Furthermore, P. gingivalis MVs inhibited macrophage surface CD14 expression and accelerated CD14 degradation, resulting in reduced macrophage response to LPS (Winter et al., 2014) and a concomitant lack of response to antigen-stimulated secondary infection, an immunosuppressive state that worsens the inflammatory response (Cecil et al., 2017). The gene discussed is CD14; the disease is infection.