Oxidative killing of Aspergillus fumigatus proceeds by parallel myeloperoxidase-dependent and -independent pathways.
AUTOR(ES)
Washburn, R G
RESUMO
The relative importance of several oxygen intermediates in fungicidal action against opsonized Aspergillus fumigatus conidia was investigated with monocytes from normal volunteers and patients with either chronic granulomatous disease or myeloperoxidase (MPO) deficiency. Results from experiments in which catalase, taurine, mannitol, or glucose-glucose oxidase were added to these phagocytes indicated that the MPO-hydrogen peroxide-halide system and an MPO-independent oxidative system exerted comparable conidiacidal activity. These findings offer a plausible explanation for the susceptibility of patients with chronic granulomatous disease to invasive Aspergillus infections; their phagocytes fail to generate hydrogen peroxide, a substrate necessary for both systems. Patients with MPO deficiency are not known to be predisposed to invasive aspergillosis, suggesting that an MPO-independent oxidative system may provide an alternative mechanism for the oxidative killing of Aspergillus spp.
ACESSO AO ARTIGO
http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=260661Documentos Relacionados
- Redundant contribution of myeloperoxidase-dependent systems to neutrophil-mediated killing of Escherichia coli.
- Protection by antibiotics against myeloperoxidase-dependent cytotoxicity to lung epithelial cells in vitro.
- Modulation of dog atrial swelling-induced chloride current by cAMP: protein kinase A-dependent and -independent pathways.
- Polyomavirus middle T antigen induces ribosomal protein S6 phosphorylation through pp60c-src-dependent and -independent pathways.
- Interleukin-2 and alpha/beta interferon down-regulate hepatitis B virus gene expression in vivo by tumor necrosis factor-dependent and -independent pathways.