Parasite immune escape: new views into host–parasite interactions

Gupta, Sunetra

doi:10.1016/j.mib.2005.06.011

Cited by 32 publications

(32 citation statements)

References 49 publications

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“…Obligate intracellular symbiotic microbes, such as Buchnera (Moran 1996) and Pneumocystis (Strobel and Arnold 2004), propagate asexually and often carry a minimal but stable genome, making them wholly dependent on life within their hosts (Wren 2000). Although both opportunistic and obligate pathogens commonly propagate by asexual means, these organisms often maintain large genomes and generate substantial genomic and phenotypic variation via genome rearrangements (Victoir and Dujardin 2002;Kline et al 2003) and heritable silencing at telomeres (Cross et al 1998;Borst 2002;Gupta 2005). Given that many commensal and apparently harmless symbionts may become invasive pathogens in immunocompromised hosts, the mechanisms underlying the maintenance of genetic variation and of the commensal state bear investigation (Levin et al 2000).…”

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confidence: 99%

Evolution inCandida albicansPopulations During a Single Passage Through a Mouse Host

et al. 2009

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The mechanisms and rates by which genotypic and phenotypic variation is generated in opportunistic, eukaryotic pathogens during growth in hosts are not well understood. We evaluated genomewide genetic and phenotypic evolution in Candida albicans, an opportunistic fungal pathogen of humans, during passage through a mouse host (in vivo) and during propagation in liquid culture (in vitro). We found slower population growth and higher rates of chromosome-level genetic variation in populations passaged in vivo relative to those grown in vitro. Interestingly, the distribution of long-range loss of heterozygosity (LOH) and chromosome rearrangement events across the genome differed for the two growth environments, while rates of short-range LOH were comparable for in vivo and in vitro populations. Further, for the in vivo populations, there was a positive correlation of cells demonstrating genetic alterations and variation in colony growth and morphology. For in vitro populations, no variation in growth phenotypes was detected. Together, our results demonstrate that passage through a living host leads to slower growth and higher rates of genomic and phenotypic variation compared to in vitro populations. Results suggest that the dynamics of population growth and genomewide rearrangement contribute to the maintenance of a commensal and opportunistic life history of C. albicans.

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confidence: 99%

Evolution inCandida albicansPopulations During a Single Passage Through a Mouse Host

et al. 2009

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“…The IL-4-dependent protective response against the parasite operates by a mechanism other than merely the gross degradation of the parasite environment brought about by the immune enteropathy (Garside et al 2000). However, the protective mechanisms involved in parasite expulsion are still unclear (Gupta 2005).…”

Section: Immunopathology Of Crohn's Diseasementioning

confidence: 99%

“…For chronic infection to occur, the parasite must first avoid clearance by the host immune system (Gupta 2005); helminths alter host mucosal and systemic immunity, inhibiting dysregulated inflammatory responses . For parasites of humans and animals that rely on vectors or on sexual contact for transmission, infection must not terminate before the occurrence of the crucial event that completes its life cycle (Gupta 2005).…”

Section: Immune Responses That Prevent Infection With Helminthsmentioning

confidence: 99%

“…For parasites of humans and animals that rely on vectors or on sexual contact for transmission, infection must not terminate before the occurrence of the crucial event that completes its life cycle (Gupta 2005). Multiple layers of immunoregulation have now been discovered in helminth infection; both cellular and complex molecular interactions are involved (Maizels and Yazdanbakhsh 2003).…”

Section: Immune Responses That Prevent Infection With Helminthsmentioning

confidence: 99%

“…Multiple layers of immunoregulation have now been discovered in helminth infection; both cellular and complex molecular interactions are involved (Maizels and Yazdanbakhsh 2003). A form of parasitological immune evasion known as antigenic variation can assist in avoiding host recognition (Gupta 2005). Increased numbers of goblet cells (GC) and qualitative changes in mucus secretion have been noted subsequent to infection with a number of nematode parasites (Nawa et al 1994).…”

Section: Immune Responses That Prevent Infection With Helminthsmentioning

confidence: 99%

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The use of Trichuris suis and other helminth therapies to treat Crohn’s disease

Reddy

Fried

2007

Parasitol Res

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Infections with gastrointestinal (GI) nematodes are prevalent worldwide, despite the fact that anti-helminthic medications are regarded as safe, efficient, and widely available globally. In this review, we highlight the potential therapeutic benefits that may be realized through the clinical use of Trichuris suis and other helminths for Crohn's disease (CD). Long-lived helminthic parasites are remarkable in their ability to down-regulate host immunity, protecting themselves from elimination, and also minimize severe pathological host changes. This review summarizes what is known about the underlying mechanisms that may account for the observed patterns in humans treated with helminths for CD. The Th2 arm of the immune system is emphasized as a component of primary importance in the association between the host immune system and GI nematode infections. Although GI nematode infections in humans cause significant morbidity and mortality, the existence and nature of protective mechanisms these helminths may confer remain largely unclear.

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