Host cell‐mediated responses to infection with Cryptosporidium

Abstract

The coccidian Cryptosporidium infects epithelial cells of a variety of vertebrate hosts and is the causative agent of cryptosporidiosis. In mammals, including humans and domestic animals, C. parvum infects the gastrointestinal tract producing an acute watery diarrhoea and weight loss. CD4+ T-cell-deficient hosts have increased susceptibility to infection with the parasite and may develop severe life-threatening complications. The host responses which induce protective immunity and contribute to pathogenesis are poorly understood. In the immunological control of infection, recent studies with murine infection models suggest that IFN-gamma plays a key role in a partially protective innate immunity against infection identified in immunocompromised mice and also in the elimination of infection mediated by CD4+ T-cells. At the mucosal level, CD4+ intraepithelial lymphocytes are involved in the control of cryptosporidial infection, acting at least in part through production of IFN-gamma which has a direct inhibitory effect on parasite development in enterocytes. Primary infection of ruminants induces an intestinal inflammatory response in which increased numbers of various T-cell subpopulations appear in the villi. In addition, infection results in increased intestinal expression of pro-inflammatory cytokines such as IL-12, IFN-gamma and TNF-alpha. Because these cytokines appear to be important in the aetiology of inflammatory bowel disease, it is possible that they are involved in the mucosal pathogenesis of cryptosporidiosis.

Induction of Protective Immunity against Eimeria tenella, Eimeria maxima, and Eimeria acervulina Infections Using Dendritic Cell-Derived Exosomes

“…While some reports indicated that a host T h 2 mucosal immune response is associated with the control of some protozoan infections (34,46), other studies revealed that T h 1 immunity was more efficient in conferring protection against infection by apicomplexan parasites (4,19,21). Depending upon the particular pathogen and host species, the local balance between T h 1 and T h 2 cytokine production is crucial for disease outcome (31,36,38). Because in the present study a low level of T h 2 cytokine-producing cells was detected in the immunized and infected group, it is possible that these cells may play a role, to some extent, in the host's Ag-specific response against the coccidial parasites.…”

Cell phenotypic change due to Cryptosporidium parvum infection in immunocompetent mice

“…Improvements in this area have been hampered by the lack of studies in immunocompetent animal models. Most experiments have been performed in neonatal or immunocompromised mice, with lacking functional T and/or B cells, and targeted mutations on major histocompatibility complex (MHC) class-II, alpha-beta-T-cell receptor (αβ-TCR) and interferon-gamma (INF-γ) (McDonald et al 1992, Aguirre et al 1994, McDonald and Bancroft 1994, McDonald 2000.…”

Increased Susceptibility of β7-Integrin-Deficient Neonatal Mice in the Early Stage ofCryptosporidium parvumInfection

“…We therefore studied the influence of ␤7 deficiency on T-lymphocyte recruitment during C. parvum infection, as T cells are important for the control of cryptosporidiosis (14). Immunohistochemistry is not an appropriate method for following the recruitment of T cells in the mucosa, because the infection is not homogeneously spread in the ileum in the early stage of infection and because very few CD3 ϩ cells can be observed on 7-day-old neonates infected 4 days earlier (data not shown).…”