tetano
Editor, Senior Moderator
Physiol Rep
. 2025 May;13(10):e70372.
doi: 10.14814/phy2.70372. IL-6 signaling regulates the inflammatory response without impacting pathogen burden during influenza-associated pulmonary aspergillosis
Lokesh Sharma[SUP] 1 [/SUP], Ravineel B Singh[SUP] 1 [/SUP], Nathaniel J Tolman[SUP] 1 [/SUP], Caden Ngeow[SUP] 1 [/SUP], Alexis M Duray[SUP] 2 [/SUP], Nima Naghshtabrizi[SUP] 1 [/SUP], Aijaz Ahmad[SUP] 1 [/SUP], William Bain[SUP] 1 [/SUP], Keven M Robinson[SUP] 1 [/SUP]
Affiliations
Viral infections increase host susceptibility to opportunistic pathogens like Aspergillus fumigatus (AF), exacerbating disease severity and prolonging its clinical course. Interleukin-6 (IL-6) drives pathological inflammation in viral infections such as COVID-19, but its role in influenza, particularly with secondary AF infection, remains unclear. Using a mouse model of post-influenza AF infection, including IL-6 knockout mice, we found that IL-6 signaling promotes neutrophilic lung inflammation but is not required for pathogen clearance of either influenza or AF. However, IL-6 deficiency increases epithelial cell damage, as indicated by elevated RAGE levels in bronchoalveolar lavage fluid. In contrast, lung capillary permeability (measured by IgM levels in BAL) and tissue injury (assessed histologically) remain unaffected in the absence of IL-6 signaling. These findings reveal a nuanced role for IL-6 in post-influenza AF infection, underscoring its contribution to lung inflammation and epithelial integrity.
Keywords: IL‐6 signaling; aspergillus; inflammation; influenza; influenza associated pulmonary aspergillosis.
. 2025 May;13(10):e70372.
doi: 10.14814/phy2.70372. IL-6 signaling regulates the inflammatory response without impacting pathogen burden during influenza-associated pulmonary aspergillosis
Lokesh Sharma[SUP] 1 [/SUP], Ravineel B Singh[SUP] 1 [/SUP], Nathaniel J Tolman[SUP] 1 [/SUP], Caden Ngeow[SUP] 1 [/SUP], Alexis M Duray[SUP] 2 [/SUP], Nima Naghshtabrizi[SUP] 1 [/SUP], Aijaz Ahmad[SUP] 1 [/SUP], William Bain[SUP] 1 [/SUP], Keven M Robinson[SUP] 1 [/SUP]
Affiliations
- PMID: 40420617
- DOI: 10.14814/phy2.70372
Viral infections increase host susceptibility to opportunistic pathogens like Aspergillus fumigatus (AF), exacerbating disease severity and prolonging its clinical course. Interleukin-6 (IL-6) drives pathological inflammation in viral infections such as COVID-19, but its role in influenza, particularly with secondary AF infection, remains unclear. Using a mouse model of post-influenza AF infection, including IL-6 knockout mice, we found that IL-6 signaling promotes neutrophilic lung inflammation but is not required for pathogen clearance of either influenza or AF. However, IL-6 deficiency increases epithelial cell damage, as indicated by elevated RAGE levels in bronchoalveolar lavage fluid. In contrast, lung capillary permeability (measured by IgM levels in BAL) and tissue injury (assessed histologically) remain unaffected in the absence of IL-6 signaling. These findings reveal a nuanced role for IL-6 in post-influenza AF infection, underscoring its contribution to lung inflammation and epithelial integrity.
Keywords: IL‐6 signaling; aspergillus; inflammation; influenza; influenza associated pulmonary aspergillosis.