ArticleScientific reports2024
Differential requirement of formyl peptide receptor 1 in macrophages and neutrophils in the host defense against Mycobacterium tuberculosis Infection.
Article in Scientific reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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4 citing papers in PubMed.
- From Gene Expression to Candidate Biomarkers in Ulcerative Colitis: Aquaporin-9 in Neutrophil Extracellular Traps Formation Pathways.Iranian journal of medical sciences · 2026Article
- Development and validation of a nomogram for predicting unfavorable treatment outcomes in patients with pulmonary tuberculosis and diabetes mellitus.Frontiers in medicine · 2026Article
- Integrated multi-omics profiling reveals immune-related biomarkers and regulatory networks for early prediction of tuberculosis in type 2 diabetes mellitus.Frontiers in immunology · 2026Article
- Assessing the potential of bacterial signal peptides for radiopharmaceutical applications.Scientific reports · 2025Article
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Abstract
Formyl peptide receptors (FPR), part of the G-protein coupled receptor superfamily, are pivotal in directing phagocyte migration towards chemotactic signals from bacteria and host tissues. Although their roles in acute bacterial infections are well-documented, their involvement in immunity against tuberculosis (TB) remains unexplored. Here, we investigate the functions of Fpr1 and Fpr2 in defense against Mycobacterium tuberculosis (Mtb), the causative agent of TB. Elevated levels of Fpr1 and Fpr2 were found in the lungs of mice, rabbits and peripheral blood of humans infected with Mtb, suggesting a crucial role in the immune response. The effects of Fpr1 and Fpr2 deletion on bacterial load, lung damage, and cellular inflammation were assessed in a murine TB model utilizing hypervirulent strain of Mtb from the W-Beijing lineage. While Fpr2 deletion had no impact on disease outcome, Fpr1-deficient mice demonstrated improved bacterial control, especially by macrophages. Bone marrow-derived macrophages from these Fpr1
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