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| Pàgina inicial > Articles > Articles publicats > Poststroke Lung Infection by Opportunistic Commensal Bacteria Is Not Mediated by Their Expansion in the Gut Microbiota |
(Universitat de Barcelona) (Institut d'Investigacions Biomèdiques August Pi i Sunyer) (Instituto de Investigación Sanitaria del Principado de Asturias) (Centro Nacional de Investigaciones Cardiovasculares Carlos III (CNIC)) (Institut d'Investigacions Biomèdiques August Pi i Sunyer) (Hospital Clínic i Provincial de Barcelona) (Universitat de Barcelona) (Institut d'Investigacions Biomèdiques August Pi i Sunyer) (Instituto de Investigación Sanitaria del Principado de Asturias) (Universitat Autònoma de Barcelona. Departament de Biologia Cel·lular, de Fisiologia i d'Immunologia) (Institut de Química Avançada de Catalunya) (Hospital Clínic i Provincial de Barcelona) (Hospital Clínic i Provincial de Barcelona) (Instituto de Investigación Sanitaria del Principado de Asturias) (Vall d'Hebron Institut de Recerca (VHIR)) (Institut d'Investigacions Biomèdiques August Pi i Sunyer)
| Data: | 2023 |
| Resum: | Background: Respiratory and urinary tract infections are frequent complications in patients with severe stroke. Stroke-associated infection is mainly due to opportunistic commensal bacteria of the microbiota that may translocate from the gut. We investigated the mechanisms underlying gut dysbiosis and poststroke infection. Methods: Using a model of transient cerebral ischemia in mice, we explored the relationship between immunometabolic dysregulation, gut barrier dysfunction, gut microbial alterations, and bacterial colonization of organs, and we explored the effect of several drug treatments. Results: Stroke-induced lymphocytopenia and widespread colonization of lung and other organs by opportunistic commensal bacteria. This effect correlated with reduced gut epithelial barrier resistance, and a proinflammatory sway in the gut illustrated by complement and nuclear factor-κB activation, reduced number of gut regulatory T cells, and a shift of gut lymphocytes to γδT cells and T helper 1/T helper 17 phenotypes. Stroke increased conjugated bile acids in the liver but decreased bile acids and short-chain fatty acids in the gut. Gut fermenting anaerobic bacteria decreased while opportunistic facultative anaerobes, notably Enterobacteriaceae, suffered an expansion. Anti-inflammatory treatment with a nuclear factor-κB inhibitor fully abrogated the Enterobacteriaceae overgrowth in the gut microbiota induced by stroke, whereas inhibitors of the neural or humoral arms of the stress response were ineffective at the doses used in this study. Conversely, the anti-inflammatory treatment did not prevent poststroke lung colonization by Enterobacteriaceae. Conclusions: Stroke perturbs homeostatic neuro-immuno-metabolic networks facilitating a bloom of opportunistic commensals in the gut microbiota. However, this bacterial expansion in the gut does not mediate poststroke infection. |
| Ajuts: | Agencia Estatal de Investigación PID2020-113202RB-I00 Ministerio de Economía y Competitividad AGL2017-83599-R Agencia Estatal de Investigación PID2020-117009RB-I00 "la Caixa" Foundation ID100010434 European Commission 725091 Agencia Estatal de Investigación PID2019-108157RB |
| Nota: | Altres ajuts: Fundació La Marató de TV3 (201723-30-31-32) |
| Drets: | Aquest document està subjecte a una llicència d'ús Creative Commons. Es permet la reproducció total o parcial, la distribució, i la comunicació pública de l'obra, sempre que no sigui amb finalitats comercials, i sempre que es reconegui l'autoria de l'obra original. No es permet la creació d'obres derivades.  |
| Llengua: | Anglès |
| Document: | Article ; recerca ; Versió publicada |
| Matèria: | Bacteria ; Bile acids ; Brain ; Infection ; Inflammation ; Ischemia |
| Publicat a: | Stroke, Vol. 54 Num. 7 (July 2023) , p. 1875-1887, ISSN 1524-4628 |
