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CRP Enhances the Innate Killing Mechanisms Phagocytosis and ROS Formation in a Conformation and Complement-Dependent Manner.
- Source :
-
Frontiers in immunology [Front Immunol] 2021 Aug 10; Vol. 12, pp. 721887. Date of Electronic Publication: 2021 Aug 10 (Print Publication: 2021). - Publication Year :
- 2021
-
Abstract
- Phagocytosis and the formation of reactive oxygen species (ROS) in phagocytic leukocytes are an effective killing mechanism of the innate host defense. These cellular processes of innate immunity function in a complex interplay with humoral factors. C-reactive protein (CRP) in its activated, monomeric isoform (mCRP) has been shown to activate immune cells via the classical complement pathway. We investigated the complement-dependent effects of monomeric CRP (mCRP) on neutrophils and monocyte subtypes using complement-specific inhibitors by both flow cytometry and confocal fluorescence microscopy. We demonstrate that CRP-induced ROS generation is a conformation-specific and complement-dependent process in leukocyte subsets with classical monocytes as the primary source of ROS amongst human monocyte subsets. Elucidation of this complex interplay of CRP and complement in inflammation pathophysiology might help to improve anti-inflammatory therapeutic strategies.<br />Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.<br /> (Copyright © 2021 Zeller, Bogner, Kiefer, Braig, Winninger, Fricke, Karasu, Peter, Huber-Lang and Eisenhardt.)
- Subjects :
- Host-Pathogen Interactions immunology
Humans
Leukocytes immunology
Leukocytes metabolism
Monocytes immunology
Monocytes metabolism
Neutrophils immunology
Neutrophils metabolism
C-Reactive Protein metabolism
Complement Activation immunology
Complement System Proteins immunology
Cytotoxicity, Immunologic
Immunity, Innate
Phagocytosis immunology
Reactive Oxygen Species metabolism
Subjects
Details
- Language :
- English
- ISSN :
- 1664-3224
- Volume :
- 12
- Database :
- MEDLINE
- Journal :
- Frontiers in immunology
- Publication Type :
- Academic Journal
- Accession number :
- 34447388
- Full Text :
- https://doi.org/10.3389/fimmu.2021.721887