PMC:7200337 / 18768-21314 JSONTXT

{"target":"https://pubannotation.org/docs/sourcedb/PMC/sourceid/7200337","sourcedb":"PMC","sourceid":"7200337","source_url":"https://www.ncbi.nlm.nih.gov/pmc/7200337","text":"Myeloid Cells Contribution to Pathogenic Inflammation\nThe initial mode of viral pathogen-associated signal (PAMP) recognition by innate cells has a major impact on downstream myeloid signaling and cytokine secretion (de Marcken et al., 2019). While macrophages are somewhat susceptible to MERS-CoV and SARS-CoV-1 infection (Perlman and Dandekar, 2005, Zhou et al., 2014), data do not suggest that they are infected by SARS-CoV-2, although one study reported ACE2 and SARS-CoV-2 nucleocapsid protein is expressed in lymph nodes and spleen-associated CD169+ macrophages of COVID-19 patients producing IL-6 (Chen et al., 2020h). Significantly elevated systemic levels of proinflammatory cytokine IL-6 have been reported in several COVID-19 patient cohorts and shown to correlate with disease severity (Mehta et al., 2020). Increased IL-6 can also be associated with higher levels of IL-2, IL-7, IFN-ɣ, and GM-CSF, as seen in secondary hemophagocytic lymphohistiocytosis. In response to viral infections, MNPs drive IL and IFN-I and IFN-III production resulting in inflammasome activation, induction of pathogenic Th1 and Th17 cell responses, recruitment of effector immune cells, and CRS pathology (Prokunina-Olsson et al., 2020, Tanaka et al., 2016). Independently, in vitro studies have demonstrated SARS-CoV-1 infection can induce intracellular stress pathways, resulting in NLRP3-dependent inflammasome activation and macrophage pyroptosis (Chen et al., 2019, Shi et al., 2019). Functional studies are required to implicate these myeloid inflammasome pathways in COVID-19 lung pathology and to assess other immunogenic pathways such as RIPK1/3-dependent necroptosis (Nailwal and Chan, 2019). In conclusion, the strength and duration of myeloid ISG)signaling potentially dictate COVID-19 disease severity, but rigorous studies are warranted to confirm this.\nLastly, more work is needed to ascertain the mechanistic role played by lung-resident and recruited granulocytes in SARS-CoV-2 control and pathogenesis (Camp and Jonsson, 2017, Flores-Torres et al., 2019). In contrast to their early protective role, neutrophil NETosis and macrophage crosstalk can drive later-stage inflammatory cascades (Barnes et al., 2020), underscoring the overall pathogenic nature of damage-sensing host responses (Figure 2).\nCollectively, the current knowledge of CoVs and SARS-CoV-2 infection, in particular, points to an inadvertent collusion involving myeloid cells in COVID-19 pathogenesis, despite their critical role in early sensing and antiviral 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