Journal
MOLECULAR CARCINOGENESIS
Volume 51, Issue 12, Pages 993-1002Publisher
WILEY
DOI: 10.1002/mc.20870
Keywords
neutrophils; T cells; KC; lung; tumor
Categories
Funding
- NIH [R01CA134433]
- Advancing a Healthier Wisconsin
- High Speed Cell Sorter Core at the Alvin J. Siteman Cancer Center (Washington U.) [P30CA91842]
- Richard Hotchkiss laboratory for use of the Luminex machine (Washington U.)
- Flow Cytometry Core at the Blood Research Institute (Milwaukee, WI)
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Multiple studies have shown a link between chronic inflammation and lung tumorigenesis. Inbred mouse strains vary in their susceptibility to methylcholanthrene (MCA)-initiated butylated hydroxytoluene (BHT)-promoted lung carcinogenesis. In the present study we investigated whether neutrophils play a role in strain dependent differences in susceptibility to lung tumor promotion. We observed a significant elevation in homeostatic levels of neutrophils in the lungs of tumor-susceptible BALB/cByJ (BALB) mice compared to tumor-resistant C57BL/6J (B6) mice. Additionally, BHT treatment further elevated neutrophil numbers as well as neutrophil chemoattractant keratinocyte-derived cytokine (KC)/chemokine (C-X-C motif) ligand 1 (Cxcl1) levels in BALB lung airways. Lung CD11c+ cells were a major source of KC expression and depletion of neutrophils in BALB mice resulted in a 71% decrease in tumor multiplicity. However, tumor multiplicity did not depend on the presence of T cells, despite the accumulation of T cells following BHT treatment. These data demonstrate that neutrophils are essential to promote tumor growth in the MCA/BHT two-step lung carcinogenesis model. (c) 2011 Wiley Periodicals, Inc.
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