Treatment of Murine Cryptosporidiosis with Anticryptosporidial Immune Rat Bile

Albert, M.; Rusnak, Janice M.; Luther, M; Graybill, John R.

doi:10.4269/ajtmh.1994.50.112

Cited by 8 publications

(4 citation statements)

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Section: Mechanisms Of Parasite Eliminationmentioning

confidence: 99%

“…Evidence that antibodies are important in the elimination of infection is limited, however. In one study, the reproduction of C. parvum was decreased in nude mice administered with sIgA from the bile of previously infected immunocompetent rats (Albert et al 1994). However, studies have demonstrated that mice depleted of B-cells and unable to produce signi®cant amounts of antibodies were no more susceptible to C. muris or C. parvum infection than control animals (Takhi-Kilani et al 1990, McDonald & Bancroft 1998.…”

Section: Mechanisms Of Parasite Eliminationmentioning

confidence: 99%

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Host cell‐mediated responses to infection with Cryptosporidium

McDonald

2000

Parasite Immunology

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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.

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Section: Mechanisms Of Parasite Eliminationmentioning

confidence: 99%

Section: Mechanisms Of Parasite Eliminationmentioning

confidence: 99%

Host cell‐mediated responses to infection with Cryptosporidium

McDonald

2000

Parasite Immunology

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“…Promising in this respect are dose response studies in animal models and, recently, the development of human tissue culture models that can be infected by Cryptosporidium . As our knowledge of infection and virulence of Cryptosporidium in human hosts increases, results from animal models and tissue culture models become more relevant, as proxies for studying the dynamics of infection, ( 9 ) influence of innate and acquired immune parameters, ( 6 , 7 , 19 , 26 ) nonimmune defensive responses, ( 2 , 14 ) influence of age, ( 22 ) or therapeutic treatment. ( 11 )…”

Section: Discussionmentioning

confidence: 99%

Cryptosporidium Dose Response Studies: Variation Between Isolates

2002

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The infectivity of three different isolates of the waterborne protozoan parasite Cryptosporidium parvum has been tested in human feeding studies. These three isolates (Iowa, TAMU, and UCP) have different ID50s, indicating substantial variation in their infectivity for humans. This finding is of great importance for quantitative risk assessment as it provides strong evidence for heterogeneity in infectivity among isolates of the same species.

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“…Promising in this respect are dose response studies in animal models and, recently, the development of human tissue culture models that can be infected by Cryptosporidium. As our knowledge of infection and virulence of Cryptosporidium in human hosts increases, results from animal models and tissue culture models become more relevant, as proxies for studying the dynamics of infection, (9) in¯uence of innate and acquired immune parameters, (6,7,19,26) nonimmune defensive responses, (2,14) in¯uence of age, (22) or therapeutic treatment. (11)…”

Section: Research Prioritiesmentioning

confidence: 99%

Cryptosporidium Dose‐Response Studies: Variation Between Hosts

Teunis¹,

Chappell²,

Okhuysen³

2002

Risk Analysis

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The issue of variation is highly important in dose-response analysis: variation among genetically related pathogens infecting the same host, but also variation among hosts, in susceptibility to infection by the same pathogen. This latter issue is addressed here for the protozoan parasite Cryptosporidium parvum, the causative agent for many outbreaks of water-borne gastrointestinal illness. In human feeding studies, infectivity has been shown to be low in subjects with high preexisting anti-Cryptosporidium IgG-levels. Here we adapt the hit theory model of microbial infection to incorporate covariables, characterizing the immune status of the susceptible host. The probability of any single oocyst in the inoculum to cause infection appears to depend on preexisting IgG-levels. This does not necessarily imply direct protection by the humoral immune system; high IgG-levels may reflect a recent episode of infection/illness, and be an epi-phenomenon associated with other protective responses. The IgG-dependence of the dose-response relation can be easily applied in quantitative risk analysis. The distribution of anti-Cryptosporidium IgG levels in the general population is accessible by analyzing serum banks, which are maintained in many Western countries. Using such an approach provides first insights into the variation of susceptibility to infection in the general population.

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Treatment of Murine Cryptosporidiosis with Anticryptosporidial Immune Rat Bile

Cited by 8 publications

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Host cell‐mediated responses to infection with Cryptosporidium

Host cell‐mediated responses to infection with Cryptosporidium

Cryptosporidium Dose Response Studies: Variation Between Isolates

Cryptosporidium Dose‐Response Studies: Variation Between Hosts

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