2026-04-29T04:09:24Zhttps://repisalud.isciii.es/rest/oai/request

oai:repisalud.isciii.es:20.500.12105/167722024-09-27T08:18:09Zcom_20.500.12105_19604com_20.500.12105_2051col_20.500.12105_19605

00925njm 22002777a 4500 dc Díaz-Marugan, Laura author Gallizioli, Mattia author Márquez-Kisinousky, Leonardo author Arboleya, Silvia author Mastrangelo, Annalaura author Ruiz-Jaén, Francisca author Pedragosa, Jordi author Casals, Climent author Morales, Francisco Javier author Ramos-Romero, Sara author Traserra, Sara author Justicia, Carles author Gueimonde, Miguel author Jiménez, Marcel author Torres, Josep Lluís author Urra, Xabier author Chamorro, Ángel author Sancho, David author de Los Reyes-Gavilán, Clara G author Miró-Mur, Francesc author Planas, Anna M author 2023-07 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. Stroke. 2023 Jul;54(7):1875-1887. http://hdl.handle.net/20.500.12105/16772 37226775 10.1161/STROKEAHA.123.042755 1524-4628 Stroke Poststroke Lung Infection by Opportunistic Commensal Bacteria Is Not Mediated by Their Expansion in the Gut Microbiota.