- Poster presentation
- Open Access
A comparison of acute lung inflammation in Klebsiella pneumoniae B5055-induced pneumonia and sepsis in BALB/c mice
© BioMed Central Ltd 2009
- Published: 11 November 2009
- Nitric Oxide
- Alveolar Macrophage
- Foam Cell
- Post Infection
Lungs play an important role in the body's defense against a variety of pathogens, but this network of immune system mediated defense can be deregulated during acute pulmonary infections.
The present study compares the acute lung inflammation (ALI) occurring during Klebsiella pneumoniae B5055-induced pneumonia and sepsis in BALB/c mice.
Pneumonia was induced by intranasal instillation of bacteria (104 CFU) while sepsis was developed by placing the fibrinthrombin clot containing a known amount of bacteria (102 CFU) into the peritoneal cavity of animals. Various cytokines (TNFα and IL-1α) levels were estimated using ELISA and degree of lung inflammation (that is, inflammatory cell infiltration) was evaluated by histopathological analysis. The other markers of inflammation (that is, nitric oxide (NO), malondialdehyde (MDA) and myeloperoxidase (MPO)) were estimated by standard biochemical methods.
Mice with sepsis showed 100% mortality within 5 post infection days 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 post infection day, after that a decline was observed, whereas in septic animals all the above-mentioned markers of inflammation kept on increasing until death of the animals. Histopathological study showed that inflammatory damage to the lungs in pneumonia was not very severe as lesser neutrophil infiltration and pulmonary damage (that is, alveolitis, bronchiolitis, endothelitis and perivascular congestion) was seen as compared with lungs taken from septic animals. This can be further strengthened by the presence of alternatively activated alveolar macrophages (AAMacs) or foam cells in lungs of mice with pneumonia after the third post infection day and their number kept on increasing until the seventh post infection day, 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 on histopathological examination, lungs were seen to be infiltrated with only neutrophils on all experimental days.
Hence, during pneumonia controlled activation of AAMacs or foam cells led to the resolution of inflammation and infection as well.