Inflammation and disease progression of non-type 2 respiratory diseases might be triggered not only by defects in cytokine secretion (Kapellos et al. 2018; Lambrecht and Hammad 2013; Stecenko et al. 2001), but also by defects in the intracellular calcium balance (Rimessi et al. 2021; Petit et al. 2019) and by phagocytosis (Belchamber and Donnelly 2017). Patients with non-type 2 inflammation are more susceptible to respiratory infections (Knobloch et al. 2011a, 2019; Jartti et al. 2020; Kiedrowski and Bomberger 2018), leading to a further increase in inflammation and finally to exacerbations (Stolz et al. 2019). There is an indication at least for COPD that the increased susceptibility might be caused by a reduced production of cytokines required for infection defense by systemic immune cells during their recruitment and activation processes (Knobloch et al. 2011a, 2019). However, the CXCL-8 and MMP-9 hyperproduction of local and resident AM in response to infectious trigger might contribute to the deleterious increase in inflammation which causes exacerbations (Knobloch et al. 2011b; Culpitt et al. 2003). These molecular pathologies might be considered by designing the urgently required new therapeutic approaches for lung diseases with non-type 2 inflammation.
Mechanistically, exacerbations might not only result from a defective clearance of bacteria but also from a substantial increase in inflammation. The latter might depend on an excessive response of AM to bacterial PAMPs regarding the release of proinflammatory cytokines and proteases like CXCL-8, CCL-2, and MMP-9 (Knobloch et al. 2011b). Therefore, the effect of OR stimulation on these key factors for non-type 2 respiratory diseases in the presence of bacterial PAMPs was investigated. We also considered IL-6, a marker whose production is rather reduced in COPD and cystic fibrosis in response to PAMPs (Knobloch et al. 2011b; Armstrong et al. 2009; John et al. 2010).
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