Rifaximin modulates the colonic microbiota of patients with Crohn's disease: an in vitro approach using a continuous culture colonic model system—authors’ response

摘要: Sir, We read with interest the comment by Cianci et al., referring to our recent publication in JAC. al. state that we cited their work incorrectly. appreciate importance of research on gut-homing T cells for understanding inflammatory conditions bowel. Further, regret sentence concerning ‘alternative mechanisms action’ rifaximin, including ‘(iii) reduction cytokine release’, did not expand complexity involvement immune system. are grateful detailed explanation and clarification regarding article referred to. would like emphasize it was intention discuss how therapeutic efficacy antibiotic rifaximin can be explained different action other than mere bactericidal effect. The latter has been reported several publications over last 2 years. In this context, is important note beyond its antimicrobial activity modulates response. Discussing aspect, references Brown Vitali clearly demonstrated overall status following administration due pro-inflammatory release, i.e. interleukin (IL)-6, IL-1b, IL-8, IL-12 interferon-g. comment, clarify investigated only modification balance cell subpopulations correlated response treatment uncomplicated diverticular disease (UDD). particular, a CD4+/CD103+ lymphocytes peripheral blood levels control subjects shown after administration, while before subpopulation significantly higher UDD patients. agree that, strict sense, cannot inferred as induced decrease cytokines or an increase anti-inflammatory measuring part investigations. Cytokine production very complex depends factors, e.g. binding ligand CD103. However, change profile ruled out. For example, paper, Wang showed lymphocyte-mediated chronic inflammation model blockage a4b7, adhesion molecule similar CD103, reduced cytokines. apologize any confusion caused clarification; thus, contributing pathology intestine.