Binding and activation of human and mouse complement by Cryptosporidium parvum (Apicomplexa) and susceptibility of C1q- and MBL-deficient mice to infection

Petry, Franz; Jakobi, Vera; Wagner, Swen; Tessema, Tesfaye Sisay; Thiel, Steffen; Loos, Michael

doi:10.1016/j.molimm.2008.04.010

Cited by 16 publications

(6 citation statements)

References 37 publications

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“…110 Mannose-binding lectin might activate complement to mediate parasite clearance. 113 Toll-like receptors on the host cell surface trigger key responses to the organism. C parvum infection increases production of antimicrobial peptides (LL-37 and human β-defensin 2).…”

Section: Therapeuticsmentioning

confidence: 99%

A review of the global burden, novel diagnostics, therapeutics, and vaccine targets for cryptosporidium

Checkley

White

Jaganath

et al. 2015

The Lancet Infectious Diseases

793

703

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Cryptosporidium spp are well recognised as causes of diarrhoeal disease during waterborne epidemics and in immunocompromised hosts. Studies have also drawn attention to an underestimated global burden and suggest major gaps in optimum diagnosis, treatment, and immunisation. Cryptosporidiosis is increasingly identified as an important cause of morbidity and mortality worldwide. Studies in low-resource settings and high-income countries have confirmed the importance of cryptosporidium as a cause of diarrhoea and childhood malnutrition. Diagnostic tests for cryptosporidium infection are suboptimum, necessitating specialised tests that are often insensitive. Antigen-detection and PCR improve sensitivity, and multiplexed antigen detection and molecular assays are underused. Therapy has some effect in healthy hosts and no proven efficacy in patients with AIDS. Use of cryptosporidium genomes has helped to identify promising therapeutic targets, and drugs are in development, but methods to assess the efficacy in vitro and in animals are not well standardised. Partial immunity after exposure suggests the potential for successful vaccines, and several are in development; however, surrogates of protection are not well defined. Improved methods for propagation and genetic manipulation of the organism would be significant advances.

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Section: Therapeuticsmentioning

confidence: 99%

A review of the global burden, novel diagnostics, therapeutics, and vaccine targets for cryptosporidium

Checkley

White

Jaganath

et al. 2015

The Lancet Infectious Diseases

793

703

View full text Add to dashboard Cite

show abstract

“…One domain is the globular "heads" domain gC1q, which is considered to act as the crucial part of C1q to recognize a wide range of pathogen-associated molecular patterns (PAMPs) [9,11,12]. The other one is the collagen-like domain (cC1q), which assembles a bouquet-like structure, and participates in the interaction and activation of C1r and C1s, the important downstream molecules of classical complement pathway [13,14].…”

Section: Introductionmentioning

confidence: 99%

A C1q domain containing protein from Crassostrea gigas serves as pattern recognition receptor and opsonin with high binding affinity to LPS

Jiang

Zhang

et al. 2015

Fish & Shellfish Immunology

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“…Infection of human biliary epithelial cells by C. parvum in vitro mimics parasitial apical invasion and epithelial innate immune responses in vivo [18]. The invasion of epithelial cells in vitro by C. parvum results in the rapid expression of anti-microbial peptides (e.g., β-defensins) and the inflammatory chemokines [19, 20]. How epithelial cells finely balance the inflammatory reactions and anti-microbial immune responses during C. parvum infection is still unclear.…”

Section: Introductionmentioning

confidence: 99%

MicroRNA‐98 andlet‐7Regulate Expression of Suppressor of Cytokine Signaling 4 in Biliary Epithelial Cells in Response toCryptosporidium parvumInfection

Hu¹,

Zhou²,

Li³

et al. 2010

J INFECT DIS

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Expression of the cytokine-inducible Src homology 2 protein (CIS) and suppressors of cytokine signaling proteins (SOCS) represents an important element of host cell reactions in response to pathogen infection. We previously demonstrated that Cryptosporidium parvum infection downregulates miR-98 and let-7 to induce CIS expression in biliary epithelial cells. We reported here that downregulation of miR-98 and let-7 also coordinates epithelial expression of SOCS4 following C. parvum infection. Targeting of SOCS4 3'-untranslated region by miR-98 or let-7 resulted in translational repression. Functional manipulation of miR-98 caused reciprocal alterations in SOCS4 protein expression. Transfection of miR-98 precursor abolished C. parvum-stimulated SOCS4 upregulation. Moreover, expression of SOCS4 in epithelial cells showed an inhibitory effect on phosphorylation of signal transducers and activators of transcription proteins induced by C. parvum. These data suggest an important role for miRNAs in the coordinated regulation of CIS/SOCS expression in epithelial cells in response to C. parvum infection.

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Binding and activation of human and mouse complement by Cryptosporidium parvum (Apicomplexa) and susceptibility of C1q- and MBL-deficient mice to infection

Cited by 16 publications

References 37 publications

A review of the global burden, novel diagnostics, therapeutics, and vaccine targets for cryptosporidium

A review of the global burden, novel diagnostics, therapeutics, and vaccine targets for cryptosporidium

A C1q domain containing protein from Crassostrea gigas serves as pattern recognition receptor and opsonin with high binding affinity to LPS

MicroRNA‐98 andlet‐7Regulate Expression of Suppressor of Cytokine Signaling 4 in Biliary Epithelial Cells in Response toCryptosporidium parvumInfection

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