Researchers assessed 298 symptomatic patients and diagnosed IBS using the Rome IV criteria, identifying 197 cases, or 66.1% of the cohort. Stool examinations found Blastocystis in 57 of those 197 patients, an infection prevalence of 28.9% within the IBS group. Parasite identification was performed by direct microscopy, while PCR with subtype-specific sequence-tagged site primers was used to classify the infections. These procedures detected two subtypes: subtype 3 accounted for 86% of Blastocystis-positive cases, and subtype 1 accounted for the remaining 14%.

To compare inflammatory responses, the investigators used a balanced random selection of 57 Blastocystis-positive IBS patients and an equal number of randomly chosen Blastocystis-negative IBS patients. Mean serum IL-8 concentration was 129.24 ± 56.28 pg/mL in the infected group, compared with 26.28 ± 9.28 pg/mL in the uninfected group. The difference was statistically significant at P < 0.001, indicating substantially elevated circulating IL-8 among the Blastocystis-positive participants. IL-8 is a chemokine involved in pro-inflammatory immune activity, making the association relevant to research on how intestinal infections may intersect with immune activation in functional gastrointestinal disorders.

The subtype analysis did not show that IL-8 concentrations differed significantly between subtype 3 and subtype 1, even though subtype 3 produced the numerically higher value. That distinction matters because subtype 3 was the predominant strain in this sample, but the study did not demonstrate a unique IL-8 response to that subtype. The authors therefore described the results as evidence of an association between Blastocystis infection and higher IL-8 in IBS rather than proof of a subtype-specific inflammatory effect.

Multivariable analysis identified younger age, diarrhea, and presentation during spring as independent predictors of Blastocystis infection. These variables were associated with the likelihood that an IBS patient carried the parasite; they do not establish that any of them caused infection or directly produced gastrointestinal symptoms. The sample was drawn from a single tertiary clinic and included symptomatic patients rather than a population-based control group. The cross-sectional comparison, modest number of infected participants, lack of longitudinal follow-up and absence of direct measurements of inflammation within the intestinal mucosa further constrain conclusions about causality.

The results add evidence to a continuing debate over whether Blastocystis has a meaningful role in IBS pathogenesis. The concentration of infections in a patient group with functional gastrointestinal symptoms and the accompanying difference in IL-8 are compatible with a potential aggravating influence, but the current data cannot establish that blastocystosis causes or worsens IBS. Distinguishing the effects of infection, subtype, host immunity, symptom pattern and other clinical characteristics will require mechanistic work and prospective studies.

The researchers also called for evaluation of local inflammatory markers to investigate immune modulation within the gut and identify molecular effectors that might connect Blastocystis with IBS. Such work would help determine whether the elevated serum IL-8 observed here reflects local intestinal activity, a broader systemic response, or another feature of the affected patients. Until those questions are resolved, the findings support a measured conclusion: Blastocystis was common among these IBS patients, subtype 3 predominated, and infection was associated with higher circulating IL-8, but the direction and mechanism of the relationship remain uncertain.

Subject of Research: Association between Blastocystis infection, subtype distribution and serum IL-8 in patients with irritable bowel syndrome

Article Title: Association of Blastocystis subtype 3 with elevated IL-8–mediated inflammation in patients with irritable bowel syndrome

Article References: Morsy, S. M., Abdeltawab, M. S. A., Mahfoz, A. M., Elkerdawy, M. A., Sallam, H. S., & Ismail, A. R. (2026). Association of Blastocystis subtype 3 with elevated IL-8–mediated inflammation in patients with irritable bowel syndrome. Gut Pathogens. https://doi.org/10.1186/s13099-026-00887-5

Image Credits: AI Generated

DOI: 10.1186/s13099-026-00887-5

Keywords: Blastocystis, irritable bowel syndrome, IL-8, intestinal parasites, inflammation, gut immunity, PCR, subtype 3, cross-sectional study, Association, subtype, elevated

Persistent organic pollutants, or POPs, are a diverse class of chemicals defined by three troubling properties: they resist degradation in the environment, they accumulate in the fatty tissues of living organisms, and they can be toxic to humans. Because they travel through food chains and persist for decades, compounds that were banned or restricted years ago still circulate in the blood of people who never directly handled them. The study focused on four major families: organochlorine pesticides such as dieldrin and heptachlor epoxide, polychlorinated biphenyls known as PCBs, polybrominated diphenyl ethers or PBDEs used as flame retardants, and per- and polyfluoroalkyl substances, the widely discussed PFAS.

The research team, led by Francesca Romana Mancini of Université Paris-Saclay, Inserm and Gustave Roussy, together with colleagues including German Cano-Sancho and Jean-Philippe Antignac of the LABERCA laboratory in Nantes and Gianluca Severi, drew on a cross-sectional sample of 468 women from the E3N-Generations cohort, a long-running French epidemiological project built on data from Inserm and supported by the Mutuelle Générale de l’Education Nationale, the Gustave Roussy Institute and the French League against Cancer. Blood samples were collected between 1994 and 1999, a period that gives researchers a window into body burdens accumulated during decades when many of these chemicals were still in active use.

What makes the study technically ambitious is its sheer analytical breadth. The researchers measured concentrations of 45 different POPs in each blood sample, alongside four circulating biomarkers of systemic inflammation: C-reactive protein, or CRP, interleukin-8, known as IL-8, monocyte chemoattractant protein-1, or MCP-1, and tumor necrosis factor-alpha, or TNF-alpha. These markers are the immune system’s chemical messengers and alarm bells. CRP, produced by the liver in response to inflammatory signals, is one of the most widely used clinical gauges of systemic inflammation, while IL-8, MCP-1 and TNF-alpha are signaling molecules involved in recruiting and activating immune cells. Chronically elevated levels of such markers have been linked in earlier research to a range of conditions, from cardiovascular disease to metabolic disorders, which is why toxicologists are keen to understand what drives them upward or downward.

The analytical strategy unfolded in two stages. First, the team applied logistic regression models to test whether individual POPs were associated with the inflammatory biomarkers, which were dichotomized, meaning participants were classified as having levels above or below a threshold. This compound-by-compound approach is the traditional way to scan for signals, but it has a well-known weakness: people are never exposed to one chemical at a time. POPs tend to travel together through food, water and the environment, so a person with high dieldrin likely carries elevated levels of related compounds too, making it hard to disentangle which agent is doing what.

To address that complexity, the researchers turned to principal component analysis, a statistical technique that compresses dozens of correlated pollutant measurements into a smaller number of composite exposure profiles. Each component represents a shared pattern of co-occurring chemicals, reflecting real-world exposure mixtures rather than isolated compounds. These derived profiles were then fed back into regression models to see whether the mixtures themselves, rather than any single pollutant, tracked with inflammation. This dual approach, examining both individual compounds and mixture-based components, is increasingly seen as the gold standard in modern exposure science, where the concept of the exposome demands that researchers grapple with chemical cocktails rather than single agents.

The results split along chemical family lines in a striking way. Several organochlorine pesticides were positively associated with CRP levels, meaning women with higher blood concentrations of these legacy insecticides tended to show more of the inflammation marker. The finding held up when the mixture-based analysis was applied, lending it weight. After the researchers applied false discovery rate correction, a statistical safeguard that accounts for the many comparisons made when dozens of chemicals are tested simultaneously, two pesticides stood out as robust: cis-heptachlor epoxide, a breakdown product of the banned insecticide heptachlor, and dieldrin, another long-restricted pesticide. That these associations survived such stringent correction suggests they are unlikely to be statistical flukes, although the cross-sectional design of the study means it cannot prove that the pollutants caused the elevated inflammation.

Just as intriguing was the pattern on the other side of the ledger. Multiple PFAS compounds were inversely associated with IL-8 concentrations, both when tested individually and as part of a shared exposure component identified by the principal component analysis. Among them, PFDA, PFNA and PFOS showed the most robust associations after false discovery rate correction. In plain terms, women with higher blood levels of these fluorinated chemicals tended to have lower levels of the IL-8 inflammatory signal. The direction of this association is notable because PFAS, often called forever chemicals due to their extreme persistence, have been implicated in a wide range of health concerns in prior research, and an inverse link with an inflammatory marker does not necessarily indicate a protective effect. Biological relationships of this kind can reflect complex interactions, including the possibility that PFAS displace other compounds, alter immune signaling in unexpected ways, or correlate with other characteristics of the study participants that the models do not fully capture.

The authors are careful about what the study can and cannot say. As a cross-sectional analysis, it captures a snapshot of pollutant levels and inflammation markers at a single point in time, so reverse causation and confounding remain possibilities. Inflammation itself can change how chemicals are distributed and stored in the body, and the researchers note that immune and inflammatory dysregulation has been proposed as a key pathway underlying the adverse health effects of POPs, a hypothesis this study helps to refine rather than definitively confirm. Still, the convergence of individual-compound and mixture-based analyses on the same signals, reinforced by false discovery rate correction, gives the findings more credibility than a simple one-off association would carry.

The broader significance lies in the study’s demonstration that mixed exposures matter. By highlighting the importance of considering both individual compounds and exposure mixtures, the work aligns with a shift in environmental health research away from single-chemical risk assessment and toward methods that reflect the reality of simultaneous, low-dose, lifelong exposure. The E3N-Generations cohort, approved by the French National Commission for Data Protection and Privacy and by the Bicêtre ethics committee, with all participants giving written informed consent including for novel biomarker testing, provided the biological foundation, while the HBM platform of LABERCA, part of the France-Exposome and EIRENE research infrastructures, delivered the analytical muscle needed to quantify 45 pollutants with the precision such comparisons demand. As regulators worldwide confront mounting pressure to address PFAS contamination and as legacy pesticides continue to persist in soils and food chains, studies like this one offer a template for understanding not just whether these chemicals are present, but what they may be doing inside us. The open-access study, published on 28 September 2026, invites both replication in other populations and longitudinal follow-up to determine whether the inflammatory signatures observed here translate into tangible health outcomes over time.

Subject of Research: Associations between blood levels of persistent organic pollutants and systemic inflammation biomarkers in French women

Article Title: Blood levels of persistent organic pollutants and circulating biomarkers of systemic inflammation in French women: evidence from the E3N-generations cohort

Article References: Mancini, F. R., Frénoy, P., Cano-Sancho, G., Marques, C., Ren, X., Perrin, C., Perduca, V., Marchand, P., Le Bizec, B., Antignac, J.-P., & Severi, G. (2026). Blood levels of persistent organic pollutants and circulating biomarkers of systemic inflammation in French women: evidence from the E3N-generations cohort. Environmental Health. https://doi.org/10.1186/s12940-026-01340-5

Image Credits: AI Generated

DOI: 10.1186/s12940-026-01340-5

Keywords: persistent organic pollutants, PFAS, organochlorine pesticides, systemic inflammation, CRP, IL-8, E3N-Generations cohort, biomarkers, chemical mixtures, dieldrin, PCBs, environmental health

The therapy belongs to a class of treatments known as CAR T-cell immunotherapy. The process begins with the collection of a patient’s own T cells, the immune system’s specialized killers. In the laboratory, those cells are genetically modified so that they carry engineered receptors capable of recognizing and binding to specific molecules on the surface of cancer cells. Once reprogrammed, the cells are expanded into large numbers and returned to the patient, where they circulate, seek out their targets and attack. The technique has already produced striking results in certain blood cancers, including leukemia and lymphoma, where engineered immune cells have driven durable remissions in patients who had exhausted every other option.

Translating that success to solid tumors such as colorectal cancer has proved far more difficult. Solid tumors are physically dense, immunologically hostile environments that engineered cells struggle to infiltrate and survive in. They deploy molecular defenses that suppress or redirect immune attacks, and they present a fundamental targeting problem: researchers must find a molecule that is abundant on cancer cells but scarce on healthy tissue, so that the therapy attacks the tumor without destroying vital organs. That targeting challenge has been one of the central obstacles holding back CAR T-cell therapy for the many cancers that form solid masses rather than circulating freely in the blood.

The CU Anschutz team believes it has found a way around that obstacle by aiming at two targets at once. The first is B7-H3, a protein found on the surface of most colorectal tumors and, importantly, on a wide range of other cancers as well. Researchers at several institutions have been investigating B7-H3 as a potential cancer target precisely because of its broad presence across tumor types. The second target is IL-8, a signaling protein that helps promote tumor growth, inflammation and the spread of cancer through the body. By simultaneously targeting B7-H3 and the IL-8 pathway, the engineered cells are designed to strike both the tumor itself and one of the biological systems it uses to grow and evade immune destruction. The researchers hope that this two-pronged strategy will give the engineered cells a better chance of overcoming the defenses that have limited earlier attempts to treat solid tumors with CAR T-cell therapy.

The dual-target design also reflects a deliberate strategic choice about which patients the therapy could eventually serve. Michael Verneris, MD, professor of pediatric oncology at CU Anschutz and program co-leader of Tumor-Host Interactions at the CU Anschutz Cancer Center, said the team wanted to move away from highly narrow approaches. “This is a very different way of thinking about how we treat cancer,” Verneris said. “We wanted to find targets that are present across many different cancers rather than developing a therapy that would only apply to a small number of patients.” If the trial demonstrates that the approach is safe and effective, the researchers say it could eventually be tested against other cancers in which these pathways play a role, including some breast, lung and ovarian cancers.

Christopher Lieu, MD, professor of medical oncology at CU Anschutz and associate director of clinical research at the CU Anschutz Cancer Center, is leading the trial. He framed the therapy as a potential alternative to the blunt instruments of conventional treatment. “Chemotherapy extends survival and helps cure people,” Lieu said. “At the same time, it’s like dropping an unguided bomb on a disease. Maybe you hit your target, but you are going to do a lot of collateral damage.” He is hoping the therapy, which has proven effective in animal models, will produce far longer-lasting results than current options typically deliver. “Immunotherapy gives us the opportunity to direct the immune system toward the cancer and potentially produce a much more durable response,” he said. The goal, he added, is not measured in months but in years.

The urgency behind the trial is underscored by troubling epidemiological trends. Colorectal cancer is increasingly affecting younger adults, with rates among people under 45 rising substantially over the past several decades while researchers continue to investigate the reasons behind the shift. For patients whose disease advances despite standard therapies, options narrow rapidly. Currently, only a small percentage of patients with colorectal and other gastrointestinal cancers qualify for certain forms of immunotherapy, because those treatments depend on specific tumor biomarkers that many patients do not have. Because B7-H3 is present in a much larger proportion of colorectal cancers, the researchers hope their approach could ultimately be applicable to a far broader patient population. “Given the number of patients we are seeing, we need new approaches,” Lieu said. But he and his colleagues are careful to note that the first step is determining whether the therapy is safe in people and whether it can effectively attack cancer in the human body, as it has in animal models.

The path from concept to clinical trial also highlights the structural advantages of the CU Anschutz campus, which brings together the university’s health professional schools, Children’s Hospital Colorado, UCHealth University of Colorado Hospital and the Gates Biomanufacturing Facility within easy walking distance of one another. The experimental cells for the trial will be manufactured at the Gates Biomanufacturing Facility, meaning the entire pipeline, from basic research to cell production to patient treatment, exists on a single campus. “The whole spectrum is right here,” Verneris said. “If we didn’t have the Gates Institute, we wouldn’t be able to make our own cells. This could have remained an interesting idea. Instead, it has become a clinical trial that could have a real impact on patients.” Philanthropic support has been essential to reaching this point, Verneris noted, because trials of this kind are expensive and private donations made it possible to move the therapy from the laboratory into patients. “We are incredibly grateful to the donors who have helped make this possible,” he said.

For the patients who enroll, the trial represents something that advanced colorectal cancer currently offers in short supply: a chance at a treatment designed to last. If the engineered cells can safely navigate the hostile terrain of solid tumors and dismantle the pathways that colorectal cancers use to grow and spread, the trial could open a new front against one of the most common and increasingly prevalent cancers, and potentially against several others beyond it. The FDA’s clearance now allows that hypothesis to be tested in the place it matters most, in the bodies of the patients the therapy was designed for.

Subject of Research: A first-in-human clinical trial of dual-target CAR T-cell immunotherapy for advanced colorectal cancer

Article Title: FDA clears CU Anschutz clinical trial using engineered immune cells to fight colorectal cancer

Article References: FDA clears CU Anschutz clinical trial using engineered immune cells to fight colorectal cancer. (n.d.). Original publication

Image Credits: AI Generated

DOI: Not provided

Keywords: CAR T-cell therapy, colorectal cancer, FDA clearance, clinical trial, immunotherapy, B7-H3, IL-8, solid tumors, CU Anschutz, pediatric cancer, engineered immune cells, Gates Biomanufacturing Facility