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Ambient pollen proteins play key roles in the incidence of allergenic respiratory health, and numerous reports have focused on respiratory diseases caused by air pollutants. However, there is still a lack of understanding of the specific mechanisms underlying the involvement of microbiota in the respiratory tracts and effects induced by air pollutants. Therefore, an allergenic animal model was established to investigate the characterization of microbials in the lung induced by allergenic Platanus pollen protein (Pla a3) and ambient fine particulate matter. Our data showed that the mice exhibited strong immune and inflammatory responses after being exposed to PMs and Pla a3 protein. This included increased levels of immunoglobulins IgG and IgE, as well as elevated levels of cytokines TNF-α, IFN-γ, IL-4, and IL-13. Furthermore, the amounts of pathogenic bacteria, such as Desulfobacterota, Enterococcus, Ferruginibacter, and Pseudoxanthomonas, in the lung microbiota of the Pla a3 exposure group increased significantly. Correlation analysis revealed a strong association between specific lung bacteria and alterations in cytokines from the lung samples. Probiotic bacteria, Deferribacterota and Bifidobacterium, was associated with changes in the level of IgG and IgE. However, pathogenic bacteria, like Prevotella and Fusobacterium, were linked with the cytokines IL-4 and TNF-α. [ABSTRACT FROM AUTHOR]

Cancer development is a complex process involving both genetic and epigenetic changes. The SWI/SNF (switch/sucrose non‐fermentable) chromatin remodelling complex, one of the most studied ATP‐dependent complexes, plays an important role in coordinating chromatin structural stability, gene expression and post‐translational modifications. The SWI/SNF complex can be classified into BAF, PBAF and GBAF according to their constituent subunits. Cancer genome sequencing studies have shown a high incidence of mutations in genes encoding subunits of the SWI/SNF chromatin remodelling complex, with abnormalities in one or more of these genes present in nearly 25% of all cancers, which indicating that stabilizing normal expression of genes encoding subunits in the SWI/SNF complex may prevent tumorigenesis. In this paper, we will review the relationship between the SWI/SNF complex and some clinical tumours and its mechanism of action. The aim is to provide a theoretical basis to guide the diagnosis and treatment of tumours caused by mutations or inactivation of one or more genes encoding subunits of the SWI/SNF complex in the clinical setting. [ABSTRACT FROM AUTHOR]