title: Lipopolysaccharides facilitate colonic motor alterations associated to the sensitization to a luminal antigen in rats.
abstract: OBJECTIVE
  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 sensitiza-tion 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 eosi-nophils 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.
authors.affiliation: Department of Cell Biology, Physiology and Immunology, Universitat Autonoma de Barcelona, Spain.
authors.forename: Ferran
authors.initials: F
authors.lastname: Jardi
authors.affiliation: Department of Cell Biology, Physiology and Immunology, Universitat Autonoma de Barcelona, Spain.|Instituto de Neurociencias, Universitat Autonoma de Barcelona, Spain.
authors.forename: Monica
authors.initials: M
authors.lastname: Aguilera
authors.affiliation: Department of Cell Biology, Physiology and Immunology, Universitat Autonoma de Barcelona, Spain.|Instituto de Neurociencias, Universitat Autonoma de Barcelona, Spain.|Centro de Investigacion Biomedica en Red de Enfermedades Hepaticas y Digestivas (CIBERehd), Instituto de Salud Carlos III, Madrid, Spain.
authors.forename: Patri
authors.initials: P
authors.lastname: Vergara
authors.affiliation: Department of Cell Biology, Physiology and Immunology, Universitat Autonoma de Barcelona, Spain.|Instituto de Neurociencias, Universitat Autonoma de Barcelona, Spain.|Centro de Investigacion Biomedica en Red de Enfermedades Hepaticas y Digestivas (CIBERehd), Instituto de Salud Carlos III, Madrid, Spain.
authors.forename: Vicente
authors.identifier: http://orcid.org/0000-0001-5193-715X
authors.initials: V
authors.lastname: Martinez
keywords: Food hypersensitivity; Gastrointestinal diseases; Irritable bowel syndrome; Microbiota; Ovalbumin
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