How does strptococcus pneumoniae avoid be killed by phagocytes?

Mechanisms used by *Streptococcus pneumoniae* to evade phagocytosis:

1. Polysaccharide Capsule:

- *S. pneumoniae* possesses a thick polysaccharide capsule composed of complex sugars.

- The capsule acts as a physical barrier, preventing phagocytes from recognizing and attaching to the bacterial surface.

- Different serotypes of *S. pneumoniae* have distinct capsular polysaccharides, allowing them to evade specific antibodies and complement proteins in the host immune response.

2. Surface Proteins and Lipoproteins:

- *S. pneumoniae* expresses various surface proteins and lipoproteins that interfere with phagocytosis.

- Some of these proteins bind to host cell receptors involved in phagocytosis, disrupting the process.

- For example, the protein PspC (pneumococcal surface protein C) can bind to the complement receptor 3 (CR3) on phagocytes, interfering with opsonization and subsequent phagocytosis.

3. Alteration of Opsonization:

- *S. pneumoniae* can produce enzymes that degrade or modify host proteins involved in opsonization, such as immunoglobulins and complement proteins.

- This modification prevents efficient recognition and binding of the bacteria by phagocytes.

4. Interference with Phagocytic Signaling:

- *S. pneumoniae* can disrupt intracellular signaling pathways within phagocytes, interfering with the uptake and killing of the bacteria.

- Certain virulence factors of *S. pneumoniae* can inhibit the activation of NADPH oxidase, an enzyme crucial for reactive oxygen species (ROS) production and bacterial killing within phagosomes.

5. Intracellular Survival:

- Once internalized by phagocytes, *S. pneumoniae* can employ strategies to survive within the host cells.

- Some strains possess a specialized two-component signal transduction system called the CiaRH system, which promotes intracellular survival and replication within phagocytes.

- Moreover, *S. pneumoniae* can induce the formation of multinucleated giant cells by fusing infected host cells, creating a protected environment for bacterial survival and replication.

By employing these various mechanisms, *S. pneumoniae* evades phagocytosis and facilitates its survival and potential spread within the host, contributing to the development of diseases such as pneumonia.