Increased susceptibility of beta7-integrin-deficient neonatal mice in the early stage of Cryptosporidium parvum infection

Roselyne Mancassola; Sonia Lacroix-Lamandé; Mathieu Barrier; Muriel Naciri; Henri Salmon; Fabrice Laurent

doi:10.1128/IAI.72.6.3634-3637.2004

Increased susceptibility of beta7-integrin-deficient neonatal mice in the early stage of Cryptosporidium parvum infection

Infect Immun. 2004 Jun;72(6):3634-7. doi: 10.1128/IAI.72.6.3634-3637.2004.

Authors

Roselyne Mancassola¹, Sonia Lacroix-Lamandé, Mathieu Barrier, Muriel Naciri, Henri Salmon, Fabrice Laurent

Affiliation

¹ Laboratoire de Contrôle et Immunologie de Maladies à Protozoaires, Unité 86 BASE, INRA de Tours, 37380 Nouzilly, France.

Abstract

Numerous inflammatory cells are recruited in response to Cryptosporidium parvum infection. These cells include interferon gamma-producing T lymphocytes, which are of major importance for the resolution of infection. Here, we show that beta7 integrin is not essential for the control of infection in mice but that beta7-deficient neonatal mice are more susceptible during the early stages of infection.

MeSH terms

Animals
Animals, Newborn
Cattle
Cryptosporidiosis / immunology*
Cryptosporidiosis / parasitology
Cryptosporidiosis / physiopathology
Cryptosporidium parvum / pathogenicity*
Disease Susceptibility
Humans
Ileum / immunology
Ileum / parasitology
Integrin beta Chains / genetics*
Integrin beta Chains / metabolism*
Mice
Mice, Inbred C57BL
T-Lymphocytes / immunology
Time Factors

Substances

Integrin beta Chains
integrin beta7