Short-term Oral Antibiotics Treatment Promotes Inflammatory Activation of Colonic Invariant Natural Killer T and Conventional CD4
Autor: | Claudia Burrello, Federica Garavaglia, Fulvia Milena Cribiù, Giulia Ercoli, Silvano Bosari, Flavio Caprioli, Federica Facciotti |
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Přispěvatelé: | Burrello, C, Garavaglia, F, Cribiu, F, Ercoli, G, Bosari, S, Caprioli, F, Facciotti, F |
Rok vydání: | 2017 |
Předmět: |
0301 basic medicine
medicine.drug_class T cell Cell Antibiotics T cells Gut flora iNKT cells antibiotics microbiota T cells intestinal inflammation antibiotics 03 medical and health sciences 0302 clinical medicine Immune system intestinal inflammation microbiota Medicine iNKT cells Original Research lcsh:R5-920 biology business.industry General Medicine medicine.disease biology.organism_classification Phenotype 030104 developmental biology medicine.anatomical_structure 030220 oncology & carcinogenesis Immunology lcsh:Medicine (General) business Dysbiosis Bacteria |
Zdroj: | Frontiers in Medicine Frontiers in Medicine, Vol 5 (2018) |
ISSN: | 2296-858X |
Popis: | The gut mucosa is continuously exposed to a vast community of microorganisms, collectively defined as microbiota, establishing a mutualistic relationship with the host and contributing to shape the immune system. Gut microbiota is acquired at birth, and its composition is relatively stable during the entire adult life. Intestinal dysbiosis, defined as a microbial imbalance of gut bacterial communities, can be caused by several factors, including bacterial infections and antibiotic use, and has been associated with an increased risk to develop or exacerbate immune-mediated pathologies, such as allergic reactions, asthma and inflammatory bowel diseases (IBD). Still, the mechanisms by which antibiotic-induced gut dysbiosis may lead to development of mucosal inflammation are still matter of debate. To this end, we aimed to evaluate the impact of antibiotic treatment on phenotype and functions of intestinal immune cell populations, including invariant Natural Killer T (iNKT) cells, a subset of lipid specific T cells profoundly influenced by alterations on the commensal microbiota. To this aim, a cocktail of broad -spectrum antibiotics was administered for two weeks to otherwise healthy mice before re-colonization of the intestinal microbial community with oral gavage of eubiotic or dysbiotic mucosa-associated bacteria and luminal colonic content, followed or not by intestinal inflammation induction. Here we showed that short-term antibiotic treatment alters frequency and functions of intestinal iNKT cells, even in the absence of intestinal inflammation. The presence of a dysbiotic microbiota after antibiotic treatment imprints colonic iNKT and CD4+ T cells towards a pro-inflammatory phenotype that collectively contributes to aggravate intestinal inflammation. Nonetheless, the inflammatory potential of the dysbiotic microbiota decreases over time opening the possibility to temporally intervene on the microbial composition to re-equilibrate dysbiosis thus controlling concomitantly mucosal immune T cell activations. |
Databáze: | OpenAIRE |
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