Streptococcus pneumoniae (S. pneumoniae) employs several strategies to avoid destruction by phagocytes:

Capsule formation: S. pneumoniae produces a polysaccharide capsule, which inhibits phagocytosis by preventing the activation of complement proteins and blocking the binding of phagocytic receptors.

Immunoglobulin A1 (IgA1) protease production: S. pneumoniae secretes an enzyme that cleaves IgA1, an antibody that plays a key role in mucosal immunity, reducing its effectiveness.

Complement evasion: S. pneumoniae can bind to complement regulatory proteins, such as factor H, to prevent the activation of the complement cascade.

Phagocyte membrane disruption: S. pneumoniae can insert its cholesterol-binding toxin, pneumolysin, into the phagocyte membrane, causing membrane disruption and inhibiting phagocytosis.

Inhibition of phagolysosome fusion: S. pneumoniae can prevent the fusion of phagosomes with lysosomes, which contain digestive enzymes, thereby avoiding degradation.

Modulation of cytokine responses: S. pneumoniae can influence cytokine production, suppressing the activation of immune cells and reducing the effectiveness of the immune response.

These mechanisms enable S. pneumoniae to evade phagocytic destruction and establish infection.