Factors affecting the development of systemic inflammatory response syndrome in pneumococcal infections

Streptococcus pneumoniae continues to be responsible for significant mortality and morbidity worldwide. A better understanding of the inflammatory response generated by the interaction of this microorganism with the host and antimicrobial therapy will improve the management of patients with pneumococcal infection.

On the side of the microorganism, recent studies have identified virulence factors such as capsular polysaccharides, surface protein, pili and pneumolysin, among others, that are able to trigger a complex inflammatory network. A misbalance in this network will precipitate a specific response that generates the systemic inflammatory response syndrome. Some of these virulence factors could be used as antigens for the production of vaccines with a broader spectrum than the currently used ones. On the host side, many single-nucleotide polymorphisms in genes controlling the immune response have been associated with specific clinical presentations. Finally, some antimicrobials or adjunctive therapies have recently been evaluated as inmunomodulatory agents.

Systemic inflammatory response syndrome is the result of an anomalous activation of the inflammatory network triggered by S. pneumoniae. Pneumococcal virulence factors, host comorbidities, the genetic background and the concomitant activity of antimicrobials and adjuvant therapies modulate the magnitude of this response.