Figure 3.

Dissemination of periodontal bacteria into lung tissues may cause Lipopolysaccharide-induced senescence, which facilitates SARS-CoV-2 cell attachment, entry, and replication. Accumulation of senescent cells in lungs is a normal event during the process of aging. Recently, it was demonstrated that cells that survive P. gingivalis infection display features of accelerated aging. Thus, periodontal bacteria that colonize lung tissues could aggravate age-related accumulation of senescent cells, which may facilitate more efficient viral replication. Several morphological and functional features of senescent cells could promote this process. In agreement with this concept, the senescence-associated cytoskeletal protein vimentin acts as a coreceptor of coronaviruses’ spike protein, promoting cell binding and entry. Intriguingly, SARS-CoV-2 causes DNA damage, cell growth arrest, cytokine production, and p38 activation during the early stages of infection as a strategy to promote more efficient replication. These are prominent features of cellular senescence. On the other hand, LPS interacts with the SARS-CoV-2 spike protein, which potentiates the inflammatory reaction produced by low concentrations of LPS alone.