Colonic bacterial translocation as a possible factor in stress-worsening experimental stroke outcome.
Stress is known to be one of the risk factors of stroke, but only a few experimental studies have examined the possible mechanisms by which prior stress may affect stroke outcome. In stroke patients, infections impede neurological recovery and increase morbidity as well as mortality. We previously reported that stress induces a bacterial translocation and that prior immobilization stress worsens experimental stroke outcome through mechanisms that involve inflammatory mediators such as release of proinflammatory cytokines and enzyme activation. We now investigate whether bacterial translocation from the intestinal flora of rats with stress before experimental ischemia is involved in stroke outcome. We used an experimental paradigm consisting of exposure of Fischer rats to repeated immobilization sessions before permanent middle cerebral artery occlusion (MCAO). The presence of bacteria and the levels and expression of different mediators involved in the bacterial translocation were analyzed. Our results indicate that stress before stroke is related to the presence of bacteria in different organs (mesenteric nodes, spleen, liver, and lung) after MCAO and increases inflammatory colonic parameters (such as cyclooxygenase-2, inducible nitric oxide synthase, and myeloperoxidase), but decreases colonic immunoglobulin A, and these results are correlated with colonic inflammation and bacterial translocation. Understanding the implication of bacterial translocation during stress-induced stroke worsening is of great potential clinical relevance, given the high incidence of infections after severe stroke and their main role in mortality and morbidity in stroke patients.
Caso
Javier R
JR
Department of Pharmacology, Univesity Complutense, 28040 Madrid, Spain.
Hurtado
Olivia
O
Pereira
Marta P
MP
García-Bueno
Borja
B
Menchén
Luis
L
Alou
Luis
L
Gómez-Lus
María Luisa
ML
Moro
María A
MA
Lizasoain
Ignacio
I
Leza
Juan C
JC
D000818:Animals; D000900:Anti-Bacterial Agents / Q000494:pharmacology; D018988:Bacterial Translocation / Q000187:drug effects; D003092:Colitis / Q000209:etiology* / Q000276:immunology / Q000382:microbiology / Q000473:pathology; D003106:Colon / Q000187:drug effects / Q000276:immunology / Q000382:microbiology* / Q000473:pathology; D003345:Corticosterone / Q000097:blood; D051546:Cyclooxygenase 2 / Q000378:metabolism; D004195:Disease Models, Animal; D007070:Immunoglobulin A / Q000378:metabolism; D020244:Infarction, Middle Cerebral Artery / Q000150:complications* / Q000473:pathology; D008168:Lung / Q000382:microbiology; D008198:Lymph Nodes / Q000382:microbiology; D008297:Male; D052247:Nitric Oxide Synthase Type II / Q000378:metabolism; D010400:Penicillin G / Q000494:pharmacology; D010539:Permeability; D009195:Peroxidase / Q000378:metabolism; D051381:Rats; D011916:Rats, Inbred F344; D012149:Restraint, Physical; D012307:Risk Factors; D013154:Spleen / Q000382:microbiology; D013315:Stress, Psychological / Q000150:complications* / Q000276:immunology / Q000382:microbiology; D020521:Stroke / Q000209:etiology* / Q000276:immunology / Q000382:microbiology / Q000473:pathology
D000900:Anti-Bacterial Agents; D007070:Immunoglobulin A; D009195:Peroxidase; D052247:Nitric Oxide Synthase Type II; C496318:Nos2 protein, rat; D051546:Cyclooxygenase 2; C489691:Ptgs2 protein, rat; D010400:Penicillin G; D003345:Corticosterone