Lipopolysaccharides Facilitate Colonic Motor Alterations Associated to the Sensitization to a Luminal Antigen in Rats

Abstract

Background/Aims Enteric dysbiosis is a risk factor for dietary proteins-associated intestinal alterations, contributing to the development of food allergies and the symptomatology of functional gastrointestinal disorders, mainly irritable bowel syndrome (IBS). We explored if a dysbiotic-like state, simulated by intraperitoneal administration of bacterial lipopolysaccharides (LPS), facilitates the sensitization to a luminal antigen, ovalbumin (OVA), in rats. Methods Rats were exposed to oral OVA for 1 week, alone or with LPS. Thereafter, colonic histology, goblet cell density, mucosal eosinophils and mucosal mast cell (MMC) and connective tissue mast cell (CTMC) were evaluated. Colonic expression (real-time quantitative polymerase chain reaction) of interleukins, IFN-α1 and integrins was assessed to determine local immune responses. Luminal and wall adhered microbiota were characterized by fluorescence in situ hybridization. Colonic contractility (in vitro) served to assess functional changes associated to OVA and/or LPS. Results Neither OVA nor LPS, alone or combined, lead to structural alterations, except for a reduced goblet cell density in OVA-LPS-treated rats. MMC density was unaffected, while CTMC counts increased within the submucosa of OVA-LPS-treated animals. Marginal immune activation (IFN-α1 up-regulation) was observed in OVA-LPS-treated rats. LPS induced a dysbiotic-like state characterized by decreased luminal bacterial counts, with a specific loss of clostridia. LPS facilitated Clostridium spp. wall adherence, an effect prevented by OVA. Colonic contractility was altered in OVA-LPS-treated animals, showing increased basal activity and enhanced motor responses to OVA. Conclusions Changes in gut microbiota and/or direct effects of LPS might enhance/facilitate local neuroimmune responses to food antigens leading to motor alterations similar to those observed in IBS.

Salidroside Ameliorates Furan-Induced Testicular Inflammation in Relation to the Gut-Testis Axis and Intestinal Apoptosis

“…LPS is the complex of lipids and polysaccharides discovered in the external membrane of Gram-negative bacteria. Jardi et al showed that LPS induced the loss of Clostridia . Consistent with our results, SAL suppressed the enhanced level of LPS induced by furan.…”

“…Jardi et al showed that LPS induced the loss of Clostridia. 61 Consistent with our results, SAL suppressed the enhanced level of LPS induced by furan. As the critical receptor of LPS, TLR4 recognizes LPS and springs the entire signaling pathway.…”