Innate immune responses against <i>Cryptosporidium parvum</i> infection

McDonald, Vincent; Korbel, Daniel S.; Barakat, Farah M.; Choudhry, Naheed; Petry, Franz

doi:10.1111/pim.12020

Cited by 82 publications

(92 citation statements)

References 75 publications

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“…This effect also extended to a mouse model of Cryptosporidium biliary infection, in which recruitment of CX3CR1+ cells to the biliary tract was increased in livers of infected mice. In addition to chemokines, proinflammatory cytokines secreted by IECs and phagocytes have been shown to play a crucial role in the innate immune response to Cryptosporidium (26,30). Lastly, mannose-binding lectin (MBL), asoluble innate immune mediator secreted by hepatocytes, has been shown to be important in the protection against cryptosporidiosis.…”

Section: Immune Responses To Cryptosporidiummentioning

confidence: 99%

Systemic and Mucosal Immune Responses to Cryptosporidium—Vaccine Development

Ludington

Ward

2015

Curr Trop Med Rep

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Cryptosporidium spp is a major cause of diarrheal disease worldwide, particularly in malnourished children and untreated AIDS patients in developing countries in whom it can cause severe, chronic and debilitating disease. Unfortunately, there is no consistently effective drug for these vulnerable populations and no vaccine, partly due to a limited understanding of both the parasite and the host immune response. In this review, we will discuss our current understanding of the systemic and mucosal immune responses to Cryptosporidium infection, discuss the feasibility of developing a Cryptosporidium vaccine and evaluate recent advances in Cryptosporidium vaccine development strategies

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Section: Immune Responses To Cryptosporidiummentioning

confidence: 99%

Systemic and Mucosal Immune Responses to Cryptosporidium—Vaccine Development

Ludington

Ward

2015

Curr Trop Med Rep

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“…Upon Crypto-sporidium infection, epithelial cells quickly initiate a series of innate immune reactions, including production of antimicrobial peptides (e.g. β-defensins and LL-37) and release of inflammatory cytokines/ chemokines, such as interleukin-8 (IL-8) (Borad and Ward, 2010; Petry et al 2010; McDonald et al 2013). Production and secretion of antimicrobial peptides can kill Cryptosporidium or inhibit parasite growth.…”

Section: Mucosal Epithelial Cells Are Critical Players In the Host’s mentioning

confidence: 99%

Non-coding RNAs in epithelial immunity toCryptosporidiuminfection

2014

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SUMMARY Cryptosporidium spp. is a protozoan parasite that infects the gastrointestinal epithelium and causes diarrhoeal disease worldwide. It is one of the most common pathogens responsible for moderate to severe diarrhoea in children younger than 2 years. Because of the ‘minimally invasive’ nature of Cryptosporidium infection, mucosal epithelial cells are critical to the host’s anti-Cryptosporidium immunity. Gastrointestinal epithelial cells not only provide the first and most rapid defence against Cryptosporidium infection, they also mobilize immune effector cells to the infection site to activate adaptive immunity. Recent advances in genomic research have revealed the existence of a large number of non-protein-coding RNA transcripts, so called non-coding RNAs (ncRNAs), in mammalian cells. Some ncRNAs may be key regulators for diverse biological functions, including innate immune responses. Specifically, ncRNAs may modulate epithelial immune responses at every step of the innate immune network following Cryptosporidium infection, including production of antimicrobial molecules, expression of cytokines/chemokines, release of epithelial cell-derived exosomes, and feedback regulation of immune homoeostasis. This review briefly summarizes the current science on ncRNA regulation of innate immunity to Cryptosporidium, with a focus on microRNA-associated epithelial immune responses.

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“…As mentioned, intestinal epithelial cells represent highly immune-reactive cells (McDonald et al 2013), which are capable to synthesize a broad spectrum of proimmunoregulatory molecules, such as chemokines and cytokines (Wang et al 2007;McDonald et al 2013;Imaeda et al 2013) to recruit leukocytes to the site of infection (Astarci et al 2012;Lane et al 2013). It appears likely that E. bovis merozoites I invasion and development could induce host intestinal epithelial cell activation resulting in the synthesis of proinflammatory chemokines/ cytokines.…”

Section: Introductionmentioning

confidence: 98%

Suitable in vitro culture of Eimeria bovis meront II stages in bovine colonic epithelial cells and parasite-induced upregulation of CXCL10 and GM-CSF gene transcription

et al. 2015

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We here established a suitable in vitro cell culture system based on bovine colonic epithelial cells (BCEC) for the development of Eimeria bovis merozoites I and the characterization of early parasite-induced innate epithelial host cell reactions as gene transcription of proinflammatory molecules. Both primary and permanent BCEC (BCEC (rim) and BCEC(perm)) were suitable for E. bovis merozoite I invasion and subsequent development of meronts II leading to the release of viable merozoites II. E. bovis merozoite II failed to develop any further neither into gamont nor oocyst stages in BCEC in vitro. E. bovis merozoite I induced innate epithelial host cell reactions at the level of CXC/CCL chemokines (CXCL1, CXCL8, CXCL10, CCL2), IL-6, and GM-CSF gene transcription. Overall, both BCEC types were activated by merozoite I infections since they showed significantly enhanced gene transcript levels of the immunomodulatory molecules CXCL10 and GM-CSF. However, gene transcription profiles of BCEC(prim) and BCEC(perm) revealed different reaction patterns in response to merozoite I infection with regard to quality and kinetics of chemokine/cytokine gene transcription. Although both BCEC types equally showed most prominent responses for CXCL10 and GM-CSF, the induction of CXCL1, CXCL8, CCL2, and IL-6 gene transcripts varied qualitatively and quantitatively. Our results demonstrate that BCEC seem capable to respond to E. bovis merozoite I infection by the upregulation of CXCL10 and GM-CSF gene transcription and therefore probably contribute to host innate effector mechanisms against E. bovis.

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Innate immune responses against Cryptosporidium parvum infection

Cited by 82 publications

References 75 publications

Systemic and Mucosal Immune Responses to Cryptosporidium—Vaccine Development

Systemic and Mucosal Immune Responses to Cryptosporidium—Vaccine Development

Non-coding RNAs in epithelial immunity toCryptosporidiuminfection

Suitable in vitro culture of Eimeria bovis meront II stages in bovine colonic epithelial cells and parasite-induced upregulation of CXCL10 and GM-CSF gene transcription

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