MicroRNA-223-mediated neutrophilic inflammation in Community Acquired Pneumonia

Abstract

Community Acquired Pneumonia remains one of the front running causes of mortality worldwide, with Streptococcus pneumoniae being the leading causative pathogen. Neutrophils are the first types of various immune cells recruited to the sites of pulmonary bacterial infection in high numbers, acting rapidly to clear the pathogenic threat by mounting inflammation and exerting their effector functions. Uncontrolled neutrophil responses, however, may prove detrimental to the host due to the toxicity of neutrophil effector molecules and mechanisms, leading to host-cell-mediated tissue injury. MicroRNAs have in recent years described to play an important role in inflammatory processes, and microRNA-223 has been described to be highly expressed in hematopoietic cells, especially in mature neutrophils. In our findings, we sought to understand the relevance and importance of microRNA-223 in neutrophilic inflammation in a murine model of pneumococcal pneumonia. Through the analyses of Streptococcus pneumonia-infected wild-type and microRNA-223-deficient mice, we aimed at understanding the difference in the magnitude of the cellular immune response, inflammatory cytokine/chemokine profile, microRNA expression pattern and degree of tissue destruction/inflammation following infection.