Mouse data from PR8 influenza A virus infection with OM-85 intervention
Description
This study investigated the immunological mechanisms by which OM-85 modulates host responses during influenza A virus infection. The central hypothesis is that OM-85 enhances antiviral protection by promoting pulmonary CD4⁺ memory-like T-cell responses, particularly CD4⁺ tissue-resident memory-like (TRM-like) cells, thereby improving viral clearance and reducing lung inflammation. To test this hypothesis, a murine model of influenza A virus infection (PR8 strain) was established. Mice were pretreated intranasally with OM-85 for 10 consecutive days prior to viral challenge. Lung tissues, bronchoalveolar lavage fluid (BALF), and systemic samples were collected at defined time points after infection. Viral burden was assessed using TCID50 assays and quantitative PCR for viral genes (NP and NS1). Lung inflammation was evaluated by histopathology (H&E staining) and cytokine expression analysis (RT-qPCR and/or ELISA). Pulmonary immune cell populations were analyzed by flow cytometry, focusing on CD4⁺ and CD8⁺ memory-like T cells and CD4⁺ TRM-like subsets. The data show that OM-85 pretreatment significantly reduces pulmonary viral load and attenuates inflammatory lung injury following PR8 infection. Importantly, OM-85 enhances the expansion of pulmonary CD4⁺ memory-like T cells after infection, with CD4⁺ TRM-like cells representing the dominant responding subset, particularly during early infection. CD8⁺ memory-like T-cell responses were also observed but were less pronounced compared with CD4⁺ responses. Mechanistically, CD4-specific PLZF conditional knockout mice demonstrated impaired OM-85-induced CD4⁺ TRM-like responses and reduced antiviral protection. In addition, modulation of IL-15/IL-15Rα signaling using pharmacological agonists partially restored CD4⁺ memory-like T-cell responses and improved inflammatory outcomes, supporting a contributory role of this pathway. Data were generated from controlled in vivo experiments with biological replicates, and all assays were performed using standard immunological and molecular biology techniques. Data should be interpreted as evidence of an association between OM-85-induced modulation of pulmonary CD4⁺ memory-like T-cell responses and improved antiviral protection, rather than as proof of direct causality.
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Institutions
- Fudan UniversityShanghai, Shanghai