Abstract
Objectives. Interactions between the host and gut microbial community contribute to the pathogenesis of Crohn's disease (CD). In this study, we aimed to detect lipopolysaccharide (LPS) and 1,3-β-D-glucan (BG) in the sera of CD patients and clarify the potential role in the diagnosis and therapeutic approaches. Materials and Methods. Serum samples were collected from 46 patients with active CD (A-CD), 22 CD patients at remission stage (R-CD), and 20 healthy controls, and the levels of LPS, BG, and TNF in sera were determined by ELISA. Moreover, sixteen patients with A-CD received anti-TNF monoclonal antibody therapy (infliximab, IFX) at a dose of 5 mg/kg body weight at weeks 0, 2, and 6, and the levels of LPS and BG were also tested at week 12 after the first intravenous infusion. Results. Serum levels of LPS and BG were found to be markedly increased in A-CD patients compared with R-CD patients and healthy controls (P < 0.05). They were also observed to be positively correlated with CDAI, ESR, and SES-CD, respectively (P < 0.05). Furthermore, the levels of TNF in sera had a significant correlation with LPS and BG, respectively. The concentrations of LPS and BG were demonstrated to be significantly downregulated in the sera of A-CD patients 12 weeks after IFX treatment (P < 0.05), suggesting that blockade of TNF could inhibit bacterial endotoxin absorption, partially through improving intestinal mucosal barrier. Conclusions. Serum levels of LPS and BG are significantly increased in A-CD patients and positively correlated with the severity of the disease. Blockade of intestinal mucosal inflammation with IFX could reduce the levels of LPS and BG in sera. Therefore, this study has shed some light on measurement of serum LPS and BG in the diagnosis and treatment of CD patients.
Highlights
Crohn’s disease (CD), belonging to inflammatory bowel disease (IBD), is one of the most prevalent chronic gastrointestinal diseases in the world, characterized by severe intestinal inflammation of the small and/or large intestine leading to abdominal pain, recurrent diarrhea, perianal fistula, and clinical manifestations of bowel obstruction [1]
Evidence has demonstrated that T helper (Th) cells are involved in the production of chronic intestinal inflammation and that Th1- and Th17mediated immune responses are dominant in the gut mucosa during the progress of CD [5]
There are greater densities of bacterial species, which are known as intestinal flora, and the common bacterial divisions are Firmicutes, Bacteroidetes, Actinobacteria, Proteobacteria, and Verrucomicrobia [23, 24]
Summary
Crohn’s disease (CD), belonging to inflammatory bowel disease (IBD), is one of the most prevalent chronic gastrointestinal diseases in the world, characterized by severe intestinal inflammation of the small and/or large intestine leading to abdominal pain, recurrent diarrhea, perianal fistula, and clinical manifestations of bowel obstruction [1]. Gut flora, which can coexist with the host throughout the digestive tract in variable concentrations (the upper limit is 1011–1012/g of luminal contents in the colon), is referred to as the largest microbial reservoir in the body [6] This community plays the vital roles in the host, ranging from helping various enzymes processing indigestible materials to regulating the immune system and constituting intestinal mucosal barrier [7]. An external “anatomical” barrier and an inner “functional” immunological barrier consist of gut mucosal barrier The former constitutes a large amount of coexisted gut flora, the mucous layer, and the intestinal epithelial monolayer, while the latter is comprised of a complex network of immune cells and gut-associated lymphoid tissues, which is organized in a specialized and compartmentalized system [8]. These components together sustain the maintenance of the delicate balance of intestinal homeostasis
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