Batf3-Dependent Intestinal Dendritic Cells Play a Critical Role in the Control of Cryptosporidium parvum Infection.

Understanding the protective immune response to Cryptosporidium parvum infection is of critical importance to reduce the widespread impact caused by this disease in young individuals. Here, we analyzed the various subsets of CD103+ and CD103- intestinal dendritic cells (DCs) of wild-type and Batf3-/- neonatal mice at homoeostasis and investigated their role during infection. Neonatal Batf3-/- mice had a low CD103+/CD103- DC ratio, resulting in higher susceptibility to the acute phase of the infection and they could not cure the infection.

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

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.

CCL20 Displays Antimicrobial Activity Against Cryptosporidium parvum, but Its Expression Is Reduced During Infection in the Intestine of Neonatal Mice.

CCL20 is a chemokine with antimicrobial activity. We investigated its expression and role during neonatal cryptosporidiosis, a worldwide protozoan enteric disease leading to severe diarrhea. Surprisingly, during infection by Cryptosporidium parvum, CCL20 production by the intestine of neonatal mice is reduced by a mechanism independent both of the enteric flora and of interferon γ, a key cytokine for the resolution of this infection.