Division of Oral Biology, College of Dentistry, The Ohio State University, Columbus, Ohio, USA.
Infect Immun. 2013 Sep;81(9):3253-63. doi: 10.1128/IAI.00278-13. Epub 2013 Jun 24.
Stressor exposure has been shown to enhance host susceptibility and the severity of a plethora of illnesses, including gastrointestinal disease. In mice, susceptibility to Citrobacter rodentium has been shown to be dependent on host genetics as well as the composition of the intestinal microbiota, but the effects of stressor exposure on this gastrointestinal pathogen have not been elucidated fully. Previously, our lab showed that exposure to the prolonged-restraint stressor prior to a challenge with C. rodentium alters the intestinal microbiota community structure, including a reduction of beneficial genera such as Lactobacillus, which may contribute to stressor-enhanced C. rodentium-induced infectious colitis. To test the effects of stressor exposure on C. rodentium infection, we exposed resistant mice to a prolonged-restraint stressor concurrent with pathogen challenge. Exposure to prolonged restraint significantly enhanced C. rodentium-induced infectious colitis in resistant mice, as measured by increases in colonic histopathology, colonic inflammatory mediator gene production, and pathogen translocation from the colon to the spleen. It was further tested if the beneficial bacterium Lactobacillus reuteri could reduce the stressor-enhanced susceptibility to C. rodentium-enhanced infectious colitis. While L. reuteri treatment did not reduce all aspects of stressor-enhanced infectious colitis, it did significantly reduce pathogen translocation from the colon to the spleen. Taken together, these data demonstrate the deleterious effects that prolonged stressor exposure can have at the onset of a gastrointestinal infection by its ability to render a resistant mouse highly susceptible to C. rodentium. Probiotic treatment ameliorated the systemic manifestations of stress on colonic infection.
应激源暴露已被证明会增强宿主易感性和多种疾病的严重程度，包括胃肠道疾病。在小鼠中，已经证明对柠檬酸杆菌的易感性取决于宿主遗传以及肠道微生物群落的组成，但应激源暴露对这种胃肠道病原体的影响尚未完全阐明。以前，我们的实验室表明，在柠檬酸杆菌挑战之前暴露于长时间束缚应激源会改变肠道微生物群落结构，包括有益属如乳酸杆菌的减少，这可能有助于应激源增强柠檬酸杆菌诱导的传染性结肠炎。为了测试应激源暴露对柠檬酸杆菌感染的影响，我们将抗性小鼠暴露于与病原体挑战同时进行的长时间束缚应激源中。暴露于长时间束缚应激源显著增强了抗性小鼠柠檬酸杆菌诱导的传染性结肠炎，如结肠组织病理学、结肠炎症介质基因产生和病原体从结肠转移到脾脏的增加所测量的那样。进一步测试了有益细菌罗伊氏乳杆菌是否可以降低应激源增强柠檬酸杆菌诱导的传染性结肠炎的易感性。虽然罗伊氏乳杆菌治疗并没有减轻应激源增强传染性结肠炎的所有方面，但它确实显著减少了病原体从结肠向脾脏的转移。总之，这些数据表明，长时间应激源暴露可以通过使抗性小鼠对柠檬酸杆菌高度易感染来对胃肠道感染的发生产生有害影响。益生菌治疗改善了应激对结肠感染的全身表现。
