Alimentary Pharmacology & Therapeutics, Journal Year: 2025, Volume and Issue: unknown
Published: April 10, 2025
Language: Английский
Alimentary Pharmacology & Therapeutics, Journal Year: 2025, Volume and Issue: unknown
Published: March 26, 2025
We commend Spinelli et al. [1] for their comprehensive meta-analysis of 19 studies encompassing 1.7 million subjects, which substantially advances our understanding Helicobacter pylori (Hp) infection's potential protective role against eosinophilic oesophagitis (EoE). Their findings demonstrate a notable 46% reduction in the odds EoE development among Hp-exposed individuals. Notwithstanding meticulous synthesis existing data, several methodological refinements and research directions warrant consideration to further elucidate this intriguing epidemiological relationship. First, stratification by Hp virulence factors strain specificity could illuminate mechanistic insights. While aggregated all infections, growing evidence suggests strain-specific immunomodulatory effects—particularly cagA+ strains, elicit more robust Th1 responses [2]. Subgroup analyses comparing versus cagA− infections might reveal differential protection EoE, as observed other Th2-mediated conditions such asthma [3]. Second, geographic heterogeneity warrants deeper exploration. Although found comparable reductions Eastern (odds ratio: 0.53) Western 0.52) cohorts, infection prevalence diverged remarkably (43% vs. 14%, respectively). This paradox region-specific confounders, genetic or endemic helminth synergising with Hp's immunoregulatory effects [4]. Regression models accounting regional socioeconomic indices, sanitation standards antibiotic stewardship disentangle these interactions further. Third, temporality Hp–EoE relationship remains unresolved. The stronger inverse association post-2019 (56% 37% reduction) is accordance EoE's rising incidence but raises questions about birth cohort [5]. Case–control nested within longitudinal cohorts clarify whether early-life acquisition may confer greater than adult exposure, hypothesised allergic diseases. Additionally, Mendelian randomisation using variants proxies susceptibility better establish causality whilst minimising confounding [6]. Fourthly, did not elaborate on mucosal cytokine profiles, transcriptomic alterations, microbiome signatures associated modification infection. contend that non-invasive biomarkers including autoantibodies inflammatory mediators [7], investigation relation Hp. status. Finally, clinical trials involving patients [8-10], it would be valuable analyse examine how influence therapeutic outcomes. In conclusion, broadening investigations encompass effects, geospatial determinants, life course exposures, transform signal highlighted into actionable biological insights preventative strategies. Notably, declining resulting from eradication campaigns necessitates urgent translational research, animal evaluate Hp-derived molecules mitigate oesophageal inflammation—potentially offering novel approaches. Enzo Emanuele: writing – original draft. Piercarlo Minoretti: review editing. article linked al papers. To view articles, visit https://doi.org/10.1111/apt.70042 https://doi.org/10.1111/apt.70099. authors have nothing report.
Language: Английский
Citations
1
Alimentary Pharmacology & Therapeutics, Journal Year: 2025, Volume and Issue: unknown
Published: April 10, 2025
Language: Английский
Citations
1
Alimentary Pharmacology & Therapeutics, Journal Year: 2025, Volume and Issue: unknown
Published: March 26, 2025
We sincerely appreciate the constructive comments from Drs. Emanuele and Minoretti [1] on our meta-analysis of potential protective role Helicobacter pylori (H. pylori) infection against eosinophilic oesophagitis (EoE) [2], are keen to address each point they raised. The cagA protein has a well-known virulence effect in positive strains, its enhancement Th1 response may play reducing Th2 characteristic EoE. Although comparison patients with H. based their status would be interest, we were unable make this subgroup analysis due lack availability pertinent data included studies. also acknowledge that significant differences prevalence between Eastern Western cohorts explained by region-specific confounders, which further depicted regression models. However, highlight odds ratios two almost equal (0.53 v. 0.52). This suggests that, regardless specific geographical infection, related mechanisms protection similar worldwide. agree evidence, arising case–control studies nested within longitudinal birth Mendelian randomisation studies, clarify whether early associated lower did not observe reduction for EoE paediatric infected pylori. Possible explanations limited number influence genetic factors over environment [2]. evidence is needed relationship life. well aware non-invasive biomarkers an unmet need EoE, diagnosis monitoring currently rely totally upper endoscopy histology. Several tests emerging as candidates monitor disease activity, but application clinical practice still under validation [3-5]. In addition, omics technologies offer new insights into immunologic research nascent [6, 7]. Finally, incorporating ongoing [8-10] utmost interest because it could help plays treatment should considered factor therapeutic decision-making. thank careful work contribution important discussion. Irene Spinelli: conceptualization, investigation, methodology, curation, resources, project administration, validation, visualization, writing – original draft, review editing, formal analysis. Gianluca Ianiro: supervision, authors' declarations personal financial interests unchanged those article linked Spinelli et al papers. To view these articles, visit https://doi.org/10.1111/apt.70042 https://doi.org/10.1111/apt.70075. Data sharing applicable no created or analyzed study.
Language: Английский
Citations
0
Alimentary Pharmacology & Therapeutics, Journal Year: 2025, Volume and Issue: unknown
Published: April 10, 2025
Language: Английский
Citations
0