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Microorganisms
Volume 13
Issue 1
10.3390/microorganisms13010110
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Article

Mycobacteria Exploit Host GPR84 to Dampen Pro-Inflammatory Responses and Promote Infection in Macrophages

by
Reziya Wumaier
1,†,
Ke Zhang
2,†,
Jing Zhou
3,
Zilu Wen
3,
Zihan Chen
3,4,
Geyang Luo
3,
Hao Wang
3,
Juliang Qin
5,
Bing Du
5,
Hua Ren
5,
Yanzheng Song
3,
Qian Gao
1,* and
Bo Yan
3,*
1
Key Laboratory of Medical Molecular Virology (MOE/NHC/CAMS), School of Basic Medical Sciences, Shanghai Medical College, Shanghai Public Health Clinical Center, Fudan University, Shanghai 200433, China
2
Shanghai Institute of Infectious Disease and Biosecurity, Fudan University, Shanghai 200032, China
3
Shanghai Public Health Clinical Center, Fudan University, Shanghai 201508, China
4
Pathology Department, The First Affiliated Hospital of Shenzhen University, Shenzhen Second People’s Hospital, Shenzhen 518035, China
5
Shanghai Frontiers Science Center of Genome Editing and Cell Therapy, Shanghai Key Laboratory of Regulatory Biology and School of Life Sciences, East China Normal University, Shanghai 200241, China
*
Authors to whom correspondence should be addressed.
†
These authors contributed equally to this work.
Microorganisms 2025, 13(1), 110; https://doi.org/10.3390/microorganisms13010110
Submission received: 26 November 2024 / Revised: 24 December 2024 / Accepted: 31 December 2024 / Published: 8 January 2025
(This article belongs to the Special Issue Diagnosis, Characterization and Treatment of Emerging Pathogens, Second Edition)
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Abstract

Tuberculosis (TB) remains the major cause of mortality and morbidity, causing approximately 1.3 million deaths annually. As a highly successful pathogen, Mycobacterium tuberculosis (Mtb) has evolved numerous strategies to evade host immune responses, making it essential to understand the interactions between Mtb and host cells. G-protein-coupled receptor 84 (GPR84), a member of the G-protein-coupled receptor family, contributes to the regulation of pro-inflammatory reactions and the migration of innate immune cells, such as macrophages. Its role in mycobacterial infection, however, has not yet been explored. We found that GPR84 is induced in whole blood samples from tuberculosis patients and Mycobacterium marinum (Mm)-infected macrophage models. Using a Mm-wasabi infection model in mouse tails, we found that GPR84 is an important determinant of the extent of tissue damage. Furthermore, from our studies in an in vitro macrophage Mm infection model, it appears that GPR84 inhibits pro-inflammatory cytokines expression and increases intracellular lipid droplet (LD) accumulation, thereby promoting intracellular bacterial survival. Our findings suggest that GPR84 could be a potential therapeutic target for host-directed anti-TB therapeutics.
Keywords: tuberculosis (TB); G-protein-coupled receptors 84 (GPR84); pro-inflammatory cytokines tuberculosis (TB); G-protein-coupled receptors 84 (GPR84); pro-inflammatory cytokines

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MDPI and ACS Style

Wumaier, R.; Zhang, K.; Zhou, J.; Wen, Z.; Chen, Z.; Luo, G.; Wang, H.; Qin, J.; Du, B.; Ren, H.; et al. Mycobacteria Exploit Host GPR84 to Dampen Pro-Inflammatory Responses and Promote Infection in Macrophages. Microorganisms 2025, 13, 110. https://doi.org/10.3390/microorganisms13010110

AMA Style

Wumaier R, Zhang K, Zhou J, Wen Z, Chen Z, Luo G, Wang H, Qin J, Du B, Ren H, et al. Mycobacteria Exploit Host GPR84 to Dampen Pro-Inflammatory Responses and Promote Infection in Macrophages. Microorganisms. 2025; 13(1):110. https://doi.org/10.3390/microorganisms13010110

Chicago/Turabian Style

Wumaier, Reziya, Ke Zhang, Jing Zhou, Zilu Wen, Zihan Chen, Geyang Luo, Hao Wang, Juliang Qin, Bing Du, Hua Ren, and et al. 2025. "Mycobacteria Exploit Host GPR84 to Dampen Pro-Inflammatory Responses and Promote Infection in Macrophages" Microorganisms 13, no. 1: 110. https://doi.org/10.3390/microorganisms13010110

APA Style

Wumaier, R., Zhang, K., Zhou, J., Wen, Z., Chen, Z., Luo, G., Wang, H., Qin, J., Du, B., Ren, H., Song, Y., Gao, Q., & Yan, B. (2025). Mycobacteria Exploit Host GPR84 to Dampen Pro-Inflammatory Responses and Promote Infection in Macrophages. Microorganisms, 13(1), 110. https://doi.org/10.3390/microorganisms13010110

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