title: Absence of TLR2 influences survival of neutrophils after infection with Candida albicans.
abstract: Candida albicans is an opportunistic pathogen, which causes local and/or disseminated diseases in immunosuppressed humans. Phagocytic cells play a critical role in the immune response against C. albicans. Toll like receptors (TLR) are important in the identification of invading microorganisms and in the regulation of neutrophil survival. TLR2 has been shown to participate in the response against pathogenic yeasts and to increase the functional life span of neutrophils. In view of these observations, we studied the involvement of TLR2 in neutrophil function after C. albicans infection. The absence of TLR2 resulted in lower chemotaxis of neutrophils to the site of infection. This in turn was associated with lower levels of chemokines from neutrophils, facilitating the dissemination of the pathogen to the lymph nodes and spleen. A high frequency of apoptotic neutrophils and macrophages in the inflammatory exudates from TLR2(-/-) mice was found. In addition, the phagocytic activity of neutrophils and macrophages, nitric oxide production and myeloperoxidase activity were diminished in cells from TLR2(-/-) mice. Together, these data demonstrate the importance of TLR2 signals for neutrophils activation and survival after C. albicans infection.
authors.affiliation: Department of Biological Sciences, Bauru Dental School, University of São Paulo, Bauru, SP, Brazil.
authors.forename: Venessa
authors.initials: V
authors.lastname: Tessarolli
authors.forename: Thaís Helena
authors.initials: TH
authors.lastname: Gasparoto
authors.forename: Hayana Ramos
authors.initials: HR
authors.lastname: Lima
authors.forename: Eduardo Aleixo
authors.initials: EA
authors.lastname: Figueira
authors.forename: Thiago Pompermaier
authors.initials: TP
authors.lastname: Garlet
authors.forename: Sérgio Aparecido
authors.initials: SA
authors.lastname: Torres
authors.forename: Gustavo Pompermaier
authors.initials: GP
authors.lastname: Garlet
authors.forename: João Santana
authors.initials: JS
authors.lastname: Da Silva
authors.forename: Ana Paula
authors.initials: AP
authors.lastname: Campanelli
mesh_terms: D000818:Animals; D002176:Candida albicans / Q000276:immunology* / Q000472:pathogenicity*; D002177:Candidiasis / Q000276:immunology* / Q000382:microbiology; D002470:Cell Survival; D002633:Chemotaxis / Q000276:immunology; D016207:Cytokines / Q000378:metabolism; D004195:Disease Models, Animal; D005122:Exudates and Transudates / Q000166:cytology; D006801:Humans; D008198:Lymph Nodes / Q000382:microbiology; D008297:Male; D051379:Mice; D008807:Mice, Inbred BALB C; D018345:Mice, Knockout; D009504:Neutrophils / Q000276:immunology* / Q000382:microbiology*; D009569:Nitric Oxide / Q000378:metabolism; D009195:Peroxidase / Q000378:metabolism; D010587:Phagocytosis; D013154:Spleen / Q000382:microbiology; D051195:Toll-Like Receptor 2 / Q000172:deficiency / Q000276:immunology*
chemical_list: D016207:Cytokines; D051195:Toll-Like Receptor 2; D009569:Nitric Oxide; D009195:Peroxidase