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.