PMC:7346000 / 4985-6594 JSONTXT

{"target":"https://pubannotation.org/docs/sourcedb/PMC/sourceid/7346000","sourcedb":"PMC","sourceid":"7346000","source_url":"https://www.ncbi.nlm.nih.gov/pmc/7346000","text":"Viral entry and infection elicit an immune response, which is initiated by the establishment of an inflammatory cascade by innate immune cells. Although the receptor(s) and signaling pathways involved in the immune recognition of Aspergillus and the downstream production of inflammatory mediators are relatively well characterized [15], not much is known regarding how the immune system senses and responds to SARS-CoV-2. Based on the available knowledge for infections with other coronaviruses, two possible mechanisms can be anticipated and are likely to explain the development of ARDS and consequently CAPA. The first involves the release of danger-associated molecular patterns (DAMPs), signal molecules released by dying or damaged cells that act as endogenous danger signals to promote and exacerbate the immune and inflammatory response leading to lung injury [16]. It is noteworthy that DAMPs have also been shown to regulate inflammation in fungal diseases [17]. The DAMP/receptor for advanced glycation end-products axis was found to integrate with Toll-like receptors (TLRs) to generate and amplify the inflammatory response in experimental aspergillosis [18]. Moreover, recipients of allogeneic stem-cell transplantation harboring genetic variants underlying a hyperactivation of danger signaling in response to infection displayed an increased risk of developing IPA [19]. This emerging concept could help explain fungal pathogenesis in conditions of exuberant inflammation such as that observed in COVID-19 patients and highlights DAMP targeting as potential immunomodulatory strategy in 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