期刊
FRONTIERS IN IMMUNOLOGY
卷 13, 期 -, 页码 -出版社
FRONTIERS MEDIA SA
DOI: 10.3389/fimmu.2022.978152
关键词
Aspergillus fumigatus; complement system; infectious disease; innate immunity; systemic aspergillosis
类别
资金
- Department of Biotechnology, India [BT/PR28506/MED/29/1307/2018]
- Pasteur-Roux-Cantarini postdoctoral fellowship
- [ANR-16S-CE110020-01]
- [ANR-21-CE17-0032]
Invasive aspergillosis is a life-threatening fungal infection for immunocompromised hosts. The study found that complement deficiency increases susceptibility to systemic infection by Aspergillus fumigatus.
Invasive aspergillosis (IA) is a life-threatening fungal infection for immunocompromised hosts. It is, therefore, necessary to understand the immune pathways that control this infection. Although the primary infection site is the lungs, aspergillosis can disseminate to other organs through unknown mechanisms. Herein we have examined the in vivo role of various complement pathways as well as the complement receptors C3aR and C5aR1 during experimental systemic infection by Aspergillus fumigatus, the main species responsible for IA. We show that C3 knockout (C3(-/-)) mice are highly susceptible to systemic infection of A. fumigatus. Intriguingly, C4(-/-) and factor B (FB)(-/-) mice showed susceptibility similar to the wild-type mice, suggesting that either the complement pathways display functional redundancy during infection (i.e., one pathway compensates for the loss of the other), or complement is activated non-canonically by A. fumigatus protease. Our in vitro study substantiates the presence of C3 and C5 cleaving proteases in A. fumigatus. Examination of the importance of the terminal complement pathway employing C5(-/-) and C5aR1(-/-) mice reveals that it plays a vital role in the conidial clearance. This, in part, is due to the increased conidial uptake by phagocytes. Together, our data suggest that the complement deficiency enhances the susceptibility to systemic infection by A. fumigatus.
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