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B induction profiles during lung inflammation induced by sub-chronic cigarette smoke exposure in mice
1 Department of Medicine, Cooperative Research Center for Chronic Inflammatory Diseases (CRC-CID), The University of Melbourne, Parkville, Victoria, Australia
2 Department of Pharmacology, The University of Melbourne, Parkville, Victoria, Australia
3 Marine and Atmospheric Research, Commonwealth Scientific and Industrial Research Organisation, Aspendale, Victoria, Australia
4 Department of Respiratory Medicine, Royal Melbourne Hospital, Parkville, Victoria, Australia
5 Department of Medicine, Cooperative Research Center for Chronic Inflammatory Diseases (CRC-CID), The University of Melbourne, Parkville, Victoria, Australia; Department of Pharmacology, The University of Melbourne, Parkville, Victoria, Australia
* To whom correspondence should be addressed. E-mail: rossv{at}unimelb.edu.au.
Cigarette smoke exposure is a major determinant of adverse lung health but the molecular processes underlying its effects on inflammation and immunity remain poorly understood. Therefore, we sought to understand whether inflammatory and host defense determinants were affected during sub-chronic cigarette smoke exposure. Dose-response and time-course studies of lungs from Balb/C mice exposed to cigarette smoke generated from 3, 6 and 9 cigarettes/day for 4 days showed macrophage- and S100A8 positive neutrophil-rich inflammation in lung tissue and BALF matrix metalloproteinase and serine protease induction, sustained NF
B translocation and binding, mucus cell induction but very small numbers of CD3+CD4+ and CD3+CD8+ lymphocytes. Cigarette smoke had no effect on phopsho-Akt but caused a small up-regulation of phopsho-Erk1/2. AP-1 and phospho-p38MAPK could not be detected. QPCR showed up-regulation of chemokines (MIP-2, MCP-1), inflammatory mediators (TNF-
, IL-1
), leukocyte growth and survival factors (GM-CSF, CSF-1, CSF1R), TGF-, matrix degrading MMP-9 and MMP-12, and Toll-like receptor TLR2, broadly mirroring NFB activation. No up-regulation was observed for, MMP-2, uPA, tPA and the TLRs 3, 4, and 9. In mouse strain comparisons the rank order of susceptibility was Balb/C>C3H/HeJ>129SvJ>C57BL6. Partition of responses into BAL macrophages versus lavaged lung strongly implicated macrophages in the inflammatory responses. Strikingly, with the exception of IL-10 and MMP-12, macrophage and lung gene profiles in Balb/C and C57BL6 mice were very similar. The response pattern we observed in our data suggests that sub-chronic cigarette smoke exposure may be useful to understand pathogenic mechanisms triggered by cigarette smoke in the lungs including inflammation and alteration of host defense.
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