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Lipopolysaccharide induces the early enhancement of mice colonic mucosal paracellular permeability mainly mediated by mast cells

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dc.contributor.authorSun, Tingyi
dc.contributor.authorWang, Yaxi
dc.contributor.authorHu, Shilong
dc.contributor.authorSun, Haimei
dc.contributor.authorYang, Shu
dc.contributor.authorWu, Bo
dc.contributor.authorJi, Fengqing
dc.contributor.authorZhou, Deshan
dc.date.accessioned2022-06-08T12:00:47Z
dc.date.available2022-06-08T12:00:47Z
dc.date.issued2019
dc.description.abstractThe alteration of intestinal mucosal barrier is considered to be the central pathophysiological process in response to gastrointestinal infections, and mucosal microstructural damage is a major factor for enhancing epithelial permeability in persistent bacterial infections. However, the mechanism involved in hyperpermeability in the early stage of acute bacterial infections is not fully understood. In the present study, fluorescein isothiocyanate-dextran across and transepithelial resistance measured in Ussing chambers were used to assess the intestinal paracellular permeability. Mast cell activation was evaluated by western blotting for the presence of tryptase released from mast cells. Serum levels of interleukin-6 were evaluated using enzymelinked immunosorbent assay. Our results indicated that mast cells played a pivotal role in colonic mucosal hyperpermeability in wild type mice treated with lipopolysaccharide (LPS) for 2 h. And the effect of LPS was mainly dependent on mast cell degranulation, while no change in permeability was observed in the mast celldeficient mice (Wads-/- ) after LPS administration. No obvious changes of the mucosal structure including histomorphological architecture and expression of intercellular junction proteins were obtained in either wild type or Wads-/- mice after LPS stimulation by hematoxylin and eosin staining, immunofluorescence staining and western blot analysis. Furthermore, the selfrenewal of intestinal epithelia, detected by using proliferation marker 5’-bromo-2’-deoxyuridine, was not involved in increased permeability. Collectively, activation of mast cells induced by LPS mediated intestinal hyperpermeability in the initial stage, and played a crucial role in barrier dysfunction rather than mucosal microstructural damage in acute enterogenous bacterial infection.es
dc.formatapplication/pdfes
dc.format.extent10es
dc.identifier.citationHistology and Histopathology, Vol.34, nº2, (2019)
dc.identifier.doiDOI: 10.14670/HH-18-039
dc.identifier.issn1699-5848
dc.identifier.issn0213-3911
dc.identifier.urihttp://hdl.handle.net/10201/121067
dc.languageenges
dc.publisherUniversidad de Murcia. Departamento de Biología Celular e Histologíaes
dc.relationSin financiación externa a la Universidades
dc.rightsinfo:eu-repo/semantics/openAccesses
dc.rightsAttribution-NonCommercial-NoDerivatives 4.0 Internacional*
dc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/4.0/*
dc.subjectLipopolysaccharidees
dc.subjectDegranulationes
dc.subjectMast cellses
dc.subjectIntestinal permeabilityes
dc.subjectAcute infectiones
dc.subject.otherCDU::6 - Ciencias aplicadas::61 - Medicina::616 - Patología. Medicina clínica. Oncologíaes
dc.titleLipopolysaccharide induces the early enhancement of mice colonic mucosal paracellular permeability mainly mediated by mast cellses
dc.typeinfo:eu-repo/semantics/articlees
dspace.entity.typePublicationes
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Histology and histopathology Vol.34, nº2 (2019)