Cryptosporidium parvum increases intestinal permeability through interaction with epithelial cells and IL‐1β and TNFα released by inflammatory monocytes

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 barri...

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Bibliographic Details
Published in:Cellular microbiology 2016-12, Vol.18 (12), p.1871-1880
Main Authors: Sablet, Thibaut, Potiron, Laurent, Marquis, Mathilde, Bussière, Françoise I., Lacroix‐Lamandé, Sonia, Laurent, Fabrice
Format: Article
Language:English
Subjects:
Animals
Animals, Newborn
Antigens, Ly - genetics
Antigens, Ly - immunology
beta Catenin - genetics
beta Catenin - immunology
Cadherins - genetics
Cadherins - immunology
Cryptosporidiosis - genetics
Cryptosporidiosis - immunology
Cryptosporidiosis - parasitology
Cryptosporidium parvum
Cryptosporidium parvum - growth & development
Cryptosporidium parvum - immunology
Cryptosporidium parvum - pathogenicity
Epithelial Cells - immunology
Epithelial Cells - parasitology
Gene Expression Regulation
Host-Pathogen Interactions
Interleukin-1beta - genetics
Interleukin-1beta - immunology
Intestinal Mucosa - immunology
Intestinal Mucosa - parasitology
Life Sciences
Mice
Mice, Inbred C57BL
Mice, Knockout
Microbiology and Parasitology
Monocytes - immunology
Monocytes - parasitology
Permeability
Signal Transduction
Tumor Necrosis Factor-alpha - genetics
Tumor Necrosis Factor-alpha - immunology
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Summary: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.
ISSN:1462-5814
1462-5822
DOI:10.1111/cmi.12632