Abstract
Humans have frequent contact with pneumococcus that commonly results in carriage, occasionally causes disease, and rarely causes death. Mucosal exposure to pneumococcus is managed with a high degree of immunological tolerance, where carriage is chaperoned by regulatory T cells. Alveolar macrophages are sentinels at whose signal the airspaces are aggressively defended, predominantly by neutrophils, and the ensuing debris efficiently managed by a role change among the remaining resident alveolar macrophages. Bloodstream invasion and meningitis cause chaos for host and pathogen, with dysregulated inflammation threatening both; extensive bacterial killing occurs despite pathogen survival strategies, and the host requires substantial support to maintain organ functions. In this chapter, the tissue-specific mechanisms for these compartmentalized responses are discussed in the context of translational research aiming for improved prevention and treatment of pneumococcal disease.
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