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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| Veröffentlicht in: | Cellular immunology Jg. 405-406; S. 104886 |
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| Format: | Journal Article |
| Sprache: | Englisch |
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01.11.2024
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| ISSN: | 0008-8749, 1090-2163, 1090-2163 |
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| Abstract | [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. |
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| AbstractList | 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.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. [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. 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 F4/80 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. |
| ArticleNumber | 104886 |
| Author | Francisco da Silva, Tiago Cordeiro Valadão, Iuri Carvalho Carneiro, Milena Morais Freitas, Vanessa Akemi Amamura, Thaís Paula Lepique, Ana Isaac, Lourdes |
| Author_xml | – sequence: 1 givenname: Tiago surname: Francisco da Silva fullname: Francisco da Silva, Tiago organization: Department of Immunology, Institute of Biomedical Sciences, University of São Paulo, São Paulo, SP, Brazil – sequence: 2 givenname: Thaís surname: Akemi Amamura fullname: Akemi Amamura, Thaís organization: Department of Immunology, Institute of Biomedical Sciences, University of São Paulo, São Paulo, SP, Brazil – sequence: 3 givenname: Iuri surname: Cordeiro Valadão fullname: Cordeiro Valadão, Iuri organization: Tumor Microenvironment Laboratory, Institute of Biomedical Sciences, University of São Paulo, São Paulo, SP, Brazil – sequence: 4 givenname: Milena surname: Carvalho Carneiro fullname: Carvalho Carneiro, Milena organization: Department of Immunology, Institute of Biomedical Sciences, University of São Paulo, São Paulo, SP, Brazil – sequence: 5 givenname: Vanessa surname: Morais Freitas fullname: Morais Freitas, Vanessa organization: Tumor Microenvironment Laboratory, Institute of Biomedical Sciences, University of São Paulo, São Paulo, SP, Brazil – sequence: 6 givenname: Ana surname: Paula Lepique fullname: Paula Lepique, Ana organization: Laboratory of Immunomodulation, Institute of Biomedical Sciences, University of São Paulo, São Paulo, SP, Brazil – sequence: 7 givenname: Lourdes surname: Isaac fullname: Isaac, Lourdes email: louisaac@icb.usp.br organization: Department of Immunology, Institute of Biomedical Sciences, University of São Paulo, São Paulo, SP, Brazil |
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| Keywords | C3 Complement system C3 deficiency Macrophages |
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•The lack of C3 causes morphological alterations in peritoneal macrophages.•The lack of C3 increases the levels of CD11c in macrophages.•The... 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... |
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| SubjectTerms | 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 |
| Title | Complement system component 3 deficiency modulates the phenotypic profile of murine macrophages |
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