tetano
Editor, Senior Moderator
Int J Mol Sci
. 2025 Oct 28;26(21):10487.
doi: 10.3390/ijms262110487. Influenza A Virus and Mycoplasma pneumoniae Coinfection Mediates Immune Dysregulation and Exacerbates Disease Severity
Yanan Wu[SUP] 1 [/SUP], Qi Zhu[SUP] 1 [/SUP], Jing Liu[SUP] 1 [/SUP], Hongyun Chuan[SUP] 1 [/SUP], Lingyu He[SUP] 2 [/SUP], Mingqing Wang[SUP] 3 [/SUP], Lilan Xu[SUP] 1 [/SUP], Runfang Zhang[SUP] 1 [/SUP], Yao Liu[SUP] 3 [/SUP], Guoyang Liao[SUP] 1 [/SUP], Weidong Li[SUP] 3 [/SUP], Chengquan Sun[SUP] 4 [/SUP], Jian Zhou[SUP] 4 [/SUP]
Affiliations
Coinfection with influenza virus and Mycoplasma pneumoniae (MP) increases mortality during influenza pandemics; however, its specific impact on Mycoplasma Pneumoniae Pneumonia (MPP) patients or animal models remains unclear. The underlying mechanisms of influenza A virus (IAV)-MP interactions are not fully understood. To investigate the causes of heightened mortality, we established a lethal sequential coinfection mouse model using H3N2 influenza and MP. Coinfection led to prolonged viral persistence, enhanced pulmonary immune cell infiltration, and significantly elevated levels of inflammatory cytokines (IL-6, CCL3, CCL4, and G-CSF; p < 0.05-0.001), culminating in severe pneumonia. Notably, coinfected mice exhibited impaired CD8+ T-cell responses (p < 0.05) and increased pulmonary IL-6 and IL-1α levels (p < 0.05) compared with the controls. Our findings demonstrate that IAV-MP coinfection induces immune-mediated lung injury, which likely contributes to the observed mortality. This study provides critical insights into the immunopathogenesis of coinfection and suggests potential therapeutic targets for managing coinfected patients.
Keywords: Mycoplasma pneumoniae; coinfection; influenza; mouse model.
. 2025 Oct 28;26(21):10487.
doi: 10.3390/ijms262110487. Influenza A Virus and Mycoplasma pneumoniae Coinfection Mediates Immune Dysregulation and Exacerbates Disease Severity
Yanan Wu[SUP] 1 [/SUP], Qi Zhu[SUP] 1 [/SUP], Jing Liu[SUP] 1 [/SUP], Hongyun Chuan[SUP] 1 [/SUP], Lingyu He[SUP] 2 [/SUP], Mingqing Wang[SUP] 3 [/SUP], Lilan Xu[SUP] 1 [/SUP], Runfang Zhang[SUP] 1 [/SUP], Yao Liu[SUP] 3 [/SUP], Guoyang Liao[SUP] 1 [/SUP], Weidong Li[SUP] 3 [/SUP], Chengquan Sun[SUP] 4 [/SUP], Jian Zhou[SUP] 4 [/SUP]
Affiliations
- PMID: 41226526
- PMCID: PMC12607711
- DOI: 10.3390/ijms262110487
Coinfection with influenza virus and Mycoplasma pneumoniae (MP) increases mortality during influenza pandemics; however, its specific impact on Mycoplasma Pneumoniae Pneumonia (MPP) patients or animal models remains unclear. The underlying mechanisms of influenza A virus (IAV)-MP interactions are not fully understood. To investigate the causes of heightened mortality, we established a lethal sequential coinfection mouse model using H3N2 influenza and MP. Coinfection led to prolonged viral persistence, enhanced pulmonary immune cell infiltration, and significantly elevated levels of inflammatory cytokines (IL-6, CCL3, CCL4, and G-CSF; p < 0.05-0.001), culminating in severe pneumonia. Notably, coinfected mice exhibited impaired CD8+ T-cell responses (p < 0.05) and increased pulmonary IL-6 and IL-1α levels (p < 0.05) compared with the controls. Our findings demonstrate that IAV-MP coinfection induces immune-mediated lung injury, which likely contributes to the observed mortality. This study provides critical insights into the immunopathogenesis of coinfection and suggests potential therapeutic targets for managing coinfected patients.
Keywords: Mycoplasma pneumoniae; coinfection; influenza; mouse model.