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Fpr2/CXCL1/2 Controls Rapid Neutrophil Infiltration to Inhibit Streptococcus agalactiae Infection
Zeyu Sun1, Wenhua Huang1, Yuling Zheng1
1State Key Laboratory of Pathogen and Biosecurity, Institute of Microbiology and Epidemiology, Academy of Military Medical Sciences, Beijing, China.
Abstract:
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.
Insights
Formyl peptide receptor 2 (Fpr2) is crucial for controlling Group B Streptococcus (GBS) infections. Its absence impairs neutrophil response and increases mortality, highlighting Fpr2's role in innate immunity.
Area of Science:
- Immunology
- Microbiology
- Molecular Biology
Background:
- Group B Streptococcus (GBS) is a significant pathogen causing severe infections in newborns and immunocompromised individuals.
- Neutrophils are key innate immune cells combating GBS, and their function is regulated by chemotactic receptors.
- Formyl peptide receptor 2 (Fpr2) is a neutrophil receptor with complex pro- and anti-inflammatory roles.
Purpose of the Study:
- To investigate the role of Fpr2 in host defense against GBS infection.
- To elucidate the mechanisms by which Fpr2 influences neutrophil function and immune response to GBS.
Main Methods:
- Utilized Fpr2 knockout (Fpr2-/-) mice to assess susceptibility to GBS.
- Employed RNA-sequencing and Luminex assays to analyze molecular signaling pathways.
- Investigated the impact of Fpr2 deficiency on neutrophil chemotaxis and bactericidal activity.
Main Results:
- Fpr2-/- mice exhibited increased susceptibility to GBS, characterized by high mortality, reduced neutrophil chemotaxis, and impaired neutrophil bactericidal capacity.
- Fpr2 activation was found to induce downstream signaling molecules and the production of chemokines CXCL1/2, essential for neutrophil recruitment.
- Depletion of CXCL1/2 or neutrophils mimicked the susceptibility observed in Fpr2-/- mice.
Conclusions:
- Fpr2 plays a critical role in controlling GBS infection by directly recruiting neutrophils and regulating chemokine production.
- Impaired Fpr2 function leads to deficiencies in chemokine production (CXCL1/2) and neutrophil recruitment, compromising host defense against GBS.
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