Conclusions.
Both infection and individual dysfunctional immune response elicited by SARS-CoV-2 have been reported to contribute to COVID-19 pathogenesis. Thus, it is more than a speculation that controlling the inflammatory response may be as important as targeting the virus. The evidences here reported suggest a potential role for the NLRP3 inflammasome pathway as cross-talk mechanism involved in both cellular events. Indeed, pharmacological targeting of NLRP3 inflammasome could be a feasible approach to counteract the pathology at multiple levels, ranging from the interference with viral infection to the reassessment of unbalanced immune responses. In addition, patients with exacerbated disease might reveal an impaired resolution process, which could again reflect on NLRP3 hyper-activation contributing to the “cytokine storm”. Interestingly, some of the pharmacological strategies under investigation for COVID-19 therapy include drugs able to directly disrupt the NLRP3 inflammasome cascade or to affect the transcriptional activity of factors involved in the synthesis of the main components of the NLRP3 inflammasome complex. Further studies are needed to better elucidate the pathophysiological involvement of NLRP3 inflammasome in this specific context and to prove the efficacy and safety of related pharmacological strategies. Overall, the findings here reviewed underlie intriguing perspective within the intricate mechanisms involved in the COVID-19 pathogenesis, and, thus, they may contribute to raise hope for discovering new strategies to battle one of the main pandemic of our modern times.