Fpr2/CXCL1/2 Controls Rapid Neutrophil Infiltration to Inhibit Streptococcus agalactiae Infection

Streptococcus agalactiae, also known as group B streptococcus (GBS), can cause pneumonia, meningitis, and bacteremia, making it a pathogen that can increase the risk of death in newborns and immunodeficient individuals. Neutrophils are the first barrier to a host’s innate immune defense against thes...

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Autores principales:	Zeyu Sun, Wenhua Huang, Yuling Zheng, Peng Liu, Wenbo Yang, Zinan Guo, Decong Kong, Qingyu Lv, Xinyu Zhou, Zongmin Du, Hua Jiang, Yongqiang Jiang
Formato:	article
Lenguaje:	EN
Publicado:	Frontiers Media S.A. 2021
Materias:	Streptococcus agalactiae (GBS) formyl peptide receptor 2 (FPR2) CXCL1 = chemokine (CXC) ligand 1 chemokine (C-X-C motif) ligand 2 neutrophil (PMN) Immunologic diseases. Allergy RC581-607
Acceso en línea:	https://doaj.org/article/f05a8912b8b7461a8e6c1b2eeda562e8
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spelling	oai:doaj.org-article:f05a8912b8b7461a8e6c1b2eeda562e82021-11-30T18:29:22ZFpr2/CXCL1/2 Controls Rapid Neutrophil Infiltration to Inhibit Streptococcus agalactiae Infection1664-322410.3389/fimmu.2021.786602https://doaj.org/article/f05a8912b8b7461a8e6c1b2eeda562e82021-11-01T00:00:00Zhttps://www.frontiersin.org/articles/10.3389/fimmu.2021.786602/fullhttps://doaj.org/toc/1664-3224Streptococcus agalactiae, also known as group B streptococcus (GBS), can cause pneumonia, meningitis, and bacteremia, making it a pathogen that can increase the risk of death in newborns and immunodeficient individuals. Neutrophils are the first barrier to a host’s innate immune defense against these infections. Fpr2(Formyl peptide receptor 2) is an important chemotactic receptor of neutrophils, though its activation would cause pro- and anti-inflammatory effects. In this study, we found that mice without Fpr2 receptor were highly susceptible to GBS infections. These mice demonstrated decreased chemotaxis to neutrophils, decreased bactericidal ability of neutrophils, and high mortality. RNA-seq and Luminex assay indicated that Fpr2 activates key signal molecules downstream and produces chemokines CXCL1/2 to chemotaxis neutrophils. Like Fpr2-/-, CXCL1/2 or neutrophil depletion impairs host’s ability to defend against GBS infection. Altogether, these data indicate that Fpr2 contributes to a host’s ability to control GBS infection and that a lack of Fpr2 was associated with selective impairment during the production of chemokines CXCL1 and CXCL2 as well as neutrophil recruitment. Here, We clarified that Fpr2, as a chemotactic receptor, could not only directly chemotactic neutrophils, but also regulate the production of chemokines to control infection by chemotactic neutrophils.Zeyu SunWenhua HuangYuling ZhengPeng LiuWenbo YangZinan GuoDecong KongQingyu LvXinyu ZhouZongmin DuHua JiangYongqiang JiangFrontiers Media S.A.articleStreptococcus agalactiae(GBS)formyl peptide receptor 2 (FPR2)CXCL1 = chemokine (CXC) ligand 1chemokine (C-X-C motif) ligand 2neutrophil (PMN)Immunologic diseases. AllergyRC581-607ENFrontiers in Immunology, Vol 12 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	Streptococcus agalactiae (GBS) formyl peptide receptor 2 (FPR2) CXCL1 = chemokine (CXC) ligand 1 chemokine (C-X-C motif) ligand 2 neutrophil (PMN) Immunologic diseases. Allergy RC581-607
spellingShingle	Streptococcus agalactiae (GBS) formyl peptide receptor 2 (FPR2) CXCL1 = chemokine (CXC) ligand 1 chemokine (C-X-C motif) ligand 2 neutrophil (PMN) Immunologic diseases. Allergy RC581-607 Zeyu Sun Wenhua Huang Yuling Zheng Peng Liu Wenbo Yang Zinan Guo Decong Kong Qingyu Lv Xinyu Zhou Zongmin Du Hua Jiang Yongqiang Jiang Fpr2/CXCL1/2 Controls Rapid Neutrophil Infiltration to Inhibit Streptococcus agalactiae Infection
description	Streptococcus agalactiae, also known as group B streptococcus (GBS), can cause pneumonia, meningitis, and bacteremia, making it a pathogen that can increase the risk of death in newborns and immunodeficient individuals. Neutrophils are the first barrier to a host’s innate immune defense against these infections. Fpr2(Formyl peptide receptor 2) is an important chemotactic receptor of neutrophils, though its activation would cause pro- and anti-inflammatory effects. In this study, we found that mice without Fpr2 receptor were highly susceptible to GBS infections. These mice demonstrated decreased chemotaxis to neutrophils, decreased bactericidal ability of neutrophils, and high mortality. RNA-seq and Luminex assay indicated that Fpr2 activates key signal molecules downstream and produces chemokines CXCL1/2 to chemotaxis neutrophils. Like Fpr2-/-, CXCL1/2 or neutrophil depletion impairs host’s ability to defend against GBS infection. Altogether, these data indicate that Fpr2 contributes to a host’s ability to control GBS infection and that a lack of Fpr2 was associated with selective impairment during the production of chemokines CXCL1 and CXCL2 as well as neutrophil recruitment. Here, We clarified that Fpr2, as a chemotactic receptor, could not only directly chemotactic neutrophils, but also regulate the production of chemokines to control infection by chemotactic neutrophils.
format	article
author	Zeyu Sun Wenhua Huang Yuling Zheng Peng Liu Wenbo Yang Zinan Guo Decong Kong Qingyu Lv Xinyu Zhou Zongmin Du Hua Jiang Yongqiang Jiang
author_facet	Zeyu Sun Wenhua Huang Yuling Zheng Peng Liu Wenbo Yang Zinan Guo Decong Kong Qingyu Lv Xinyu Zhou Zongmin Du Hua Jiang Yongqiang Jiang
author_sort	Zeyu Sun
title	Fpr2/CXCL1/2 Controls Rapid Neutrophil Infiltration to Inhibit Streptococcus agalactiae Infection
title_short	Fpr2/CXCL1/2 Controls Rapid Neutrophil Infiltration to Inhibit Streptococcus agalactiae Infection
title_full	Fpr2/CXCL1/2 Controls Rapid Neutrophil Infiltration to Inhibit Streptococcus agalactiae Infection
title_fullStr	Fpr2/CXCL1/2 Controls Rapid Neutrophil Infiltration to Inhibit Streptococcus agalactiae Infection
title_full_unstemmed	Fpr2/CXCL1/2 Controls Rapid Neutrophil Infiltration to Inhibit Streptococcus agalactiae Infection
title_sort	fpr2/cxcl1/2 controls rapid neutrophil infiltration to inhibit streptococcus agalactiae infection
publisher	Frontiers Media S.A.
publishDate	2021
url	https://doaj.org/article/f05a8912b8b7461a8e6c1b2eeda562e8
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Fpr2/CXCL1/2 Controls Rapid Neutrophil Infiltration to Inhibit Streptococcus agalactiae Infection

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