Early immune innate hallmarks and microbiome changes across the gut during Escherichia coli O157: H7 infection in cattle

Abstract

The zoonotic enterohemorrhagic Escherichia coli (EHEC) O157: H7 bacterium causes diarrhea, hemorrhagic colitis, and hemolytic uremic syndrome (HUS) in humans. Cattle are primary reservoirs and EHEC O157: H7; the bacteria predominately inhabit the colon and recto-anal junctions (RAJ). The early innate immune reactions in the infected gut are critical in the pathogenesis of EHEC O157: H7. In this study, calves orally inoculated with EHEC O157: H7 showed infiltration of neutrophils in the lamina propria of ileum and RAJ at 7 and 14 days post-infection. Infected calves had altered mucin layer and mast cell populations across small and large intestines. There were differential transcription expressions of key bovine β defensins, tracheal antimicrobial peptide (TAP) in the ileum, and lingual antimicrobial peptide (LAP) in RAJ. The main Gram-negative bacterial/LPS signaling Toll-Like receptor 4 (TLR4) was downregulated in RAJ. Intestinal infection with EHEC O157: H7 impacted the gut bacterial communities and influenced the relative abundance of Negativibacillus and Erysipelotrichaceae in mucosa-associated bacteria in the rectum. Thus, innate immunity in the gut of calves showed unique characteristics during infection with EHEC O157: H7, which occurred in the absence of major clinical manifestations but denoted an active immunological niche.

Escherichia coli 0157:H7 virulence factors and the ruminant reservoir

“…These animals shed 100 to 1000 times more E. coli O157:H7 than average shedders [139 & ,150]. Composition of GIT commensals differs between supershedders and nonshedders, suggesting that the RAJ microbiota may be influenced by or affected by E. coli O157:H7 [135,[151][152][153][154]. E. coli O157:H7 regulates gene expression for assimilation of carbon and nitrogen, the stress response, and respiration to survive various GIT conditions [155,156].…”

Exposure to High Aerial Ammonia Causes Hindgut Dysbiotic Microbiota and Alterations of Microbiota-Derived Metabolites in Growing Pigs

“…Earlier research reported that the colonization of Clostridium_sensu_stricto_1 could improve the aggregation of T cells regulated by CD41 in the colon of sterile mice (35) and strengthen the resistance of infant gut bacteria by hindering the colonization of pathogenic microbiota (36), which might explain the decrement of Clostridium_sensu_stricto_1 induced by ammonia exposure in this study. Pathogenic bacteria Negativibacillus associated with gut dysbiosis or pediatric Crohn's disease (37,38) was dramatically increased in this research after ammonia exposure. The results on specific different genera caused by ammonia exposure of the hindgut were quite different from those of the previous study on the small intestine (11), which is probably due to undigested or unabsorbed nutrients (induced by ammonia exposure in the small intestine) from the small intestine to enter the hindgut, interacting with ammonia exposure of the hindgut.…”

The combined impact of xylo-oligosaccharides and gamma-irradiated astragalus polysaccharides on the immune response, antioxidant capacity, and intestinal microbiota composition of broilers

“…Negativibacillus genus is a kind of bacillus with a Gram-negative cell wall structure. It has been clearly demonstrated that the increased Negativibacillus proportion caused a distal gut dysbiosis after calves infected with Escherichia coli O157: H7 ( Larzabal, et al, 2020 ). In addition, Negativibacillus genus was higher in cecal contents of mice with obesity-related disorders ( Wang et al, 2019 ).…”