Streptococcuspneumoniae is a major human pathogen at the extremes of age. The elderly are particularly vulnerable to S.pneumoniae, the most common causative agent of
bacterial pneumonia in this population. Despite the availability of
vaccines and
antibiotics, mortality rates associated with
pneumococcal pneumonia in this age group remain high. In light of globally increasing life-expectancy, a better understanding of the patho-mechanisms of elderly
pneumococcal pneumonia, including alterations in innate immune responses, is needed to develop improved
therapies. In this study we aimed at investigating how increased susceptibility to
pneumococcal infection relates to
inflammation kinetics in the aged mouse
pneumonia model by determining pulmonary
cytokine and
chemokine levels and comparing these parameters to those measured in young adult mice. Firstly, we detected overall higher pulmonary
cytokine and
chemokine levels in aged mice. However, upon induction of
pneumococcal pneumonia in aged mice, delayed production of certain analytes, such as IFN-γ, MIG (CXCL9), IP-10 (CXCL10), MCP-1 (CCL2), TARC (CCL17) and MDC (CCL22) became apparent. In addition, aged mice were unable to control excess inflammatory responses: while young mice showed peak inflammatory responses at 20 h and subsequent resolution by 48 h post intranasal challenge, in aged mice increasing
cytokine and
chemokine levels were measured. These findings highlight the importance of considering multiple time points when delineating inflammatory responses to S.pneumoniae in an age-related context. Finally, correlation between pulmonary bacterial burden and
cytokine or
chemokine levels in young mice suggested that appropriately controlled inflammatory responses support the host to fight
pneumococcal infection.