Abstract
BackgroundThis study investigated the protective effects of L. reuteri ZJ617 on intestinal and liver injury and the underlying mechanisms in modulating inflammatory, autophagy, and apoptosis signaling pathways in a piglet challenged with lipopolysaccharide (LPS).MethodsDuroc × Landrace × Large White piglets were assigned to 3 groups (n = 6/group): control (CON) and LPS groups received oral phosphate-buffered saline for 2 weeks before intraperitoneal injection (i.p.) of physiological saline or LPS (25 μg/kg body weight), respectively, while the ZJ617 + LPS group was orally inoculated with ZJ617 for 2 weeks before i.p. of LPS. Piglets were sacrificed 4 h after LPS injection to determine intestinal integrity, serum biochemical parameters, inflammatory signaling involved in molecular and liver injury pathways.ResultsCompared with controls, LPS stimulation significantly increased intestinal phosphorylated-p38 MAPK, phosphorylated-ERK and JNK protein levels and decreased IκBα protein expression, while serum LPS, TNF-α, and IL-6 concentrations (P < 0.05) increased. ZJ617 pretreatment significantly countered the effects induced by LPS alone, with the exception of p-JNK protein levels. Compared with controls, LPS stimulation significantly increased LC3, Atg5, and Beclin-1 protein expression (P < 0.05) but decreased ZO-1, claudin-3, and occludin protein expression (P < 0.05) and increased serum DAO and D-xylose levels, effects that were all countered by ZJ617 pretreatment. LPS induced significantly higher hepatic LC3, Atg5, Beclin-1, SOD-2, and Bax protein expression (P < 0.05) and lower hepatic total bile acid (TBA) levels (P < 0.05) compared with controls. ZJ617 pretreatment significantly decreased hepatic Beclin-1, SOD2, and Bax protein expression (P < 0.05) and showed a tendency to decrease hepatic TBA (P = 0.0743) induced by LPS treatment. Pretreatment of ZJ617 before LPS injection induced the production of 5 significant metabolites in the intestinal contents: capric acid, isoleucine 1TMS, glycerol-1-phosphate byproduct, linoleic acid, alanine-alanine (P < 0.05).ConclusionsThese results demonstrated that ZJ617 pretreatment alleviated LPS-induced intestinal tight junction protein destruction, and intestinal and hepatic inflammatory and autophagy signal activation in the piglets.
Highlights
L. reuteri species are an obligate heterofermentative strain that exerts beneficial effects on the health of the host [1]
L. reuteri has great potential to exert its probiotic effects given its tolerance to the gastrointestinal environment and the secretion of special bacteriostatic substances such as reuterin which is produced by glycerol metabolism [3, 4]
The lumen of the gut is always exposed to a plethora of microorganism, food antigens, and toxins, it is susceptible to triggering immune responses and inducing intestinal dysfunction and dysbiosis, which lead to various intestinal diseases, such as irritable bowel syndrome (IBS) [11] and diarrhea [12]
Summary
L. reuteri species are an obligate heterofermentative strain that exerts beneficial effects on the health of the host [1]. It was first isolated in 1962 and can be found endogenously in the intestines of all vertebrates and mammals [2], often in relatively low numbers. Based on the strong adhesion and broadspectrum antibacterial activity of reuterin, there have been numerous studies investigating the relationship between the effects of L. reuteri and intestinal health [5,6,7]. This study investigated the protective effects of L. reuteri ZJ617 on intestinal and liver injury and the underlying mechanisms in modulating inflammatory, autophagy, and apoptosis signaling pathways in a piglet challenged with lipopolysaccharide (LPS)
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