LPS Induces Hyper-Permeability of Intestinal Epithelial Cells

摘要: Necrotizing Enterocolitis (NEC) is a severe inflammatory disorder leading to high morbidity and mortality rates. A growing body of evidence demonstrate the key role Toll like receptor 4 (TLR4) in NEC. This membranal recognizes lipopolysaccharides (LPS) from bacterial wall triggers an response. The aim present study was elucidate effect LPS on paracellular permeability known be severely affected IEC-18 cells were treated with effects morphology, their associated gene protein expressions measured. Our results show that down regulated expression occludin ZO-1 mRNAs while up regulating Cdkn1a. In addition caused significant increase epithelial barrier damage. Finally found spatially disarrayed intercellular junctions response LPS. We conclude adversely functionality intestinal suggesting new mechanism by which infection may contribute development J. Cell. Physiol. 232: 381-390, 2017. © 2016 Wiley Periodicals, Inc.