The research team, led by Chuanyu Yang and Veronica Ancona at the Citrus Center of Texas A&M University-Kingsville in Weslaco, together with Kranthi Mandadi of Texas A&M AgriLife Research, set out to address a gap in the understanding of how antibiotic therapy affects citrus beyond its direct antimicrobial action. Oxytetracycline trunk injection has already shown promise in reducing disease severity and improving tree health and productivity in affected groves, but the researchers hypothesized that part of its benefit might come from changes to the endophytic microbiome, the community of microorganisms that live within plant tissues without causing harm.

To test this idea, the team worked with Huanglongbing-affected grapefruit trees in a field setting. Some trees received a trunk injection of oxytetracycline at a concentration of 50,000 parts per million, while control trees were injected with water. The researchers then tracked changes in the leaf endophytic microbiome at three time points: immediately before injection, fifteen days after treatment, and forty-five days after treatment. They used 16S rDNA amplicon sequencing, a technique that reads a specific region of bacterial ribosomal DNA to identify and quantify the bacterial taxa present in each sample, giving a detailed census of the microbial community inside the leaves.

Alongside the microbiome analysis, the team measured titers of Candidatus Liberibacter asiaticus, the phloem-limited bacterium responsible for Huanglongbing, as well as a suite of agronomic traits reflecting tree health and field performance. This dual approach allowed the researchers to connect shifts in the microbial community with both pathogen burden and the physical condition of the trees over the six-week observation window.

The results confirmed that trunk injection of oxytetracycline reduced the titers of the HLB-associated pathogen, improved the field performance of treated trees, and significantly altered the composition of the leaf endophytic microbiome. But the most intriguing finding concerned the timing of microbial change. Fifteen days after treatment, the researchers observed a reduction in potentially beneficial bacteria within the leaf community. By forty-five days after injection, however, those same beneficial groups had become enriched, rebounding to higher relative abundance than before.

This temporal pattern suggests a two-phase effect. In the immediate aftermath of injection, the antibiotic appears to act broadly, suppressing susceptible bacteria including some that may be helpful to the tree. As the compound dissipates or the community reorganizes, beneficial taxa recover and expand, potentially filling ecological space vacated by the pathogen and other competitors. The researchers propose that this delayed enrichment of beneficial bacteria may be involved in the observed improvement in field performance, providing a microbiome-mediated contribution to tree recovery that extends beyond the antibiotic’s direct effect on the pathogen.

Correlation analysis strengthened this interpretation. Using Spearman correlation, the team found a significantly negative relationship between the relative abundance of two bacterial genera, Sphingomonas and Aermicrobium, and the titer of Candidatus Liberibacter asiaticus. In other words, when these genera were more abundant, the pathogen was less so. This pattern positions both genera as potential antagonists of the HLB bacterium, organisms that may compete with or actively suppress it within the leaf environment.

Sphingomonas in particular has drawn attention in plant microbiome research as a genus frequently associated with disease suppression across a range of crops. Its members are known for versatile metabolic capabilities and for colonizing plant surfaces and internal tissues. The new findings suggest that within citrus leaves, this genus and the less-studied Aermicrobium may represent natural allies whose abundance could be deliberately encouraged as part of an integrated disease management strategy.

The implications reach beyond the immediate question of antibiotic treatment. If the health benefits of oxytetracycline injection depend partly on fostering beneficial endophytes, then future approaches might aim to amplify that effect directly, for example by introducing or supporting specific bacterial strains after treatment. The study provides what the authors describe as valuable information about the interactions between the pathogen and the leaf microbiome that can be explored for developing new strategies to suppress citrus Huanglongbing, a disease for which no cure currently exists and which has devastated groves in Florida, Texas, and other production regions around the world.

The work was supported by funding from the United States Department of Agriculture’s National Institute of Food and Agriculture, Texas A&M AgriLife Research, and related internal grant programs. As Huanglongbing continues to spread and threaten citrus industries globally, understanding the microbial dimension of tree health may prove as important as targeting the pathogen itself, and this study offers one of the clearest pictures yet of how a therapeutic intervention ripples through the invisible ecosystem inside a citrus leaf.

Subject of Research: Effects of trunk-injected oxytetracycline on the leaf endophytic microbiome and health of Huanglongbing-affected citrus trees

Article Title: Trunk-injected oxytetracycline alters the leaf endophytic microbiome and promotes health recovery in Huanglongbing-affected citrus

Article References: Yang, C., Pasupuleti, L. A., Mendez, R., Kolla, T. C., Mandadi, K., & Ancona, V. (2026). Trunk-injected oxytetracycline alters the leaf endophytic microbiome and promotes health recovery in Huanglongbing-affected citrus. BMC Plant Biology. https://doi.org/10.1186/s12870-026-10179-4

Image Credits: AI Generated

DOI: 10.1186/s12870-026-10179-4

Keywords: Huanglongbing, citrus greening, oxytetracycline, endophytic microbiome, Candidatus Liberibacter asiaticus, Sphingomonas, Aermicrobium, trunk injection, citrus health, 16S rDNA sequencing, plant microbiome, BMC Plant Biology

Xijiao Dihuang Decoction, abbreviated XDD, contains four ingredients: Cornu Bubali (water buffalo horn), Rehmanniae Radix (dried tuberous root of Rehmannia glutinosa), Paeoniae Radix Rubra (root of Paeonia lactiflora), and Moutan Cortex (root bark of Paeonia suffruticosa). In traditional Chinese medicine theory, the formula clears heat, cools the blood, detoxifies, and resolves blood stasis, and it has historically been prescribed for apoplexy and febrile coma. Modern pharmacological work had already hinted at protective effects in cerebrovascular disease, including regulation of inflammation, neurogenesis, angiogenesis, and TLR4–MyD88/NF-κB signaling, but the systematic mechanisms of the complete formula against CIRI remained poorly understood. The new study set out to test a specific hypothesis: that XDD protects the brain through a coordinated chain running from the formula itself, through gut microbes and their metabolites, to neuroprotection.

The first step was to determine which of the formula’s many constituents actually reach the bloodstream. Using ultra-high-performance liquid chromatography coupled to tandem mass spectrometry on an Orbitrap Exploris 120 instrument, the researchers analyzed serum from rats dosed with XDD at ten times the human-equivalent maximum dose. They identified 54 XDD-derived circulating components, none of which appeared in blank control serum. The top 30 compounds, all confirmed at the highest identification confidence level, spanned seven chemical categories dominated by sesquiterpenoids and phenylpropanoids, with terpenoids, polyketides, alkaloids, and fatty acids also represented. Among the detected molecules were well-known plant phenolics such as epicatechin, protocatechuic acid, caffeic acid, paeoniflorin, and acteoside, with mass accuracy controlled within 5 parts per million and retention-time variation within 0.3 minutes.

With the circulating chemistry in hand, the team turned to network pharmacology to predict what those compounds might do. Cross-referencing component targets from the TCMSP, ChEMBL, and STITCH databases against 136 CIRI-related targets from GeneCards, OMIM, and the Therapeutic Target Database yielded 20 shared targets. Gene Ontology enrichment pointed to biological processes including regulation of inflammatory response, response to hypoxia, extrinsic apoptotic signaling, and epithelial cell proliferation, while KEGG analysis highlighted lipid and atherosclerosis pathways and the longevity regulating pathway. Protein–protein interaction analysis ranked AKT1 and NLRP3, a central node of the inflammasome, as the highest-degree hub targets, alongside EGR1, PTGS1, HMOX1, and CCL2. Molecular docking provided computational support: epicatechin bound AKT1 with an estimated energy of −9.131 kcal/mol and protocatechuic acid bound PTGS1 at −6.350 kcal/mol, all tested pairs falling below the −5.0 kcal/mol threshold generally considered favorable. The authors caution that these docking results remain computational predictions requiring experimental validation.

The in vivo evidence came from a rat model of focal stroke. Ninety-four Sprague–Dawley rats entered the efficacy experiment, with 79 undergoing a 90-minute middle cerebral artery occlusion followed by reperfusion via the intraluminal filament method. After excluding animals that failed the predefined neurological success criterion, 75 modeled rats were randomized to receive distilled water, the antioxidant drug edaravone as a positive control, or XDD at low, medium, or high doses of 0.95, 1.9, or 3.8 grams per kilogram by daily oral gavage for seven days, beginning one hour after reperfusion. Assessments were performed by investigators blinded to group allocation. The results were striking: high-dose XDD significantly reduced neurological deficit scores at 24 hours, and infarct volume, measured by triphenyltetrazolium chloride staining, fell by 23.56 percentage points at the medium dose and 30.27 percentage points at the high dose compared with untreated stroke rats, approaching the 32.32-point reduction achieved by edaravone.

Supporting measurements reinforced the picture. XDD lowered the elevated whole-blood and plasma viscosity characteristic of the stroke model, with the largest corrections at the high dose. Histology told a consistent story: hematoxylin–eosin and Nissl staining showed that treated animals retained denser, more organized neurons in the hippocampus and cortex, with less vacuolation, nuclear pyknosis, and Nissl body loss than untreated stroke controls. Intestinal tissue, which suffered broken villi and glandular disruption after stroke, also recovered partially with high-dose XDD. Inflammation, a key driver of secondary brain injury, was measurably restrained: serum interleukin-6 fell significantly at all three XDD doses, and interleukin-1β dropped significantly at the medium and high doses, as quantified by enzyme-linked immunosorbent assay.

The study’s most novel contribution lies in the gut. Sequencing the V3–V4 region of the bacterial 16S rRNA gene from cecal contents revealed that stroke dramatically reshaped the microbial community: alpha diversity declined, and at the phylum level Firmicutes decreased while Proteobacteria and Patescibacteria expanded, a pattern long associated with dysbiosis. At the genus level, opportunistic taxa such as Escherichia, Parabacteroides, and Klebsiella rose, while beneficial Lactobacillus, Limosilactobacillus, and Duncaniella fell. XDD partially reversed these shifts in a dose-dependent manner, with medium- and high-dose communities clustering closer to healthy controls in principal coordinates analysis. The contrast was especially sharp for Klebsiella, nearly absent in sham and high-dose treatment groups but abundant after stroke, and for Duncaniella, which showed the reverse pattern.

Metabolomics added the biochemical dimension. Untargeted liquid chromatography–mass spectrometry of cecal contents, reduced from 67,727 raw features to 41,906 after quality filtering, detected 970 metabolites significantly altered by stroke. XDD treatment produced a bidirectional corrective effect on 347 of them: 143 metabolites that rose after modeling fell with treatment, and 204 moved the opposite way. Pathway analysis tied the reversing metabolites to fatty acid degradation, glyceride metabolism, sphingolipid metabolism, and alpha-linolenic acid metabolism. Notable examples included hexadecatrienoylcarnitine, an acylcarnitine linked to mitochondrial fatty-acid transport whose accumulation can stress mitochondria; adenosine, a neuroprotective purine depleted after injury; and alpha-linolenic acid, the plant-derived omega-3 fatty acid that serves as precursor to anti-inflammatory EPA and DHA. The authors suggest these findings offer a modern biochemical reading of the formula’s traditional actions of clearing heat and resolving stasis.

Integrating the two datasets across 20 paired samples, Spearman correlation analysis with false-discovery-rate correction linked specific bacteria to specific lipids. Duncaniella, Limosilactobacillus, Schaedlerella, and Ligilactobacillus correlated positively with monogalactosyl lipids, alpha- and gamma-linolenic acid, and the endocannabinoid-like NAE(18:1), a known agonist of the anti-inflammatory nuclear receptor PPAR-alpha. Klebsiella, Blautia_A, and Escherichia showed negative correlations with the same protective metabolites, raising the possibility that pathogen overgrowth depletes beneficial lipid mediators. The authors are careful to frame these as statistical co-variation, not proof of direct interaction or causality, and they acknowledge key limitations: the study cannot establish whether microbial changes cause neuroprotection, network pharmacology relied on human databases while experiments used rats, predicted targets like AKT1 and NLRP3 were not validated at the protein level, only male rats were studied, and the microbiome sample sizes were small after quality exclusions.

Even with those caveats, the work stands as one of the more complete multi-omics portraits of how a traditional formula might act on the microbiota–gut–brain axis. It proposes a testable framework in which XDD suppresses opportunistic gut pathogens, nurtures commensals associated with anti-inflammatory lipids, normalizes energy and lipid metabolism, and thereby dampens the inflammatory and cell-death cascades that amplify brain injury after reperfusion. Future experiments using antibiotic depletion, microbiota-depleted animals, and fecal transplantation, together with protein-level validation in brain tissue, will be needed to convert correlation into causation. But if the gut-brain link holds up, an herbal prescription written more than 1,300 years ago may yet find a place in the modern stroke arsenal, not as a replacement for thrombolysis or thrombectomy, but as a multi-target adjunct aimed at the secondary injury that no single-molecule drug has fully tamed.

Subject of Research: Gut microbiota and metabolic mechanisms underlying the neuroprotective effects of Xijiao Dihuang Decoction against cerebral ischemia–reperfusion injury

Article Title: Integrated multi-omics reveals gut microbiota–metabolic mechanisms underlying the neuroprotective effects of Xijiao Dihuang Decoction against cerebral ischemia–reperfusion injury

Article References: Long, Y.-Y., Feng, Y.-J., Mao, K.-N., Song, Z.-G., Liu, Y.-C., Chen, S.-Y., Zheng, C.-X., Zeng, Y.-D., Yin, S.-T., Dai, S.-S., Li, H., & Liu, W.-H. (2026). Integrated multi-omics reveals gut microbiota–metabolic mechanisms underlying the neuroprotective effects of Xijiao Dihuang Decoction against cerebral ischemia–reperfusion injury. Frontiers in Microbiology, 17, Article 1851608. https://doi.org/10.3389/fmicb.2026.1851608

Image Credits: AI Generated

DOI: 10.3389/fmicb.2026.1851608

Keywords: cerebral ischemia–reperfusion injury, Xijiao Dihuang Decoction, gut microbiota, metabolomics, 16S rDNA sequencing, network pharmacology, molecular docking, neuroinflammation, traditional Chinese medicine, microbiota–gut–brain axis, lipid metabolism, MCAO/R rat model

Researchers at Wuhan Third Hospital in China recruited 18 children with grade IV adenoid hypertrophy, the most severe category of nasopharyngeal obstruction, between August and November 2024. Nine of the children also carried a diagnosis of allergic rhinitis, while nine did not. The team deliberately excluded children with tonsillar disease, recent respiratory infections, recent use of nasal steroids, antihistamines, or antibiotics, household smoking, pets, and unusual diets, in an effort to isolate the effect of allergy alone. Serum total IgE and reflective total nasal symptom scores were significantly higher in the allergic group, confirming the clinical distinction between the two cohorts, while age, sex, body mass index, and routine blood counts were statistically comparable.

To profile the microbial landscape, the investigators collected adenoid surface secretions under general anesthesia using sterile swabs rotated five times across the tissue, taking care to avoid contamination from the oral mucosa or saliva. Bacterial DNA was then extracted and the 16S rDNA V3-V4 region was amplified and sequenced on an Illumina NovaSeq platform, a culture-independent technique that captures organisms conventional cultivation misses. In parallel, the team performed untargeted metabolomics using ultra-performance liquid chromatography coupled with high-resolution tandem mass spectrometry, annotating compounds against the KEGG and HMDB databases.

The sequencing results revealed a striking shift in community structure. Children with allergic rhinitis showed significantly higher alpha diversity, measured by both the Chao1 richness index and the Shannon index, indicating a richer and more varied bacterial population on the adenoid surface. Principal coordinate analysis based on weighted UniFrac distances confirmed that the overall composition of the microbiota differed significantly between the two groups, with a statistical separation that was highly significant. At the phylum level, Firmicutes dominated the adenoids of children without allergy, whereas Fusobacteriota and Actinobacteriota took precedence in the allergic group.

Among the top twenty differentially abundant genera, three stood out: Fusobacterium, Actinomyces, and Veillonella were all significantly enriched in children with allergic rhinitis. Linear discriminant analysis effect size analysis reinforced these differences across every taxonomic level from phylum to species. The authors note that these same genera have been previously identified among the fifteen microbial communities characteristic of the nasopharynx, but their dominance in allergic children suggests that IgE-driven inflammation may actively reshape which bacteria colonize the adenoid biofilm.

The metabolomic analysis was equally revealing. Of the 706 metabolites identified across the 18 samples, 255 changed significantly between groups, with 140 reduced and 115 increased in the allergic cohort. Partial least squares discriminant analysis cleanly separated the two groups, and KEGG pathway enrichment pointed to twelve metabolic pathways that were significantly altered, including the biosynthesis and degradation of branched-chain amino acids such as valine, leucine, and isoleucine, the pentose phosphate pathway, glycine, serine, and threonine metabolism, aromatic amino acid biosynthesis, galactose and fructose metabolism, histidine metabolism, vitamin B6 metabolism, unsaturated fatty acid biosynthesis, and glycerophospholipid metabolism.

Perhaps the most intriguing finding came from the integration of the two datasets. Spearman correlation analysis between the three differential bacterial genera and thirty differential metabolites revealed a dense web of significant associations. Fusobacterium correlated positively with eleven metabolites and negatively with five, Veillonella correlated positively with ten and negatively with two, and Actinomyces correlated positively with fourteen and negatively with eleven. These patterns suggest that the allergic inflammatory environment does not merely change which bacteria are present but also alters what those bacteria produce, creating a feedback loop in which microbial metabolites may further stimulate adenoid immune activation and tissue growth.

The clinical implications are considerable. Adenoidectomy remains the standard treatment for severe disease, but it carries risks of bleeding and infection, and roughly 13 to 15 percent of children require a second procedure because of regrowth. Some researchers have argued that surgery offers no clear benefit for the majority of children who have both allergic rhinitis and adenoid hypertrophy. If the three bacterial genera identified here prove to be reliable biomarkers, they could eventually support non-invasive diagnosis through nasopharyngeal swabs and guide targeted anti-allergic or microbiome-directed therapies before surgery becomes necessary.

The authors are careful to acknowledge the limitations of their work. The sample size is small, the cohort was drawn from a single tertiary center rather than the general population, and the observed correlations between microbes and metabolites do not establish causation. Future studies using microbiota transplantation or longitudinal sampling will be needed to confirm whether the allergic microbiome actively drives adenoid enlargement or simply accompanies it. Nevertheless, the study provides a compelling molecular framework for a clinical observation that has puzzled pediatricians for decades, and it opens a concrete path toward interventions that target the nasopharyngeal ecosystem rather than the tissue alone.

Subject of Research: The effect of allergic rhinitis on nasopharyngeal microbiota and metabolomics in children with severe adenoid hypertrophy

Article Title: The impact of allergic rhinitis on nasopharyngeal microbiota and metabolomics in children with severe adenoid hypertrophy

Article References: Wang, B., Chen, T., Gao, S., Jin, H., Liang, G., Gong, G., & Xiao, L. (2026). The impact of allergic rhinitis on nasopharyngeal microbiota and metabolomics in children with severe adenoid hypertrophy. Frontiers in Medicine, 13, Article 1895589. https://doi.org/10.3389/fmed.2026.1895589

Image Credits: AI Generated

DOI: 10.3389/fmed.2026.1895589

Keywords: allergic rhinitis, adenoid hypertrophy, pediatric otolaryngology, microbiome, metabolomics, 16S rDNA sequencing, nasopharyngeal microbiota, IgE, impact, allergic, rhinitis, nasopharyngeal

The technical leap matters enormously. Most previous studies of the prostate microbiome relied on short-read sequencing of the 16S ribosomal DNA gene, a workhorse method that can reliably identify bacteria only down to the genus level. Because closely related species within a genus can behave very differently in the body, that resolution limit left researchers guessing about which specific organisms might matter. By sequencing the full-length 16S gene and processing the reads into amplicon sequence variants, or ASVs, the MICROPROSTK team could distinguish individual species with far greater confidence. The payoff was a catalog of remarkable breadth: across prostate biopsy samples alone, the researchers identified 22 phyla, 31 classes, 83 orders, 158 families, 330 genera, and 959 species. In total, 11,922 ASVs were characterized in prostate tissue, alongside 3,741 in urine and 15,424 in rectal samples.

The cohort itself was designed to reflect real clinical practice. All participants were men with a clinical suspicion of prostate cancer, triggered by an abnormal digital rectal examination, elevated prostate-specific antigen, or suspicious findings on magnetic resonance imaging. After excluding patients who had recently taken antibiotics, dropped out, or deviated from the protocol, the final analysis included 122 men with biopsy-confirmed prostate cancer and 113 without malignancy. In the subgroup with adequate DNA yield from all three sample types, 72 cancer patients were compared against 69 controls. The two groups were broadly similar, though cancer patients were slightly older, with a mean age of 70.0 versus 67.0 years, and had higher comorbidity scores. Notably, PSA levels did not differ significantly between the groups, underscoring the well-known limitations of that blood test and the need for complementary biomarkers.

Because prostate biopsies yield very little tissue, and therefore very little DNA, the researchers took extraordinary precautions against contamination, a notorious pitfall in low-biomass microbiome studies. Sampling procedures were standardized across all six centers, DNA extraction and sequencing followed uniform protocols, and a blank control was included in every extraction batch to monitor for stray genetic material. Stringent quality filtering and bioinformatic processing were then applied to reduce the impact of potential contaminants. Even so, the authors acknowledge that low-level residual contamination cannot be entirely excluded in studies of this kind, a caveat that applies to virtually all tissue microbiome research and one they weigh carefully in interpreting their results.

The headline finding concerns diversity. In prostate biopsies, both species richness and Shannon diversity, a standard metric that combines the number of species with how evenly they are distributed, were significantly higher in men with prostate cancer than in those without, with p-values of 0.046 and 0.019 respectively. No significant differences emerged in urine or rectal samples, although both diversity indices trended higher in cancer patients across all sample types. Intriguingly, beta diversity analyses, which assess whether whole microbial communities differ in composition, showed no significant separation between cancer and non-cancer patients in any sample type. But the beta diversity comparisons did confirm something else important: the prostate, urine, and rectum each harbor clearly distinct microbial communities, reinforcing the idea that the prostate hosts its own resident ecosystem rather than merely collecting bacteria drifting in from neighboring sites.

When the researchers drilled down to which bacteria were actually enriched in cancerous tissue, a distinctive pattern emerged. At the phylum level, Synergistota stood out as significantly more abundant in prostate cancer patients. At the genus level, Bacteroides, Agathobacter, Ruminococcus, Cutibacterium, and Lachnoclostridium were enriched in cancer tissue, while Chryseobacterium was more abundant in non-cancer samples. The species-level results were even more striking: Eubacterium rectale, Cutibacterium acnes, Bacteroides dorei, Ruminococcus torques, Bacteroides massiliensis, Ruminococcus lactaris, Eubacterium halii, Bilophila wadsworthia, Clostridium disporicum, and Clostridium spiroforme were all significantly enriched in prostate cancer patients. Five of these species, E. rectale, C. acnes, B. dorei, L. reuteri, and R. torques, showed mean relative abundances above one percent in at least one of the two groups, marking them as the strongest candidates for future validation.

Some of these organisms carry compelling biological backstories. Cutibacterium acnes, formerly known as Propionibacterium acnes, has been repeatedly detected in prostate tissue in prior studies and is known to provoke chronic inflammation and modulate immune responses. Mouse models using human prostate cancer-derived isolates of the bacterium have induced chronic prostatic inflammation, and laboratory work suggests the organism can induce immunosuppressive gene expression in macrophages and even invade prostate epithelial cells. Eubacterium rectale, meanwhile, has been implicated in inflammation-related colorectal carcinogenesis, raising the speculative but tantalizing question of whether similar mechanisms could operate in the prostate. On the protective side of the ledger, Lactobacillus reuteri was significantly more abundant in the non-cancer group, and this species has documented anti-inflammatory properties, including the production of reuterin, a compound shown in other work to suppress colorectal cancer growth by altering redox balance in cells.

The study’s design carries inherent limitations that the authors confront directly. Every participant received a single oral dose of the antibiotic ciprofloxacin two hours before biopsy as standard prophylaxis, a uniform exposure across both groups that may nonetheless have altered microbial composition. Because taking prostate biopsies from healthy men is not ethically justifiable, the comparison group consisted of men biopsied for suspected cancer whose histology showed no malignancy, a clinically relevant but imperfect control group that included some patients with prostatitis or benign prostatic abnormalities. The predominance of low-grade tumors, with ISUP grade 1 accounting for roughly 41 percent of cancers, means the findings mainly reflect early-stage disease, which is ideal for biomarker discovery but may not extend to aggressive cancers. And because the study was cross-sectional, capturing a single moment in time, it cannot determine whether the observed microbial differences contribute to cancer development or merely accompany it.

What comes next could determine whether this research translates into clinical tools. The team proposes validating the bacterial signatures with species-specific quantitative PCR and culturomics on prostate tissue, then extending the search to urine and rectal samples, specimens that can be collected without a needle in the prostate. If microbial signatures reliably detectable in urine track with the tissue findings, the door opens to non-invasive screening tests that could complement PSA, MRI, and biopsy. Functional studies in laboratory and animal models will then be needed to establish whether the enriched bacteria actively drive tumorigenesis or simply flourish in the altered environment of a tumor. Prostate cancer remains the second most frequently diagnosed cancer in men worldwide and the fifth leading cause of cancer death, with an estimated 473,011 new cases and 115,182 deaths in Europe alone in 2022. No specific prevention strategy can currently be recommended, and existing treatments, however effective, often compromise sexual function and quality of life. Against that backdrop, the idea that a handful of bacterial species, some potentially targetable with antibiotics, probiotics, or other interventions, might influence prostate cancer risk represents one of the most consequential open questions in urological oncology today.

Subject of Research: Prostate tissue microbiota dysbiosis and its association with prostate cancer

Article Title: Prostate tissue microbiota dysbiosis associated with prostate cancer: results from the MICROPROSTK multicenter study

Article References: Lotte, R., Gaudart, A., Cruzel, C., Droupy, S., Lavigne, J., Bruyère, F., Lanotte, P., Lechevallier, E., Dubourg, G., Fournier, P., Haider, R., Lotte, L., Youssef, K., Emery, A., Madany, R., Payen, M., Pfauwadel, L., Tibi, B., Ahallal, Y., … Ruimy, R. (2026). Prostate tissue microbiota dysbiosis associated with prostate cancer: results from the MICROPROSTK multicenter study. New Microbes and New Infections, Article 101862. https://doi.org/10.1016/j.nmni.2026.101862

Image Credits: AI Generated

DOI: 10.1016/j.nmni.2026.101862

Keywords: prostate cancer, microbiota, dysbiosis, 16S rDNA sequencing, Cutibacterium acnes, Eubacterium rectale, Lactobacillus reuteri, MICROPROSTK, biomarkers, urinary microbiome, inflammation, multicenter study

Rice blast has long been regarded as the most important fungal disease of rice, a staple crop that feeds roughly half of the global population. The pathogen, Magnaporthe oryzae, infects leaves, stems, and panicles, producing the characteristic diamond-shaped lesions that can decimate yields under favorable humid conditions. Conventional control relies heavily on fungicide applications and the deployment of resistance genes in cultivars, but the fungus is notorious for its adaptive capacity, repeatedly overcoming single resistance genes in the field. This has driven scientists to look beyond the plant’s own genome for partners in defense, and the rhizosphere microbiome has emerged as a compelling frontier.

The rhizosphere—the narrow zone of soil influenced by root exudates—harbors some of the densest and most metabolically active microbial communities on Earth. Plant roots actively recruit and nourish specific microbes through the release of sugars, organic acids, and signaling compounds, and in return, certain bacteria can suppress pathogens, modulate plant hormones, or prime immune responses. Whether the rhizosphere communities of disease-resistant rice cultivars are fundamentally different from those of susceptible ones, and how those communities respond when the blast pathogen attacks, had remained incompletely resolved. The new greenhouse study set out to answer precisely those questions.

The research team, led by Tingting Yang and Di Han of the College of Plant Protection at Shenyang Agricultural University, together with colleagues at Liaoning Academy of Agricultural Sciences, grew blast-resistant and blast-susceptible rice cultivars under controlled greenhouse conditions and compared their rhizobacterial communities both before and after challenge with M. oryzae. Using 16S rDNA amplicon sequencing—a technique that catalogs bacterial taxa by amplifying a conserved genetic marker—they profiled the diversity and composition of the root-associated bacteria across the experimental treatments.

The sequencing results revealed statistically significant differences in rhizobacterial diversity and community composition between resistant and susceptible cultivars, confirming that the plant genotype leaves a measurable imprint on which bacteria congregate around its roots. More striking was what happened after pathogen infection: both cultivar types underwent distinct community shifts, but the direction and magnitude of those shifts differed between resistant and susceptible plants. The researchers detected differential microbial enrichment patterns across cultivars and disease states, indicating that the rhizosphere is not a passive bystander in the rice–blast interaction but a dynamic environment that responds to both plant genotype and pathogen pressure.

Among the taxa whose abundance changed, one genus stood out. Bacillus species were consistently enriched in the rhizospheres of healthy plants of resistant cultivars and, tellingly, in infected plants of susceptible cultivars. This dual pattern suggests that Bacillus populations may be associated with disease status in both contexts—either helping to maintain health in resistant plants or responding to infection in susceptible ones. Bacillus species are well known in agricultural microbiology for their ability to produce antimicrobial compounds, form protective biofilms on roots, and induce systemic resistance in host plants, which makes their enrichment patterns particularly noteworthy for biocontrol-oriented research.

To probe the structure of these microbial communities more deeply, the team applied network analysis, a computational approach that maps co-occurrence and potential ecological interactions among taxa. The analysis showed that cultivar resistance was associated with measurable differences in the architecture of the rhizosphere microbial community. In practical terms, resistant and susceptible rice varieties appear to host rhizobacterial networks with different organization, hinting that community structure—not merely the presence or absence of particular species—may contribute to the disease-suppressive potential of the root environment.

The study then moved from community profiling to the isolation and characterization of individual candidates. From the rhizosphere of healthy rice plants, the researchers recovered a bacterial strain designated Bacillus velezensis H2. The strain was characterized through a combination of morphological and biochemical tests, 16S rRNA gene sequencing, and single-nucleotide polymorphism (SNP) profiling to confirm its taxonomic identity. B. velezensis is a species that has attracted considerable attention in biocontrol research because many of its strains carry extensive biosynthetic machinery for antimicrobial secondary metabolites.

Whole-genome analysis using the antiSMASH platform—an algorithmic pipeline that scans bacterial genomes for biosynthetic gene clusters—identified multiple clusters in the H2 genome involved in secondary metabolite production. Among these were genes encoding nonribosomal peptide synthetases, the giant multifunctional enzymes responsible for assembling many of the lipopeptide antibiotics that Bacillus species are famous for, such as members of the surfactin, iturin, and fengycin families. The presence of these clusters provides a genomic rationale for the strain’s observed biological activity and suggests that H2 is genetically equipped to interfere with fungal pathogens in the root zone.

Laboratory assays confirmed that promise in practice. In vitro tests demonstrated that B. velezensis H2 exhibits strong antifungal activity against Magnaporthe oryzae, directly inhibiting the growth of the blast pathogen. While in vitro inhibition does not guarantee field-level disease suppression—greenhouse and field validation remain essential next steps—the combination of rhizosphere origin, rich biosynthetic potential, and demonstrable antagonism makes H2 a compelling candidate for development as a biocontrol agent. If it can colonize rice roots effectively and express its antifungal arsenal under realistic soil conditions, it could contribute to reducing the chemical fungicide burden in rice production systems.

The broader significance of the study lies in its integrated perspective. Rather than treating plant immunity and the microbiome as separate domains, the work links cultivar resistance, rhizobacterial community structure, pathogen-induced shifts, and a concrete antagonistic isolate into a single narrative. It reinforces a growing consensus in plant pathology: breeding for resistance and engineering beneficial microbiomes may be complementary strategies. Rice blast remains a moving target, but evidence that resistant cultivars cultivate distinct and potentially protective bacterial communities—and that strains like B. velezensis H2 can directly oppose the pathogen—offers a scientifically grounded path toward more sustainable, microbiome-aware crop protection.

Subject of Research: Rhizosphere bacterial community shifts in rice blast-resistant cultivars and the antagonistic activity of Bacillus velezensis against the rice blast pathogen

Article Title: Rhizosphere Bacterial Community Shifts in Rice Blast–Resistant Cultivars and the Antagonistic Activity of Bacillus velezensis

Article References: Yang, T., Han, D., Ding, A., Du, S., Wang, W., Huang, Y., & Ahsan, T. (2026). Rhizosphere Bacterial Community Shifts in Rice Blast–Resistant Cultivars and the Antagonistic Activity of Bacillus velezensis. Microbial Ecology. https://doi.org/10.1007/s00248-026-02858-4

Image Credits: AI Generated

DOI: 10.1007/s00248-026-02858-4

Keywords: rhizosphere microbiome, rice blast disease, Bacillus velezensis, Magnaporthe oryzae, biocontrol, 16S rDNA sequencing, secondary metabolites, nonribosomal peptide synthetases, antiSMASH, disease resistance, Rhizosphere, Bacterial