The infection and damage of alveolar pneumocytes results in a cascade of physiological changes, beginning with an increased production of proinflammatory cytokines, such as interleukin (IL)-1 (IL-1), IL-6, IL-8, tumor necrosis factor-alpha (TNF-α), and elevated levels of C-reactive protein (CRP) and D-dimer [51,52,53,54,55]. This evidence concerns the gene TNF and infection.