What is the role of adherence and invasion in the pathophysiology of pneumococcal infection?

Updated: Aug 27, 2018
  • Author: Claudia Antonieta Nieves Prado, MD; Chief Editor: John L Brusch, MD, FACP  more...
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Answer

S pneumoniae is an extracellular bacterial pathogen that can adhere avidly to the respiratory epithelium and mucus. It exhibits different surface proteins that recognize and attach to human cells. Pneumococcal surface protein C (PspC) binds to the poly-Ig receptor on epithelial cells, pneumococcal surface antigen A (PsaA) binds to E-cadherin on epithelial cells, pneumococcal adhesion and virulence factor A (PavA) binds to fibronectin, and enolase (Eno) binds to plasminogen that may bridge binding to host cells. Phospho-cholines interact with the receptor for platelet-activating on activated epithelial cells. Capsule, pneumolysin, and the ABC transporter Ami have also been implicated in adherence. [27] S pneumoniae produces biofilm after binding to host cells. Biofilm production is regulated by external factors, such as temperature.

Invasion is promoted by phospho-cholines. After interacting with the PAF receptor, it is inserted into the host cell via endocytosis, causing translocation of bacteria through the endothelium. This is particularly important for translocation over the blood-brain barrier during meningitis development. Bacteria surface coat is changed via gene expression to avoid host defenses and complete translocation. Invasion is also mediated by adhesins and pneumolysin; pneumolysin is a cytotoxin that induces apoptosis of epithelial cells by membrane pore formation, resulting in access to subendothelium. Intraalveolar replication of pneumococci, penetration into the interstitium, and dissemination into the bloodstream are among other functions of pneumolysin. [28]

Much of the clinical severity of pneumococcal disease results from the activation of the complement pathways and cytokine release, which induce a significant inflammatory response. S pneumoniae cell wall components, along with the pneumococcal capsule, activate the alternative complement pathway; antibodies to the cell wall polysaccharides activate the classic complement pathway. Cell wall proteins, autolysin, and DNA released from bacterial breakdown all contribute to the production of cytokines, inducing further inflammation.


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