Short-term exposure of mice to cigarette smoke and/or residual oil fly ash produces proximal airspace enlargements and airway epithelium remodeling

Imagem de Miniatura
Arquivos
art_BISELLI_Shortterm_exposure_of_mice_to_cigarette_smoke_andor_2011.PDF (1.93 MB)
Citações na Scopus
31
Tipo de produção
article
Data de publicação
2011
Scopus
Web of Science
PubMed
Título da Revista
ISSN da Revista
Título do Volume
Editora
ASSOC BRAS DIVULG CIENTIFICA
Autores
BISELLI, P. J. C.
MORIYA, H. T.
Citação
BRAZILIAN JOURNAL OF MEDICAL AND BIOLOGICAL RESEARCH, v.44, n.5, p.460-468, 2011
Projetos de Pesquisa
Unidades Organizacionais
Fascículo
Resumo
Chronic obstructive pulmonary disease (COPD) is associated with inflammatory cell reactions, tissue destruction and lung remodeling. Many signaling pathways for these phenomena are still to be identified. We developed a mouse model of COPD to evaluate some pathophysiological mechanisms acting during the initial stage of the disease. Forty-seven 6- to 8-week-old female C57/BL6 mice (approximately 22 g) were exposed for 2 months to cigarette smoke and/or residual oil fly ash (ROFA), a concentrate of air pollution. We measured lung mechanics, airspace enlargement, airway wall thickness, epithelial cell profile, elastic and collagen fiber deposition, and by immunohistochemistry transforming growth factor-beta 1 (TGF-beta 1), macrophage elastase (MMP12), neutrophils and macrophages. We observed regional airspace enlargements near terminal bronchioles associated with the exposure to smoke or ROFA. There were also increases in airway resistance and thickening of airway walls in animals exposed to smoke. In the epithelium, we noted a decrease in the ciliated cell area of animals exposed to smoke and an increase in the total cell area associated with exposure to both smoke and ROFA. There was also an increase in the expression of TGF-beta 1 both in the airways and parenchyma of animals exposed to smoke. However, we could not detect inflammatory cell recruitment, increases in MMP12 or elastic and collagen fiber deposition. After 2 months of exposure to cigarette smoke and/or ROFA, mice developed regional airspace enlargements and airway epithelium remodeling, although no inflammation or increases in fiber deposition were detected. Some of these phenomena may have been mediated by TGF-beta 1.
Palavras-chave
Emphysema, Cigarette smoke, Airways, TGF-beta 1, Mouse airway epithelium remodeling, Proximal airspace enlargements
URI
https://observatorio.fm.usp.br/handle/OPI/23501
Referências
  1. Valenca SS, 2004, TOXICOL PATHOL, V32, P351, DOI 10.1080/01926230490431466
  2. Yao HW, 2010, P NATL ACAD SCI USA, V107, P15571, DOI 10.1073/pnas.1007625107
  3. Guerassimov A, 2004, AM J RESP CRIT CARE, V170, P974, DOI 10.1164/rccm.200309-1270oc
  4. Henson Peter M, 2006, Proc Am Thorac Soc, V3, P713, DOI 10.1513/pats.200605-104SF
  5. Kasahara Y, 2000, J CLIN INVEST, V106, P1311, DOI 10.1172/JCI10259
  6. Di Stefano A, 1998, AM J RESP CRIT CARE, V158, P1277
  7. Saetta M, 1997, AM J RESP CRIT CARE, V156, P1633
  8. HANTOS Z, 1992, J APPL PHYSIOL, V72, P168
  9. Churg A, 2006, AM J RESP CRIT CARE, V174, P1327, DOI 10.1164/rccm.200605-585OC
  10. Barnes PJ, 2003, EUR RESPIR J, V22, P672, DOI 10.1183/09031936.03.00040703
  11. DiStefano A, 1996, AM J RESP CRIT CARE, V153, P629
  12. Ghio AJ, 2002, ENVIRON HEALTH PERSP, V110, P89
  13. Churg A, 2002, AM J RESP CELL MOL, V27, P368, DOI 10.1165/rcmb.4791
  14. Anderson HR, 1997, EUR RESPIR J, V10, P1064, DOI 10.1183/09031936.97.10051064
  15. Tuder RM, 2003, AM J RESP CELL MOL, V29, P88, DOI 10.1165/rcmb.2002.0228OC
  16. SAETTA M, 1993, AM REV RESPIR DIS, V147, P301
  17. Chen ZH, 2010, P NATL ACAD SCI USA, V107, P18880, DOI 10.1073/pnas.1005574107
  18. Cavarra E, 2001, AM J RESP CRIT CARE, V164, P886
  19. Di Stefano A, 2004, CLIN EXP ALLERGY, V34, P1156, DOI 10.1111/j.1365-2222.2004.02030.x
  20. Arantes-Costa FM, 2008, TOXICOL PATHOL, V36, P680, DOI 10.1177/0192623308317427
  21. Foronjy RF, 2006, AM J RESP CRIT CARE, V173, P623, DOI 10.1164/rccm.200506-850OC
  22. Shapiro SD, 2003, AM J PATHOL, V163, P2329, DOI 10.1016/S0002-9440(10)63589-4
  23. Demedts IK, 2006, RESP RES, V7, DOI 10.1186/1465-9921-7-53
  24. Lopes FDTQS, 2009, ENVIRON RES, V109, P544, DOI 10.1016/j.envres.2009.03.002
  25. Hautamaki RD, 1997, SCIENCE, V277, P2002, DOI 10.1126/science.277.5334.2002
  26. Adair-Kirk TL, 2008, AM J RESP CELL MOL, V39, P400, DOI 10.1165/rcmb.2007-0295OC
  27. Yang QY, 2005, ENVIRON RES, V99, P99, DOI 10.1016/j.envres.2004.09.014
  28. Mahadeva R, 2002, THORAX, V57, P908, DOI 10.1136/thorax.57.10.908
  29. Takubo Y, 2002, AM J RESP CRIT CARE, V166, P1596, DOI 10.1164/rccm.2202001
  30. Rennard Stephen I, 2006, Proc Am Thorac Soc, V3, P703, DOI 10.1513/pats.200605-121SF
  31. Klass BR, 2009, POSTGRAD MED J, V85, P9, DOI 10.1136/pgmj.2008.069831
  32. Wang RD, 2005, AM J RESP CELL MOL, V33, P387, DOI 10.1165/rcmb.2005-02030C
  33. Brandsma CA, 2008, INHAL TOXICOL, V20, P183, DOI 10.1080/08958370701821342
  34. Gaschler Gordon J, 2008, Am J Respir Cell Mol Biol, V38, P218
  35. Global Initiative for Chronic Obstructive Pulmonary Disease (GOLD), 2010, GLOB STRAT DIAGN MAN
  36. *I LAB AN RES COMM, 1996, GUID CAR US LAB AN
  37. MacNee W., 2000, CHEST, V117, P303
  38. RANGASAMY T, 2009, AM J PHYSIOL-LUNG C, V296, P888
  39. Wan WYH, 2010, RESP RES, V11, DOI 10.1186/1465-9921-11-126
  40. YAO H, 2008, AM J PHYSIOL-LUNG C, V294, P1174

Coleções
Artigos e Materiais de Revistas Científicas - FM/MPT
Artigos e Materiais de Revistas Científicas - FM/MCM
Artigos e Materiais de Revistas Científicas - HC/ICHC
Artigos e Materiais de Revistas Científicas - HC/InCor
Artigos e Materiais de Revistas Científicas - LIM/05
Artigos e Materiais de Revistas Científicas - LIM/20