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Candida albicans escapes from mouse neutrophils
Umeå universitet, Medicinska fakulteten, Institutionen för klinisk mikrobiologi, Klinisk bakteriologi.
Umeå universitet, Medicinska fakulteten, Institutionen för klinisk mikrobiologi, Klinisk bakteriologi.
Umeå universitet, Medicinska fakulteten, Institutionen för klinisk mikrobiologi, Klinisk bakteriologi.
Department of Hematology, National University Hospital, Copenhagen, Denmark..
Vise andre og tillknytning
2013 (engelsk)Inngår i: Journal of Leukocyte Biology, ISSN 0741-5400, E-ISSN 1938-3673, Vol. 94, nr 2, s. 223-236Artikkel i tidsskrift (Fagfellevurdert) Published
Abstract [en]

Candida albicans, the most commonly isolated human fungal pathogen, is able to grow as budding yeasts or filamentous forms, such as hyphae. The ability to switch morphology has been attributed a crucial role for the pathogenesis of C. albicans. To mimic disseminated candidiasis in humans, the mouse is the most widely used model organism. Neutrophils are essential immune cells to prevent opportunistic mycoses. To explore potential differences between the rodent infection model and the human host, we compared the interactions of C. albicans with neutrophil granulocytes from mice and humans. We revealed that murine neutrophils exhibited a significantly lower ability to kill C. albicans than their human counterparts. Strikingly, C. albicans yeast cells formed germ tubes upon internalization by murine neutrophils, eventually rupturing the neutrophil membrane and thereby, killing the phagocyte. On the contrary, growth and subsequent escape of C. albicans are blocked inside human neutrophils. According to our findings, this blockage in human neutrophils might be a result of higher levels of MPO activity and the presence of α-defensins. We therefore outline differences in antifungal immune defense between humans and mouse strains, which facilitates a more accurate interpretation of in vivo results.

sted, utgiver, år, opplag, sider
Bethesda: Federation of American societies for experimental biology , 2013. Vol. 94, nr 2, s. 223-236
Emneord [en]
killing, immune evasion, myeloperoxidase, defensins
HSV kategori
Identifikatorer
URN: urn:nbn:se:umu:diva-80700DOI: 10.1189/jlb.0213063ISI: 000329744300004PubMedID: 23650619OAI: oai:DiVA.org:umu-80700DiVA, id: diva2:651098
Tilgjengelig fra: 2013-09-24 Laget: 2013-09-24 Sist oppdatert: 2018-06-08bibliografisk kontrollert

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Ermert, DavidNiemiec, Maria JoannaRöhm, MarcUrban, Constantin F.

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