Department of Infectious Diseases and Pathology, University of Florida, Gainesville, Florida, United States of America; Division of Gastroenterology, Hepatology and Nutrition, Department of Medicine, University of Florida, Gainesville, Florida, United States of America.
Division of Gastroenterology, Department of Pediatrics, University of Florida, Gainesville, Florida, United States of America.
PLoS One. 2014 Jun 19;9(6):e100532. doi: 10.1371/journal.pone.0100532. eCollection 2014.
Gastrointestinal (GI) anthrax results from the ingestion of Bacillus anthracis. Herein, we investigated the pathogenesis of GI anthrax in animals orally infected with toxigenic non-encapsulated B. anthracis Sterne strain (pXO1+ pXO2-) spores that resulted in rapid animal death. B. anthracis Sterne induced significant breakdown of intestinal barrier function and led to gut dysbiosis, resulting in systemic dissemination of not only B. anthracis, but also of commensals. Disease progression significantly correlated with the deterioration of innate and T cell functions. Our studies provide critical immunologic and physiologic insights into the pathogenesis of GI anthrax infection, whereupon cleavage of mitogen-activated protein kinases (MAPKs) in immune cells may play a central role in promoting dysfunctional immune responses against this deadly pathogen.
胃肠道（GI）炭疽是由炭疽杆菌摄入引起的。在此，我们研究了经口感染无荚膜产毒炭疽芽孢杆菌 Sterne 株（pXO1+pXO2-）孢子的动物中 GI 炭疽的发病机制，这导致动物迅速死亡。炭疽芽孢杆菌 Sterne 诱导显著的肠道屏障功能破坏，并导致肠道菌群失调，不仅导致炭疽芽孢杆菌，还导致共生菌的全身传播。疾病进展与先天和 T 细胞功能的恶化显著相关。我们的研究为 GI 炭疽感染的发病机制提供了重要的免疫学和生理学见解，在此过程中，免疫细胞中丝裂原活化蛋白激酶（MAPKs）的切割可能在促进针对这种致命病原体的功能失调免疫反应中起核心作用。
