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Fritz JM, Tennis MA, Orlicky DJ, et al. Depletion of tumor-associated macrophages slows the growth of chemically induced mouse lung adenocarcinomas. Front Immunol. 2014;5:587doi: 10.3389/fimmu.2014.00587.
Fritz, J. M., Tennis, M. A., Orlicky, D. J., Lin, H., Ju, C., Redente, E. F., Choo, K. S., Staab, T. A., Bouchard, R. J., Merrick, D. T., Malkinson, A. M., & Dwyer-Nield, L. D. (2014). Depletion of tumor-associated macrophages slows the growth of chemically induced mouse lung adenocarcinomas. Frontiers in immunology, 5587. https://doi.org/10.3389/fimmu.2014.00587
Fritz, Jason M, et al. "Depletion of tumor-associated macrophages slows the growth of chemically induced mouse lung adenocarcinomas." Frontiers in immunology vol. 5 (2014): 587. doi: https://doi.org/10.3389/fimmu.2014.00587
Fritz JM, Tennis MA, Orlicky DJ, Lin H, Ju C, Redente EF, Choo KS, Staab TA, Bouchard RJ, Merrick DT, Malkinson AM, Dwyer-Nield LD. Depletion of tumor-associated macrophages slows the growth of chemically induced mouse lung adenocarcinomas. Front Immunol. 2014 Nov 25;5:587. doi: 10.3389/fimmu.2014.00587. eCollection 2014. PMID: 25505466; PMCID: PMC4243558.
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Front Immunol. 2014 Nov 25;5:587. doi: 10.3389/fimmu.2014.00587. eCollection 2014.

Depletion of tumor-associated macrophages slows the growth of chemically induced mouse lung adenocarcinomas.

Frontiers in immunology

Jason M Fritz, Meredith A Tennis, David J Orlicky, Hao Lin, Cynthia Ju, Elizabeth F Redente, Kevin S Choo, Taylor A Staab, Ronald J Bouchard, Daniel T Merrick, Alvin M Malkinson, Lori D Dwyer-Nield

Affiliations

  1. Department of Pharmaceutical Sciences, Skaggs School of Pharmacy and Pharmaceutical Sciences, University of Colorado Denver , Aurora, CO , USA.
  2. Pulmonary Division, School of Medicine, University of Colorado Denver , Aurora, CO , USA.
  3. Department of Pathology, School of Medicine, University of Colorado Denver , Aurora, CO , USA.
  4. Department of Pediatrics, National Jewish Health , Denver, CO , USA.
  5. Research Division, Eastern Colorado Veterans Administration Medical Center , Denver, CO , USA.

PMID: 25505466 PMCID: PMC4243558 DOI: 10.3389/fimmu.2014.00587

Abstract

Chronic inflammation is a risk factor for lung cancer, and low-dose aspirin intake reduces lung cancer risk. However, the roles that specific inflammatory cells and their products play in lung carcinogenesis have yet to be fully elucidated. In mice, alveolar macrophage numbers increase as lung tumors progress, and pulmonary macrophage programing changes within 2 weeks of carcinogen exposure. To examine how macrophages specifically affect lung tumor progression, they were depleted in mice bearing urethane-induced lung tumors using clodronate-encapsulated liposomes. Alveolar macrophage populations decreased to ≤50% of control levels after 4-6 weeks of liposomal clodronate treatment. Tumor burden decreased by 50% compared to vehicle treated mice, and tumor cell proliferation, as measured by Ki67 staining, was also attenuated. Pulmonary fluid levels of insulin-like growth factor-I, CXCL1, IL-6, and CCL2 diminished with clodronate liposome treatment. Tumor-associated macrophages expressed markers of both M1 and M2 programing in vehicle and clodronate liposome-treated mice. Mice lacking CCR2 (the receptor for macrophage chemotactic factor CCL2) had comparable numbers of alveolar macrophages and showed no difference in tumor growth rates when compared to similarly treated wild-type mice suggesting that while CCL2 may recruit macrophages to lung tumor microenvironments, redundant pathways can compensate when CCL2/CCR2 signaling is inactivated. Depletion of pulmonary macrophages rather than inhibition of their recruitment may be an advantageous strategy for attenuating lung cancer progression.

Keywords: clodronate; inflammation; lung tumor; macrophage; programing

References

  1. Blood. 1991 Aug 15;78(4):1112-6 - PubMed
  2. Acta Endocrinol (Copenh). 1993 Feb;128(2):168-72 - PubMed
  3. Am J Physiol Lung Cell Mol Physiol. 2012 Apr 1;302(7):L711-8 - PubMed
  4. Blood. 2006 Mar 1;107(5):2112-22 - PubMed
  5. Anticancer Res. 2009 Dec;29(12):5095-101 - PubMed
  6. Mol Cancer Ther. 2007 Jul;6(7):1993-2002 - PubMed
  7. Nat Rev Immunol. 2014 Feb;14(2):81-93 - PubMed
  8. Mol Cancer. 2011 Jun 24;10:76 - PubMed
  9. Expert Rev Anticancer Ther. 2007 Oct;7(10):1405-21 - PubMed
  10. Cancer Res. 2008 Sep 1;68(17):7237-45 - PubMed
  11. Oncol Rep. 1998 May-Jun;5(3):649-52 - PubMed
  12. J Immunol. 2011 Dec 1;187(11):5703-11 - PubMed
  13. Respir Med. 2007 Aug;101(8):1738-43 - PubMed
  14. Am J Respir Cell Mol Biol. 2008 Jan;38(1):8-15 - PubMed
  15. Lancet. 2011 Jan 1;377(9759):31-41 - PubMed
  16. Immunol Cell Biol. 2014 Jul;92(6):543-52 - PubMed
  17. FASEB J. 2004 Nov;18(14):1716-8 - PubMed
  18. Lung Cancer. 2001 Jun;32(3):265-79 - PubMed
  19. Int J Cancer. 2013 May 1;132(9):1977-85 - PubMed
  20. Nature. 2002 Dec 19-26;420(6917):860-7 - PubMed
  21. Anticancer Res. 2001 May-Jun;21(3B):1749-55 - PubMed
  22. J Leukoc Biol. 1989 Feb;45(2):97-104 - PubMed
  23. Proc Natl Acad Sci U S A. 1994 Apr 26;91(9):3652-6 - PubMed
  24. Nat Immunol. 2014 May;15(5):423-30 - PubMed
  25. Nat Methods. 2012 Jul;9(7):671-5 - PubMed
  26. Neuropeptides. 2000 Apr;34(2):98-107 - PubMed
  27. Am J Physiol Lung Cell Mol Physiol. 2006 Jun;290(6):L1260-6 - PubMed
  28. Cancer Sci. 2008 Aug;99(8):1595-602 - PubMed
  29. J Natl Cancer Inst. 2011 Jul 20;103(14):1112-22 - PubMed
  30. Epidemiology. 1994 Mar;5(2):138-46 - PubMed
  31. Diabetes. 2010 May;59(5):1171-81 - PubMed
  32. J Clin Invest. 1982 Oct;70(4):806-22 - PubMed
  33. Toxicology. 2001 Dec 1;169(1):1-15 - PubMed
  34. Science. 2011 Jun 10;332(6035):1284-8 - PubMed
  35. Clin Cancer Res. 2008 Oct 15;14(20):6364-70 - PubMed
  36. Toxicol Lett. 1998 Aug;96-97:85-95 - PubMed
  37. Cancer Res. 2004 Apr 1;64(7):2307-16 - PubMed
  38. Clin Cancer Res. 2013 Jul 1;19(13):3404-15 - PubMed
  39. Am J Respir Cell Mol Biol. 2014 Apr;50(4):825-37 - PubMed
  40. Am J Physiol Lung Cell Mol Physiol. 2007 Aug;293(2):L383-92 - PubMed
  41. Proc Natl Acad Sci U S A. 2012 Nov 13;109 (46):E3186-95 - PubMed
  42. J Leukoc Biol. 1996 Sep;60(3):365-71 - PubMed
  43. Am J Physiol Lung Cell Mol Physiol. 2005 May;288(5):L805-12 - PubMed
  44. Toxicology. 1997 Nov 21;123(1-2):53-100 - PubMed
  45. Int J Cancer. 2010 Dec 15;127(12):2893-917 - PubMed
  46. J Leukoc Biol. 2010 Jul;88(1):159-68 - PubMed
  47. PLoS One. 2011;6(12):e28133 - PubMed
  48. Am J Physiol Lung Cell Mol Physiol. 2009 Jun;296(6):L936-46 - PubMed
  49. Cancer Chemother Pharmacol. 2008 Sep;62(4):605-20 - PubMed
  50. Cancer Immunol Immunother. 2013 Mar;62(3):563-70 - PubMed
  51. J Natl Cancer Inst. 1991 Aug 21;83(16):1142-8 - PubMed
  52. J Immunol. 2006 Nov 15;177(10):7303-11 - PubMed
  53. Am J Pathol. 2010 Jun;176(6):2972-85 - PubMed
  54. Lung Cancer. 2007 Apr;56(1):25-33 - PubMed
  55. Nat Rev Immunol. 2008 Dec;8(12):958-69 - PubMed
  56. Clin Cancer Res. 2004 Oct 15;10(20):6865-71 - PubMed
  57. Br J Cancer. 2006 Aug 7;95(3):272-81 - PubMed
  58. Front Immunol. 2011 Nov 08;2:57 - PubMed
  59. Cell. 2006 Jan 27;124(2):263-6 - PubMed
  60. J Exp Med. 1989 Aug 1;170(2):499-509 - PubMed
  61. Methods Mol Biol. 2010;605:189-203 - PubMed
  62. Clin Cancer Res. 2000 Aug;6(8):3282-9 - PubMed
  63. Am J Pathol. 2007 Feb;170(2):693-708 - PubMed
  64. Exp Lung Res. 2001 Apr-May;27(3):197-216 - PubMed
  65. PLoS One. 2014 Apr 15;9(4):e94188 - PubMed
  66. Cancer Sci. 2007 Dec;98(12):2009-18 - PubMed
  67. Gene Ther. 2000 Feb;7(4):292-9 - PubMed
  68. Am J Physiol Lung Cell Mol Physiol. 2001 Jun;280(6):L1282-9 - PubMed
  69. J Thorac Oncol. 2008 Aug;3(8):815-8 - PubMed
  70. Clin Exp Immunol. 2006 Jul;145(1):162-72 - PubMed

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