Role of Inflammatory Risk Factors in the Pathogenesis of Streptococcus pneumoniae

Abstract

Streptococcus pneumoniae (Spn) is a colonizer of the human nasopharynx (NP), causing a variety of infections in humans including otitis media, pneumonia, sepsis, and meningitis. The NP is an immune permissive site which allows for the persistence of commensal bacteria. Acute or chronic respiratory airway inflammation constitutes a significant risk factor for the manifestation of Spn infections. The inflammatory conditions caused by an upper respiratory viral infection or respiratory conditions such as allergic asthma and chronic obstructive pulmonary disorders (COPDs) are implicated in the dysregulation of airway inflammation and tissue damage, which compromise the respiratory barrier integrity. These immune events promote bacterial outgrowth leading to Spn dissemination and invasion into the bloodstream. Therefore, suppression of inflammation and restoration of respiratory barrier integrity could contain Spn infections manifesting in the backdrop of an inflammatory disease condition. The gained knowledge could be harnessed in the design of novel therapeutic interventions to circumvent Spn bacterial infections.

Keywords: carriage; co-infection; inflammation; pathogenesis; pneumococcus.

Figure 1

Transition of Spn commensal colonization to disease. Acute or chronic airway inflammation caused by influenza virus or chronic conditions such as COPD or allergic asthma promote Spn bacterial outgrowth and compromises respiratory tissue barrier function, which leads to the invasion of Spn bacteria into the bloodstream establishing invasive infection. Colored dots (green, yellow, red, blue) represent chemokines and cytokines.