Changes in the expression of TLR9 in PBMCs and pulmonary macrophages during allergic rhinitis and asthma attacks

In recent years, the role of the monocyte macrophage system and Toll like receptor 9 (TLR9) in the pathogenesis of allergic diseases has attracted attention, but little is known about the relationship between changes in TLR9 expression on monocytes and macrophages and allergic rhinitis (AR) and allergic asthma (AA). This article uses flow cytometry to analyze the expression changes of TLR9+ monocytes in peripheral blood of patients with AR, AA, and allergic rhinitis combined with asthma (ARA). And the AR and AA models of wild-type (WT) and FcεRⅠ gene knockout (FcεRⅠ KO) mice were used to investigate the expression changes of TLR9 in monocytes and macrophages in lung tissue of mice after allergen stimulation. It was found that the proportion of TLR9+ cells in the peripheral blood mononuclear cell population of AR, AA, and ARA patients was significantly increased, indicating an increase in MFI expression representing the number of TLR9 molecules expressed in each mononuclear cell. Artemisia selengensis allergen extract (ASWE), house dust mite allergen extract (HDME), wutong pollen allergen extract (PPE) stimulate to increase the proportion of TLR9+ monocytes in the blood of AR and AA model mice, upregulate the expression level of TLR9 MFI in monocytes, and make the expression level of TLR9 in macrophages in lung tissue higher than that of control mice. In AR and AA mouse models with high-affinity IgE receptor (FcεRⅠ) KO, ASWE, especially HDME, can also induce upregulation of TLR9+ cell percentage and TLR9 MFI in monocytes. Based on the significant reduction in the proportion of TLR9+ cells and TLR9 MFI expression levels in AR and AA mice compared to wild-type (WT) mice, it can be concluded that the increase in the proportion of blood monocytes induced by allergen extract and the upregulation of TLR9 expression levels in monocytes are achieved through both FcεRⅠ dependent and non-dependent pathways. Similarly, compared with WT mice, the AA model mice of FcεRⅠ KO showed a significant increase in the proportion of lung tissue macrophages induced by allergen extract and a significant decrease in the upregulation of TLR9 expression level. In summary, monocytes may participate in the pathophysiological processes of AR, AA, and ARA through upregulation of TLR9 expression. The upregulation of TLR9 expression in lung tissue macrophages further suggests that monocytes and macrophages may form a new inflammatory signal amplification loop in local tissues through high expression of TLR9 under allergen stimulation, providing new ideas for understanding the pathogenesis of allergic airway diseases.