Pulmonary innate immune system plays an important role in host defence against pathogens and variety air allergens. Any breach in the pulmonary innate immune system may prove lethal. This study was designed to evaluate comparative pulmonary innate immune response during bacterial pneumonia and sepsis in BALB/c mice. Pneumonia was induced by intranasal instillation of bacteria (104 CFU) while sepsis was established by placing 102 CFU bacteria in peritoneal cavity of mice. Various cytokine (TNF-α, IL-1α and IL-10) levels were measured and the degree of lung inflammation was evaluated.
Mice with sepsis showed 100% mortality within 5 post infection days (PIDs) whereas all the animals with pneumonia survived. In animals suffering from K. pneumoniae B5055-induced pneumonia all the inflammatory parameters (TNFα, IL-1α, MPO, MDA and NO) were found to be maximum until the third PID, after that a decline was observed, whereas in septic animals all the above-mentioned markers of inflammation kept on increasing on all PIDs. Inflammatory damage to the lungs in pneumonia was not very severe. This can be further strengthened by the presence of alternatively activated alveolar macrophages (AAMacs) or foam cells in lungs of mice with pneumonia, which might have contributed to the induction of resolution of inflammation and clearance of the infection. But no such AAMacs or foam cells were seen in lungs of septic mice.
Thus, controlled activation of AAMacs during pneumonia may have helped in resolution of inflammation and infection as well, while this mechanism of prevention of acute lung injury was absent in sepsis associated ALI.