The newts were collected in June 2017 from temporary ponds on the periphery of Jena, with permission from the city’s nature conservation authority. Two females and three males, all in their aquatic stage, were brought to the laboratory of the Zoological Institute of the University of Jena. The original aim of the study had nothing to do with parasites at all: the researchers wanted to understand how the feeding system of the species works. Only when the specimens were prepared for detailed anatomical analysis did the ciliates come to light, clinging in remarkable numbers to the lining of the animals’ mouths and throats.

To document the finding, the team employed two complementary techniques. For histological investigation, one male and one female newt were preserved in Bouin’s solution for two months, with the solution changed weekly. After decalcification, the samples were dehydrated in a graded ethanol-isopropanol series, embedded in paraffin, and cut into seven-micrometer semi-serial sections using rotatory microtomes. The sections were stained with periodic acid Schiff and a combination of hematoxylin-eosin, then examined under a light microscope. For scanning electron microscopy, three additional newts were processed: the floor of the mouth was removed and fixed in modified Karnovsky solution for eighteen hours, postfixed in osmium tetroxide, treated with dilute hydrochloric acid to wash mucus from the surface, dehydrated, critically point dried, gold-coated, and imaged in a scanning electron microscope.

Both methods revealed the same striking picture. The ciliate zooids were firmly attached to the oral epithelium and abundant throughout the oral cavity. The greatest concentration, roughly fifteen zooids per fifty square micrometers, occurred on the dorsal surface of the tongue. Under the scanning electron microscope, the ciliates appeared funnel-shaped, each with a narrow stalk anchoring it to the epithelial substrate and a broad peristomal disc fringed with numerous cilia. Horizontal annular striations, running perpendicular to the newt’s body axis, were clearly visible on the zooids. Histological sections showed granular structures within the ciliate bodies that stained positive for both alcian blue and periodic acid Schiff. Based on these morphological features, the researchers assigned the protists to the phylum Ciliophora, subclass Peritrichia, order Peritrichida, suborder Sessilina, genus Apiosoma.

Sessilid peritrich ciliates are no strangers to aquatic animals. They live as epibionts on a wide variety of aquatic invertebrates and also occur on vertebrates. Some species act as commensals, others as ectoparasites, and heavy infestations can even prove fatal to the host. Among amphibians, the best-documented peritrichs are the trichodinids, which inhabit the gills and skin of aquatic species and have occasionally been detected as endoparasites. Sessile peritrichs are well known as fish parasites, colonizing the body surface and gills. Historical accounts stretch back a century: as early as 1924, researchers reported various peritrich genera, including Vorticella, Opercularia, Rhabdostyla, and Epistylis, on the skin and gills of anuran larvae, some apparently restricted to the tadpole surface. In 1982, seven peritrich species were found on the skin of agile frog tadpoles, and one species, Apiosoma tintinnabulum, was recorded on the skin of the smooth newt itself.

What makes the new finding unusual is the location. Ciliates on skin and gills have been described many times, but a heavy infestation inside the oropharyngeal cavity of an amphibian is a rarely documented phenomenon. The researchers suggest such infestations may in fact be frequently overlooked, because the ciliates are invisible to the naked eye and the elaborate laboratory methods needed to detect them are rarely available in field studies. Without histology or electron microscopy, an infested newt would look perfectly normal even as its mouth harbored thousands of protists.

The ecological implications may be considerable, and here the study moves from observation to hypothesis. Smooth newts rely on water-dependent mechanisms for capturing prey and transporting it within the mouth during their aquatic phase. Like other vertebrates that feed by suction underwater, they lack prominent structures in the oropharynx, because anything protruding into the mouth can disrupt the rapid intraoral water flow on which suction feeding depends. Efficient suction feeding demands smooth, streamlined internal anatomy.

Smooth newts, in fact, display a remarkable form of phenotypic flexibility that makes this point vividly. During their aquatic season, their tongue surface is smooth, an adaptation thought to benefit underwater suction feeding. When they migrate to land, they grow a carpet of densely packed longitudinal lingual papillae, which presumably aids terrestrial feeding by helping grip prey. The seasonal transformation of the tongue is a textbook example of how morphology tracks ecological function. But the infested newts from Jena complicate this elegant picture: the ciliates covering their tongues were about the same size as the dorsal lingual papillae the animals would develop in their terrestrial stage. In effect, the protists had manufactured a papillae-like texture on a tongue that should have been hydrodynamically smooth.

The researchers hypothesize that this massive infestation functionally counteracts the newts’ sophisticated seasonal flexibility. A smooth tongue surface provides hydrodynamic benefits for suction feeding; cover it with numerous relatively large ciliates, and the water flows during suction may be disrupted. The densely packed zooids could cause drag within the waterflow in the bidirectional feeding situation characteristic of salamanders, and they may induce turbulent microflows within the lingual portion of the mouth. In practical terms, a newt whose tongue is carpeted with ciliates might suck water less efficiently, capture prey less successfully, and suffer reduced ecological performance — all without any visible sign of disease.

For fish, the consequences of external ciliate infestations are better understood: affected tissue on the skin and gills may produce excess mucus, and afflicted animals show loss of condition and characteristic behaviors such as flashing and piping. Researchers have also noted that the presence of numerous parasitic ciliates can signal deteriorated water quality, making these protists useful bioindicators. Whether the oropharyngeal Apiosoma of the Jena newts indicate something about the condition of their temporary ponds, or simply reflect an underappreciated and widespread phenomenon, remains open. What is clear is that a whole layer of amphibian–protist interaction may have been hiding in plain sight, inside the mouths of animals that scientists have studied for generations, visible only when the right microscopes are pointed at the right surfaces. As the authors conclude, an oropharyngeal cavity packed with ciliates is a phenomenon that deserves far more attention than it has ever received.

Subject of Research: Sessile peritrich ciliates of the genus Apiosoma colonizing the oropharyngeal cavity of smooth newts

Article Title: On the presence of the sessilid peritrich Apiosoma in the oro-pharynx of Lissotriton vulgaris ( Urodela , Vertebrata )

Article References: Natchev, N., & Heiss, E. (2026). On the presence of the sessilid peritrich Apiosoma in the oro-pharynx of Lissotriton vulgaris (Urodela, Vertebrata). Herpetozoa, 39, 23-26. https://doi.org/10.3897/herpetozoa.39.e173880

Image Credits: AI Generated

DOI: 10.3897/herpetozoa.39.e173880

Keywords: Apiosoma, smooth newt, Lissotriton vulgaris, peritrich ciliates, oropharynx, suction feeding, histology, scanning electron microscopy, amphibian parasites, phenotypic flexibility, tongue papillae, Germany

Respiratory viral infections remain a leading global cause of illness and death, with influenza virus alone responsible for an estimated 3 to 5 million severe cases and up to 650,000 deaths each year. Older adults bear a disproportionate share of this burden, experiencing substantially higher mortality than younger populations. Vaccination remains the main strategy to reduce influenza disease, but its effectiveness in people aged 60 and older is markedly lower than in younger adults, with most studies reporting protection of roughly 20 to 50 percent in older individuals compared with 60 to 90 percent in younger groups. This gap has created an urgent need for approaches that safeguard aging populations against influenza and other respiratory infections, and the upper respiratory tract microbiota has emerged as a promising target.

The human respiratory tract is divided into upper and lower compartments. The upper tract includes the anterior nares, nasal passages, paranasal sinuses, nasopharynx, and oropharynx, while the lower tract comprises the larynx, trachea, bronchi, and alveoli. Because the upper tract is the primary entry point for inhaled air and hosts the highest microbial density, it acts as a gatekeeper to the lower airways. Within it, the nasopharynx and oropharynx provide distinct environments shaped by immune activity, mucus flow, temperature, tissue architecture, and cell composition. Bacterial biomass varies dramatically by site, with around 1,000 bacteria in the nasopharynx and up to 1 million in the oropharynx. Disruption of these ecosystems by viral infection can reduce colonization resistance, worsen local inflammatory responses, and facilitate the spread of pathogens into the lower respiratory tract, leading to more severe disease.

Although the role of the upper-airway microbiome in respiratory health is increasingly recognized, evidence on how aging shapes these communities remains limited. Studies in older adults have shown reduced oropharyngeal diversity, changes in community composition, and a loss of niche distinctness compared with younger individuals. These age-related shifts are discussed in relation to immunosenescence and chronic low-grade inflammation and may contribute to the higher burden of respiratory infections in older adults. However, little has been known about upper-airway microbiota dynamics during acute respiratory illness in this population and its interaction with the host, leaving an important gap in understanding infection risk and resilience.

To address this gap, Kool and colleagues analyzed nasopharyngeal and oropharyngeal swabs from 221 participants aged 60 to 88, including 136 who experienced influenza-like illness during the 2014-2015 season and 85 who reported no symptoms and had no detectable respiratory pathogens at the time of sampling. The researchers characterized microbial composition, bacterial load, and cytokine patterns in a healthy state and determined the impact of acute infection. Influenza-like illness was defined according to the Dutch Pel criteria, which categorize individuals as having the condition based on the presence of fever of at least 37.8 degrees Celsius and at least one additional symptom such as headache, myalgia, sore throat, coughing, rhinitis, or chest pain. Swabs were collected within 72 hours of reported symptoms, and the causative viruses and bacteria were identified using multiplex ligation-dependent probe amplification and conventional bacterial culture.

Cluster analyses of the nasopharyngeal samples revealed three distinct community state types based on their dominant genera. The first was dominated by Moraxella, the second was characterized by Haemophilus, Staphylococcus, and Streptococcus, and the third was dominated by Corynebacterium and Dolosigranulum. The Moraxella-dominated cluster had the lowest diversity and evenness, while the other two were the most diverse. Beta-diversity analysis based on Bray-Curtis dissimilarity demonstrated clear separation between the three clusters, confirmed by permutational analysis of variance with an R-squared of 0.41 and a p value of 0.001. In contrast, no meaningful clustering structure was identified in the oropharyngeal samples, suggesting that the two niches have fundamentally different microbial ecosystems.

When the researchers compared healthy and infected individuals, they found that nasopharyngeal microbiome composition differed significantly between the two groups, with a PERMANOVA R-squared of 0.025 and a p value of 0.002, while no differences were observed in the oropharyngeal microbiome. Infected individuals were significantly more frequently found in the Moraxella-dominated and mixed clusters, with 73 percent and 69 percent infected samples respectively, whereas the Corynebacterium and Dolosigranulum-dominated cluster contained an equal mix of healthy and infected individuals. Genus-level differential-abundance analysis revealed that Corynebacterium and Dolosigranulum were more abundant in healthy individuals, while Streptococcus and Haemophilus were more abundant in infected individuals. Together, these findings suggest that the nasopharynx, rather than the oropharynx, is the most reflective niche for compositional change during acute infection.

The immune response mirrored this site specificity. In nasopharyngeal samples, infection was associated with a broad local response, with pro-inflammatory and innate immune markers such as IL-6, CXCL8, CCL2, and CXCL5, antiviral and interferon-associated markers including CXCL9, CXCL10, IFN-lambda1, and granzyme A, the tissue remodeling marker CRP, and the B cell survival factor APRIL all higher in infected individuals. In contrast, the oropharyngeal niche showed only limited changes, with only B-cell activating factor and CRP increased in infected individuals. Systemically, infected individuals had higher levels of pro-inflammatory markers, antiviral and interferon-associated chemokines, and the regulatory cytokine IL-10, while eotaxin, a chemokine associated with eosinophil recruitment and allergic inflammation, was higher in healthy individuals.

To probe the host-microbe interaction, the researchers constructed a network of cytokines identified as increased in infected individuals and the bacterial genera significantly associated with them. Among the genera enriched in infected participants, Haemophilus was positively associated with IL-6 and CXCL10, Streptococcus was positively linked to CXCL9, IL-6, and CXCL10, and Moraxella showed a positive link with CXCL10. In contrast, genera enriched in healthy participants showed only negative associations. Corynebacterium was negatively associated with IL-6, CXCL9, and CXCL10, while Staphylococcus was negatively linked to granzyme A, CXCL9, and CXCL10. This negative association suggests that Corynebacterium is linked to lower local inflammation, consistent with its association with the healthy, Corynebacterium and Dolosigranulum-dominated microbiome.

The nasopharyngeal community composition was also associated with clinical features and symptom burden. The Corynebacterium and Dolosigranulum-dominated cluster was associated with significantly lower odds of several respiratory symptoms, including influenza-like illness symptoms and fever, cough, sore throat, and nasal symptoms. In contrast, the Moraxella-dominated cluster was associated with significantly higher odds of nasal symptoms only, and the mixed cluster showed no significant associations with any symptom. These findings suggest that community membership is more consistently related to local, nasal symptoms than to systemic symptoms. At the genus level, a higher number of cumulative bacterial pathogens detected was positively associated with Haemophilus, while a higher number of total and viral pathogens detected was negatively associated with Corynebacterium. Smoking was positively associated with Porphyromonas and negatively associated with Corynebacterium, aligning with previous reports that Corynebacterium is underrepresented in the nasopharyngeal microbiota of smokers.

Perhaps most strikingly, the researchers found that nasopharyngeal immune responses remained elevated 7 to 9 weeks after infection. Several markers, including IL-6, CRP, IP-10, IL-1Ra, IFN-gamma, and IL-10, remained elevated when compared with healthy controls, indicating ongoing immune activation. Although effect sizes were smaller than in the acute phase and fewer markers reached statistical significance after adjustment, immune levels had not returned to those observed in healthy individuals. A distance-to-healthy centroid analysis showed that most participants moved closer to healthy immune profiles between the acute and recovery visits, but recovery samples remained distinct from healthy controls, indicating that immune normalization was partial rather than complete. This suggests that local immune recovery in the nasopharynx is slower than symptom resolution after acute infection.

The study’s authors note that persistent immune activation at mucosal sites may reflect several biological processes. Epithelial repair and restoration of barrier integrity can require sustained chemokine signaling, residual viral RNA or antigen may continue to stimulate low-level innate responses even after symptoms decline, and immune cell populations recruited during acute infection may remain locally active during resolution. Prolonged but declining interferon and chemokine signaling in the upper airway has been described in both experimental and natural human influenza infection. Such prolonged, microbiome-associated immune activation may delay full recovery of mucosal balance and thereby increase the risk of secondary bacterial infections, particularly in older adults and other vulnerable groups.

These findings show that influenza-like illness in older adults is associated with site-specific immune and microbiome responses in the upper respiratory tract. The nasopharynx emerged as the primary site of biological change, characterized by strong local innate immune activation and associations between specific genera and inflammatory mediators. Communities enriched in infected individuals, including those characterized by Moraxella, Haemophilus, and Streptococcus, were linked to higher levels of pro-inflammatory and interferon-related cytokines, while Corynebacterium and Dolosigranulum-associated communities were linked to lower inflammatory signatures and reduced symptom burden. The oropharyngeal niche showed comparatively limited immune and microbiome changes during infection, suggesting functional specialization between upper airway niches. While the nasopharynx reflected early antiviral immune activation, the oropharynx appeared more stable at both the microbial and immune level, possibly attributed to daily influences such as saliva flow, food intake, and oral hygiene practices that promote resilience and prevent dysbiosis.

More broadly, these results highlight the importance of considering anatomical niche when studying respiratory infections in aging populations, as immune responses and microbial associations differ between the nasopharynx and oropharynx. The results also emphasize the need to monitor mucosal immune responses beyond the acute phase, as prolonged immune activation may delay the restoration of immune and microbial homeostasis and increase susceptibility to secondary infections, particularly in older individuals. Ultimately, identifying microbiome-immune patterns may help enable early risk stratification and more effective preventive strategies in older adults, a population for whom current vaccination approaches leave substantial room for improvement.

Subject of Research: Immunology

Article Title: Linking nasopharyngeal and oropharyngeal microbiota to immune responses during influenza-like illness in an aging population

Article References: Kool, J., Konstanti, P., van Dijken, H., Chu, M. L. J. N., Nanlohy, N. M., Bijvank, E., van Woudenbergh, E., van Beek, J., van Baarle, D., & Fuentes, S. (2026). Linking nasopharyngeal and oropharyngeal microbiota to immune responses during influenza-like illness in an aging population. iScience, 29(11), Article 117929. https://doi.org/10.1016/j.isci.2026.117929

Image Credits: AI Generated

DOI: 10.1016/j.isci.2026.117929

Keywords: microbiome, influenza, aging, nasopharynx, oropharynx, immune response, respiratory infection, immunosenescence, Corynebacterium, Dolosigranulum, Linking, nasopharyngeal

The original study that prompted the correspondence, conducted by Hudson and colleagues and published in the same journal, examined the microbial communities of children diagnosed with obstructive sleep apnea and children with primary snoring, comparing them against the microbial signatures found in their throats and intestines. The headline finding was twofold. First, the oropharynx, the region at the back of the mouth where the soft palate, tonsils, and tongue base conspire to block airflow during apneic events, showed dysbiosis, a disturbance of the normally balanced microbial ecosystem. Second, the gastrointestinal tract displayed a milder but still detectable compositional imbalance, suggesting that the microbial consequences of disordered breathing during sleep may not be confined to the airway alone.

That dual-site finding is what makes the study scientifically provocative. The oropharynx is the obvious suspect in sleep-disordered breathing, since it is the anatomical battleground where airway collapse occurs. But the gut connection is less intuitive and more tantalizing. Microbes swallowed in saliva continuously seed the gut, and inflammatory signals generated in inflamed airway tissue can ripple systemically through the bloodstream. A growing body of research has shown that oral taxa can enrich the lung microbiome in ways associated with a Th17-skewed inflammatory phenotype, as Segal and colleagues reported in Nature Microbiology, demonstrating that microbes originating in the mouth can travel and reshape immune behavior at distant mucosal sites. If snoring children carry a subtly different gut microbial portfolio, the question becomes whether that difference is a cause, a consequence, or merely a microbial echo of the sleep disorder itself.

Min’s correspondence engages with this question from the vantage point of an otolaryngologist who has previously published on the adenotonsillar microbiome. In earlier work with Kim, published in Clinical and Experimental Otorhinolaryngology, Min examined correlations between the microbiome of the adenoids and tonsils and the clinical characteristics of pediatric patients who snore. That line of investigation matters because the adenoids and tonsils are not passive bystanders in childhood sleep apnea; they are the most common anatomical cause of airway obstruction in snoring children and the usual target of adenotonsillectomy, the standard surgical treatment. If the immune tissues of the throat harbor a distinctive microbial community in children who snore, the microbiome could plausibly influence the inflammatory state of those tissues, their tendency to enlarge, and their contribution to airway collapse.

The correspondence also arrives amid a broader scientific reckoning with how environmental factors sculpt the human microbiome. David and colleagues demonstrated in Nature in 2014 that diet rapidly and reproducibly alters the human gut microbiome, shifting the relative abundance of microbial species within days of a dietary change. Shaw and colleagues showed in mBio in 2017 that the human salivary microbiome is shaped more by shared environment than by genetics, drawing on evidence from a large family of closely related individuals. These findings cut both ways for sleep apnea research. On one hand, they suggest that household factors such as shared meals, shared bedrooms, and shared microbial exposures could confound apparent associations between sleep disorders and microbial profiles. On the other hand, they reinforce the plausibility of a genuine link, because the same environmental variables that shape a child’s microbiome, including diet, allergen exposure, and household infections, also influence airway inflammation and adenotonsillar tissue growth.

Nasal and upper airway microbiology adds further context. Yan and colleagues, writing in Cell Host and Microbe, showed that nasal microenvironments and interspecific interactions influence the complexity of nasal microbiota and the carriage of Staphylococcus aureus, underscoring how finely structured these communities are even within the small geography of the nose. Choi and colleagues reported in Allergy that patients with chronic rhinosinusitis show decreased diversity of nasal microbiota and of the extracellular vesicles those microbes secrete, linking reduced microbial diversity to chronic inflammatory disease of the airways. Reduced diversity is a recurring theme in dysbiosis research across body sites, and the oropharyngeal findings in snoring children fit that pattern, raising the possibility that a less diverse throat community might both reflect and reinforce the chronic inflammation that accompanies repeated nighttime oxygen desaturation and arousals.

The mechanistic stakes are considerable. Obstructive sleep apnea in children is not a benign habit but a condition associated with daytime inattention, behavioral problems, impaired growth, and cardiovascular strain. Current diagnosis relies on overnight polysomnography, a resource-intensive test, and treatment hinges on surgery or, in some cases, continuous positive airway pressure. If microbial markers in the throat or gut could help identify children at risk, or if microbial dysbiosis turned out to contribute to airway inflammation and tissue hypertrophy, the field would gain both a potential screening tool and a novel therapeutic target. Probiotic or dietary interventions that reshape the gut and oral microbiomes are already being explored for other inflammatory conditions, and the correspondence implicitly asks whether such approaches deserve systematic study in pediatric sleep medicine.

Yet the correspondence also serves as a reminder of how much caution the microbiome field demands. Associations between microbial composition and disease are notoriously vulnerable to confounding by antibiotics, diet, age, geography, and sampling technique. The salivary microbiome’s sensitivity to shared environment means that siblings in the same household can carry strikingly similar oral communities regardless of their genetics, so any study comparing snoring children with non-snoring controls must carefully account for household clustering. The mildness of the gastrointestinal imbalance reported in the original study, described explicitly as a mild compositional imbalance, suggests an effect that is real but subtle, the kind of signal that requires replication in independent cohorts before it can be translated into clinical practice. Min’s letter, by engaging critically with the findings rather than simply endorsing them, exemplifies the kind of scholarly scrutiny that determines which microbiome associations survive replication.

What emerges from this exchange is a picture of pediatric sleep medicine slowly absorbing the lessons of the microbiome era. The airway is no longer viewed as a sterile tube that occasionally gets blocked by oversized tonsils; it is a living ecological interface where bacteria, immune cells, airflow, and inflammation interact continuously. The gut is no longer seen as anatomically remote from the throat; it is connected by the constant downward flow of swallowed saliva and by circulating immune mediators. The correspondence by Min, published as volume 22, article 104 of the Journal of Clinical Sleep Medicine, does not resolve whether microbes help drive childhood sleep apnea, but it sharpens the questions that the next generation of studies must answer: which specific taxa change, whether the changes precede the disorder or follow it, whether they track disease severity, and whether correcting them could help a snoring child breathe, sleep, and grow more easily. For now, the microbial trail from throat to gut in snoring children remains an open and actively contested frontier.

Subject of Research: The association between pediatric obstructive sleep apnea, primary snoring, and oropharyngeal and gastrointestinal microbiome dysbiosis

Article Title: Correspondence regarding “Obstructive sleep apnea and primary snoring in children are associated with oropharyngeal dysbiosis and a mild compositional imbalance in the gastrointestinal tract”

Article References: Min, H. J. (2026). Correspondence regarding “Obstructive sleep apnea and primary snoring in children are associated with oropharyngeal dysbiosis and a mild compositional imbalance in the gastrointestinal tract”. Journal of Clinical Sleep Medicine, 22(1), Article 104. https://doi.org/10.1007/s44470-026-00112-9

Image Credits: AI Generated

DOI: 10.1007/s44470-026-00112-9

Keywords: obstructive sleep apnea, primary snoring, children, microbiome, dysbiosis, oropharynx, gut microbiota, adenotonsillar microbiome, sleep-disordered breathing, pediatric sleep medicine, inflammation, Journal of Clinical Sleep Medicine