ABSTRACT
Enteric glial cells (EGCs) and enteric glial-derived neurotrophic factor (GDNF) are directly involved in intestinal inflammation. In this study, we sought to examine the possible mechanisms for how Bifidobacterium bifidum (B.b.) and Bacteroides fragilis (B.f.) influence EGC regulation. In this study, lipopolysaccharide (LPS) and interferon-γ (IFN-γ) were used as exogenous stimuli of EGCs to establish an intestinal inflammation model. After stimulation with LPS and IFN-γ, B.b. and B.f. supernatants were used to activate EGCs and to examine EGC immune mechanisms. For this purpose, qRT-PCR, western blotting, and laser scanning confocal microscopy (LSCM) were used to detect the expression of NLRP3, NLRP6, NGF, NT-3, IL-18, IL-1ß, and caspase-1. We found that EGCs, after stimulation with LPS and IFN-γ, could express NLRP3, NLRP6, NT-3, NGF, IL-18, IL-1ß, and caspase-1 through LSCM. In intestinal inflammation, B.b. and B.f. could trigger an increase in NGF and NT-3 expression in EGCs in order to protect the intestine. Furthermore, B.b. and B.f. could upregulate NLRP3 expression in EGCs and promote an inflammatory response. B.b. had a dual regulatory role in EGC NLRP6 expression, while B.f. inhibited NLRP6 protein expression. Moreover, B.b. could decrease the expression of IL-18, IL-1ß, and caspase-1 in EGCs in order to inhibit the inflammatory response. Contrary to this, B.f. could upregulate IL-18, IL-1ß, and caspase-1 expression in EGCs in order to promote the inflammatory response. B.b. and B.f. can influence the expression of NGF, NT-3, NLRP3, NLRP6, IL-18, IL-1ß, and caspase-1 in EGCs in order to inhibit or promote intestinal inflammation.
Subject(s)
Bacteroides fragilis/metabolism , Bifidobacterium bifidum/metabolism , Glial Cell Line-Derived Neurotrophic Factor/metabolism , Inflammasomes/metabolism , Inflammation/metabolism , Neuroglia/metabolism , Probiotics/metabolism , Animals , Gastrointestinal Microbiome , Intestines , Lipopolysaccharides/pharmacology , Male , Microscopy, Confocal , Rats , Rats, Sprague-DawleyABSTRACT
OBJECTIVE: To investigate the mechanism of impeded wound healing by exogenous hyaluronan (HA). METHODS: Wound healing models were established on 18 adult rabbit ears, which were randomly divided into 3 groups, the 2% HA treated-group (group A), the 1% HA treated-group(group B), and the PBS control group (group C). The process of wound healing was observed morphologically and histologically. The expression of alpha-smooth muscle actin in fibroblast was measured by immunohistochemical method. RESULTS: 1. The mean values of wound healing time of groups A, B and C were (11.7 +/- 0.6), (11.3 +/- 0.6), and (10.8 +/- 1.0) days respectively. Wound contraction was greater in group C than in group A and group B. 2. Compared with PBS controls, the collagen fibril was slender and arrayed regularly in HA treated wound. 3. The expression of alpha-smooth muscle actin was greater in group C than in groups A and B. CONCLUSION: It is one of reasons of impeded wound healing that exogenous HA inhibits the expression of alpha-smooth muscle protein and wound contraction. There exists dose-dependent effect.
