Open AccessCryptosporidium parvum increases intestinal permeability through interaction with epithelial cells and IL‐1β and TNFα released by inflammatory monocytes
Author(s) -
Sablet Thibaut,
Potiron Laurent,
Marquis Mathilde,
Bussière Françoise I.,
LacroixLamandé Sonia,
Laurent Fabrice
Publication year - 2016
Publication title -
cellular microbiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.542
H-Index - 138
eISSN - 1462-5822
pISSN - 1462-5814
DOI - 10.1111/cmi.12632
Subject(s) - adherens junction , cryptosporidium parvum , biology , barrier function , tight junction , microbiology and biotechnology , inflammation , tumor necrosis factor alpha , immunology , glycocalyx , enterocyte , cell , cadherin , small intestine , genetics , biochemistry
Summary Intestinal epithelial cells form a single layer separating the intestinal lumen containing nutriments and microbiota from the underlying sterile tissue and therefore play a key role in maintaining homeostasis. We investigated the factors contributing to the alteration of the epithelial barrier function during Cryptosporidium parvum infection. Infected polarized epithelial cell monolayers exhibit a drop in transepithelial resistance associated with a delocalization of E‐cadherin and β‐catenin from their intercellular area of contact, the adherens junction complex. In neonatal mice infected by C . parvum , the increased permeability is correlated with parasite development and with an important recruitment of Ly6c + inflammatory monocytes to the subepithelial space. TNFα and IL‐1β produced by inflammatory monocytes play a key role in the loss of barrier function. Our findings demonstrate for the first time that both the parasite and inflammatory monocytes contribute to the loss of intestinal barrier function during cryptosporidiosis.