ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2025
Role of Atypical MAPK p38 Signaling in the Progression of Influenza A-Induced Acute Lung Injury.
Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2025. 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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Who cites it
4 citing papers in PubMed.
- Avian coronaviruses induce inflammatory responses by activating p38/MAPK signaling and NLRP3/caspase-1 inflammasomes through sphingosine-1-phosphate receptor 1.Veterinary research · 2026Article
- Post-translational modification networks as master regulators of influenza virus replication, host adaptation, and immune evasion.Frontiers in immunology · 2026Review
- Atypical p38 Kinase Signaling in Retinal Vascular Damage and Recovery.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Article
- Role of Atypical MAPK p38 Signaling in the Progression of Influenza A-Induced Acute Lung Injury.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Article
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Authors and funding
8 authors.
Funding
Abstract
Mitogen-activated protein kinase (MAPK) p38 plays a key role in driving the pathology of acute lung injury (ALI), but effective therapeutic targeting remains elusive. Atypical p38 signaling, mediated by interaction with the adaptor protein Tumor Growth Factor β Activated Kinase 1 (TAK1) Binding Protein 1 (TAB1), has so far only been observed during pathological responses, representing a selective and alternative target during pulmonary injury. However, atypical signaling has not been investigated in the context of pulmonary injury and immune responses related to the onset and progression of ALI. Here, we utilized a genetic knock-in mouse to block influenza A-induced lung injury mediated by atypical signaling. We report that the loss of TAB1-p38 interaction reduces weight loss and recovery time, reduces histopathological scores associated with influenza-induced lung injury early during infection, and prompts earlier recruitment of monocytes to the lungs following infection. These results were found to be independent of viral replication and infectivity, representing the first evidence for the roles of atypical signaling as a driver of host-mediated pulmonary injury following influenza infection.
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Registered trials
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