Complement system component 3 deficiency modulates the phenotypic profile of murine macrophages

[Display omitted] •The lack of C3 causes morphological alterations in peritoneal macrophages.•The lack of C3 increases the levels of CD11c in macrophages.•The lack of C3 affects the phagocytosis of iC3b-opsonized particles.•The lack of C3 reduces ROS production in TPA-treated macrophages.•The lack o...

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Vydané v:	Cellular immunology Ročník 405-406; s. 104886
Hlavní autori:	Francisco da Silva, Tiago, Akemi Amamura, Thaís, Cordeiro Valadão, Iuri, Carvalho Carneiro, Milena, Morais Freitas, Vanessa, Paula Lepique, Ana, Isaac, Lourdes
Médium:	Journal Article
Jazyk:	English
Vydavateľské údaje:	Netherlands Elsevier Inc 01.11.2024
Predmet:	Animals Antigens, Differentiation - immunology Antigens, Differentiation - metabolism C3 deficiency CD11 Antigens CD11c Antigen - metabolism Complement C3 - deficiency Complement C3 - genetics Complement C3 - immunology Complement C3 - metabolism Complement C5a - immunology Complement C5a - metabolism Complement system Macrophages Macrophages - immunology Macrophages - metabolism Macrophages, Peritoneal - immunology Macrophages, Peritoneal - metabolism Male Mice Mice, Inbred C57BL Mice, Knockout Phagocytosis Phenotype Reactive Oxygen Species - metabolism Tetradecanoylphorbol Acetate - pharmacology C3 Complement system C3 deficiency Macrophages
ISSN:	0008-8749, 1090-2163, 1090-2163
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Shrnutí:	[Display omitted] •The lack of C3 causes morphological alterations in peritoneal macrophages.•The lack of C3 increases the levels of CD11c in macrophages.•The lack of C3 affects the phagocytosis of iC3b-opsonized particles.•The lack of C3 reduces ROS production in TPA-treated macrophages.•The lack of C3 reduces MAPK activation in TPA-treated macrophages. The Complement System is composed of more than 40 proteins that act in innate and adaptive immunity. C3 is the most abundant one and C3-deficient patients are more susceptible to recurrent and severe infections. Several studies have demonstrated the importance of C3 in controlling infections. However, its role in leukocyte biology is still poorly understood. This study aimed to evaluate several cellular parameters in macrophages from C3-deficient mice and compare them to similar cells from wild-type counterparts. We observed that in the absence of C3, the population of F4/80low macrophages in the peritoneal cavity of thioglycolate-treated mice is diminished, probably due to the lack of chemotactic factors like C3a and low levels of C5a. Using fluorescence microscopy analysis, we observed that macrophages from C3-deficient mice exhibited morphological alterations when compared to similar cells from wild-type mice. We observed a significant increase in the expression of CD11c, which is part of CR4 (CD11c/CD18), in macrophages from C3-deficient compared to cells from wild-type mice. Treatment with 12-o-tetradecanoylphorbol-13-acetate, stimulated ROS production and MAPK activation by macrophages. However, these parameters were lower in macrophages from C3-deficient mice when compared to wild-type counterparts. In addition, the phagocytosis of iC3b-opsonized Zymosan particles was diminished in macrophages from C3-deficient mice. Our results suggest that C3 deficiency in C57Black/6 mice may influence specific morphological and functional parameters of macrophages, cells of fundamental importance for both the innate and acquired immune responses.
Bibliografia:	ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23
ISSN:	0008-8749 1090-2163 1090-2163
DOI:	10.1016/j.cellimm.2024.104886