Ammonia exposure induced intestinal inflammation injury mediated by intestinal microbiota in broiler chickens via TLR4/TNF-α signaling pathway

Abstract

Ammonia is a known environmental pollutant that causes injury to the intestine. Growing evidence suggests that intestinal microbiota dysbiosis involves in the development of intestinal injury under environmental pollution. However, the specific mechanism remains unexplored. To do this, broiler chicken ileal exposed to ammonia was selected as the research object. Further, antibiotic depletion of intestinal microbiota and flora transplantation were used to clarify the role of intestinal microbiota in the intestinal injury. Histopathological examination indicated inhaled ammonia caused intestinal injury. Then we observed a decrease in intestinal muc-2, claudin-1, IL-6, IL-10 in ammonia inhalation, as opposed to the control group, associated with a significant increase in TLR4, MyD88, NF-κB, TNF-α, IL-1β, caspase3. Moreover, there was a significant increase of Streptococcus, Escherichia-Shigella, Faecalibacterium, [Ruminococcus]_torques_group, Ruminococcaceae_UCG-014, unclassified_f_Lachnospiraceae, Rothia, unclassified_f_Ruminococcaceae in the inhaled ammonia exposure. Correlation analysis suggested that the altered genera were positively correlated with the expression of TLR4 and TNF-α. Moreover, transferring intestinal microbiota from ammonia exposure broiler into healthy broiler caused intestinal injury and increased TLR4 and TNF-α concentrations in recipient broiler. Furthermore, antibiotic depletion of intestinal microbiota attenuated ammonia-caused intestinal injury and reduced TLR4 and TNF-α productions. In summary, TLR4/TNF-α signaling pathway was an important regulated mechanism involved in the intestinal injury mediated by intestinal microbiota dysbiosis under inhaled ammonia.