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Curr Opin Crit Care. 2010 Oct;16(5):453-9. doi: 10.1097/MCC.0b013e32833e046e.

Pathogenesis of invasive candidiasis.

Author information

  • 1Department of Medicine and Nijmegen Institute for Infection, Inflammation & Immunity (N4i), Radboud University Nijmegen Medical Center, Nijmegen, The Netherlands.

Abstract

PURPOSE OF REVIEW:

Disseminated candidiasis remains a life-threatening disease in the ICU. The development of invasive disease with Candida albicans is dependent on multiple factors, such as colonization and efficient host defense at the mucosa. In the present review, we describe the host defense mechanisms against Candida that are responsible for counteracting mucosal invasion, and eliminating the pathogen once invasion has taken place.

RECENT FINDINGS:

The newly described T-helper subset Th17 is critical for mucosal anti-Candida host defense and plays a major role in controlling C. albicans colonization, whereas the Th1 response and monocyte-dependent cytokines such as IL-1 and TNF are predominantly responsible for activation of neutrophils and macrophages during disseminated candidiasis.

SUMMARY:

This knowledge provides the basis of exploring new treatment options in the fight against invasive candidiasis. Reports of beneficial effects of recombinant cytokine therapy in fungal infections, renders them prime candidates for adjuvant immunotherapy in Candida sepsis.

PMID:
20711079
[PubMed - indexed for MEDLINE]
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