The study investigates how RELMα influences influenza A virus infection in the lung. Using constitutive and cell-specific Retnla deficiency, the authors demonstrate that epithelial-derived RELMα creates an environment permissive to viral infection and directly increases susceptibility of lung epithelial cells to influenza virus.
Retnla deficiency reduced infectious influenza virus burden in lung epithelial cells. Club cell-specific deletion reproduced this phenotype, supporting a direct epithelial role for RELMα. RELMα promoted influenza infection and altered epithelial cellular pathways that favor viral replication.
Retnla conditional Knockout / reporter mouse — genOway-developed using Cre-Lox and FLEx technology, with Retnla exons 2–4 targeted and the deleted locus replaced by a tdTomato reporter. The conditional-ready Retnla^Flox/Flox allele enables cell-specific deletion and was crossed with CC10-CreERT for club cell-specific Retnla deletion. The model was also converted to constitutive Retnla deficiency for whole-body studies.
Influenza A virus, viral infection, respiratory disease, lung epithelium, host-pathogen interaction, antiviral immunity, epithelial cell biology
Retnla conditional Knockout, Cre-Lox, FLEx technology, floxed exons 2–4, tdTomato reporter, cell-specific deletion, CC10-CreERT, club cells, constitutive deletion, influenza infection model
From model design to experimental results
Featured in 600+ scientific articles
Collaboration with 17 Top Pharmas,
170+ Biotechs and 380+ Academic Institutions
Generated with biopharma partners and in-house
and guaranteed freedom to operate
Models with certified health status from professional breeders in US and Europe
