ArticlePhysiological reports2025
IL-6 signaling regulates the inflammatory response without impacting pathogen burden during influenza-associated pulmonary aspergillosis.
Article in Physiological reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
2 citing papers in PubMed.
- Myeloid Cell States in Influenza-Associated Pulmonary Aspergillosis Are Shaped by Iron Overload and Metabolic Reprogramming.bioRxiv : the preprint server for biology · 2026Article
- IL-6 signaling regulates the inflammatory response without impacting pathogen burden during influenza-associated pulmonary aspergillosis.Physiological reports · 2025Article
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Authors and funding
9 authors.
Funding
Abstract
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.
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Registered trials
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