PRJNA718995
Hindgut dysbiotic microbiota contributes to the alterations of microbiota-derived metabolites during high ammonia exposure in growing pigs
The intestinal microbiome has been proven to affect host systematic metabolism and immune homeostasis. The current study aimed to investigate how aerial ammonia exposure influences the hindgut microbiota and its metabolites using pyrosequencing technologies in the pig model. Twelve growing pigs were randomly allocated to control or ammonia exposure (35 mg/m3) group respectively, and raised in two controlled chambers for 25d. A decreased trend of leptin (p = 0.0898) and reduced HDL-C (p = 0.0006) were found in serum after ammonia exposure. High ammonia exposure notably enhanced the alpha-diversity with higher sobs, shannon or ace index in cecum or colon and chao index in cecum (p < 0.05), indicating that high ammonia exposure increased the large intestinal microbiota species richness. Based on the bray-curtis distance and ANOSIM test, PCoA analysis demonstrated a distinct cluster clearly in cecum or colon after ammonia exposure (p < 0.01). In cecum, 17 genera were modified by ammonia exposure, followed by 6 genera in colon (FDR < 0.05). Ammonia exposure increased acetate and decreased isobutyrate or isovalerate in cecum or colon, respectively (p < 0.05). Cecal BA profiles showed that high ammonia exposure had a decreased trend of CA, HCA, LCA (p < 0.1), and decreased DCA, HDCA (p < 0.05), but increased GCDCA (p < 0.05). Contrary, an increased trend of HCA, LCA, HDCA (p < 0.1), a decreased trend of TDCA (p < 0.1) and decreased THDCA (p < 0.05) were observed in the serum BA profiles after ammonia exposure. Mantel test and correlation analysis revealed associations between microbiota-derived metabolites and ammonia exposure-responsive cecal bacteria. Collectively, our findings illustrated that high ammonia exposure induced the dysbiotic microbiota in hindgut, thereby affecting the production of microbiota-derived SCFAs and BAs, which play a pivotal role in the modulation of host systematic metabolism.