22 suppresses the expression of the antibacterial peptides β-defensin2 and β-defensin3 in airway epithelial cells as a factor in increased susceptibility to respiratory infections (Rivas-Santiago et al., 2015). Regarding the effects on innate immunity, in vivo studies have shown that PM2.5 increases the number of inflammatory cells, especially neutrophils and macrophages, and cytokines, such as IL-6, IL-1β, TNF-α, and KC (an IL-8 homolog) in bronchial lavage fluid (BALF) and lung tissues (Honda et al., 2021). These molecules activate acute inflammation (Zhang & An 2007). PM2.5 suppresses macrophage phagocytic activity and nitric oxide production during pneumococcal infection, enhancing pneumococcal infectivity and aggravating pulmonary pathogenesis (Chen et al., 2020). In an in vitro study, PM2.5 induced IL-6, IL-1β, and TNF-α in bone marrow-derived antigen-presenting cells (Honda et al., 2021). Interestingly, the inflammatory response induced by PM2.5 in antigen-presenting cells was drastically suppressed when the particles were removed as an extract (Honda et al., 2021); therefore, the shape of xenobiotics is important in triggering an immune Fig. 1 Effects of particulate matters on respiratory and immune systems. A. HONDA and T. SAGAWA response. In addition, the recognition receptors for PM have also been elucidated. SRB-1 and Siglec-14 on antigen-presenting cells recognize silica and multi-walled carbon nanotubes, respectively, leading to the production of inflammatory cytokines, such as IL-1β, and the enhancement of phagocytosis (Tsugita et al., 2017; Yamaguchi et al., 2023). ILC2 is a new player in the innate immune system and expressed in the lungs, mesentery, skin, etc. ILC2 produces IL-5 and IL-13 in response to epithelial-derived cytokines, such as IL-33, IL-25 and thymic stromal lymphopoietin (TSLP), and induces a Th2-type immune response. IL-5 facilitates eosinophil production and maturation, and IL-13 stimulates epithelial cells to secret mucins (Habib et al., 2022). Previous studies have reported that multi-walled carbon nanotubes, O3, diesel exhaust particles and cigarette smoke activate pulmonary or BALF ILC2 in the presence or absence of allergens (Estrella et al., 2019; Lee et al., 2019). Regarding the effect on acquired immunity, in the presence of allergens, PM2.5 has increased the number of

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