|
|
||||||||
Departments of 1 Environmental Health, 2 Molecular and Cellular Physiology, and 3 Medicine, University of Cincinnati, Cincinnati 45267; and 4 Human and Environmental Safety Division and Corporate Research Division, Procter and Gamble Company, Cincinnati, Ohio 45239
Pulmonary inflammation has been observed in humans
and in many animal species after ozone exposure. Inflammatory cell
accumulation involves local synthesis of chemokines, including
neutrophil chemoattractants such as macrophage inflammatory protein-2
(MIP-2), and monocyte chemoattractants, such as monocyte
chemoattractant protein-1 (MCP-1). To better understand the mechanism
of ozone-induced inflammation, we exposed mice and rats to ozone for 3 h and measured MIP-2 and MCP-1 gene expression. In C57BL/6
mice, steady-state mRNA levels for MCP-1 in the lung increased at 0.6 parts/million (ppm) ozone and were maximal at 2.0 ppm ozone. After
exposure to 2 ppm ozone, MIP-2 mRNA levels peaked at 4 h postexposure,
whereas MCP-1 mRNA levels peaked at 24 h postexposure.
Neutrophils and monocytes recovered in bronchoalveolar lavage fluid
peaked at 24 and 72 h, respectively. The accumulation of monocytes was
thus delayed relative to that of neutrophils, consistent with the
sequential expression of the corresponding chemokines. The role of
MCP-1 in monocyte accumulation was evaluated in greater detail in rats. Ozone caused an increase in monocyte chemotactic activity in
bronchoalveolar fluid that was inhibited by an antibody directed
against MCP-1. Ozone-induced MCP-1 mRNA levels were higher in lavage
cells than in whole lung tissue, indicating that lavage cells are an
important source of MCP-1. In these cells, nuclear factor-
B, a
nuclear transcription factor implicated in MCP-1 gene regulation, was also activated 20-24 h after ozone exposure. These findings
indicate that monocyte accumulation subsequent to acute lung injury can be mediated through MCP-1 and that nuclear factor-
B may play a role
in ozone-induced MCP-1 gene expression.
air pollution; asthma; inflammatory mediators; ozone
This article has been cited by other articles:
![]() |
R. A. Johnston, T. A. Theman, F. L. Lu, R. D. Terry, E. S. Williams, and S. A. Shore Diet-induced obesity causes innate airway hyperresponsiveness to methacholine and enhances ozone-induced pulmonary inflammation J Appl Physiol, June 1, 2008; 104(6): 1727 - 1735. [Abstract] [Full Text] [PDF] |
||||
![]() |
J. E. Lang, E. S. Williams, J. P. Mizgerd, and S. A. Shore Effect of obesity on pulmonary inflammation induced by acute ozone exposure: role of interleukin-6 Am J Physiol Lung Cell Mol Physiol, May 1, 2008; 294(5): L1013 - L1020. [Abstract] [Full Text] [PDF] |
||||
![]() |
M. Mita, M. Satoh, A. Shimada, M. Okajima, S. Azuma, J. S. Suzuki, K. Sakabe, S. Hara, and S. Himeno Metallothionein is a crucial protective factor against Helicobacter pylori-induced gastric erosive lesions in a mouse model Am J Physiol Gastrointest Liver Physiol, April 1, 2008; 294(4): G877 - G884. [Abstract] [Full Text] [PDF] |
||||
![]() |
R. A. Johnston, I. N. Schwartzman, L. Flynt, and S. A. Shore Role of interleukin-6 in murine airway responses to ozone Am J Physiol Lung Cell Mol Physiol, February 1, 2005; 288(2): L390 - L397. [Abstract] [Full Text] [PDF] |
||||
![]() |
R. A. Johnston, J. P. Mizgerd, and S. A. Shore CXCR2 is essential for maximal neutrophil recruitment and methacholine responsiveness after ozone exposure Am J Physiol Lung Cell Mol Physiol, January 1, 2005; 288(1): L61 - L67. [Abstract] [Full Text] [PDF] |
||||
![]() |
L. Fakhrzadeh, J. D. Laskin, and D. L. Laskin Ozone-induced production of nitric oxide and TNF-{alpha} and tissue injury are dependent on NF-{kappa}B p50 Am J Physiol Lung Cell Mol Physiol, August 1, 2004; 287(2): L279 - L285. [Abstract] [Full Text] [PDF] |
||||
![]() |
J. L. Wright, S. G. Farmer, and A. Churg Synthetic Serine Elastase Inhibitor Reduces Cigarette Smoke-induced Emphysema in Guinea Pigs Am. J. Respir. Crit. Care Med., October 1, 2002; 166(7): 954 - 960. [Abstract] [Full Text] |
||||
![]() |
A. Churg, J. Dai, H. Tai, C. Xie, and J. L. Wright Tumor Necrosis Factor-{alpha} Is Central to Acute Cigarette Smoke-induced Inflammation and Connective Tissue Breakdown Am. J. Respir. Crit. Care Med., September 15, 2002; 166(6): 849 - 854. [Abstract] [Full Text] |
||||
![]() |
S. A. Shore, R. A. Johnston, I. N. Schwartzman, D. Chism, and G. G. Krishna Murthy Ozone-induced airway hyperresponsiveness is reduced in immature mice J Appl Physiol, March 1, 2002; 92(3): 1019 - 1028. [Abstract] [Full Text] [PDF] |
||||
![]() |
L. Michalec, B. K. Choudhury, E. Postlethwait, J. S. Wild, R. Alam, M. Lett-Brown, and S. Sur CCL7 and CXCL10 Orchestrate Oxidative Stress-Induced Neutrophilic Lung Inflammation J. Immunol., January 15, 2002; 168(2): 846 - 852. [Abstract] [Full Text] [PDF] |
||||
![]() |
S. A. SHORE, I. N. SCHWARTZMAN, B. LE BLANC, G. G. KRISHNA MURTHY, and C. M. DOERSCHUK Tumor Necrosis Factor Receptor 2 Contributes to Ozone-induced Airway Hyperresponsiveness in Mice Am. J. Respir. Crit. Care Med., August 15, 2001; 164(4): 602 - 607. [Abstract] [Full Text] [PDF] |
||||
![]() |
S. R. Kleeberger, S. P. M. Reddy, L.-Y. Zhang, H.-Y. Cho, and A. E. Jedlicka Toll-like receptor 4 mediates ozone-induced murine lung hyperpermeability via inducible nitric oxide synthase Am J Physiol Lung Cell Mol Physiol, February 1, 2001; 280(2): L326 - L333. [Abstract] [Full Text] [PDF] |
||||
![]() |
P. G. Knott, P. R. Gater, P. J. Dunford, M. E. Fuentes, and C. P. Bertrand Rapid Up-Regulation of CXC Chemokines in the Airways after Ag-Specific CD4+ T Cell Activation J. Immunol., January 15, 2001; 166(2): 1233 - 1240. [Abstract] [Full Text] [PDF] |
||||
![]() |
D. W. McGraw, S. L. Forbes, J. C. W. Mak, D. P. Witte, P. E. Carrigan, G. D. Leikauf, and S. B. Liggett Transgenic overexpression of beta 2-adrenergic receptors in airway epithelial cells decreases bronchoconstriction Am J Physiol Lung Cell Mol Physiol, August 1, 2000; 279(2): L379 - L389. [Abstract] [Full Text] [PDF] |
||||
![]() |
S. R. Kleeberger, S. Reddy, L.-Y. Zhang, and A. E. Jedlicka Genetic Susceptibility to Ozone-Induced Lung Hyperpermeability . Role of Toll-Like Receptor 4 Am. J. Respir. Cell Mol. Biol., May 1, 2000; 22(5): 620 - 627. [Abstract] [Full Text] |
||||
![]() |
J. W. Christman, R. T. Sadikot, and T. S. Blackwell The Role of Nuclear Factor-{kappa} B in Pulmonary Diseases Chest, May 1, 2000; 117(5): 1482 - 1487. [Abstract] [Full Text] [PDF] |
||||
![]() |
M. T. Borchers, S. Wesselkamper, S. E. Wert, S. D. Shapiro, and G. D. Leikauf Monocyte inflammation augments acrolein-induced Muc5ac expression in mouse lung Am J Physiol Lung Cell Mol Physiol, September 1, 1999; 277(3): L489 - L497. [Abstract] [Full Text] [PDF] |
||||
![]() |
N. J. Kenyon, A. van der Vliet, B. C. Schock, T. Okamoto, G. M. McGrew, and J. A. Last Susceptibility to ozone-induced acute lung injury in iNOS-deficient mice Am J Physiol Lung Cell Mol Physiol, March 1, 2002; 282(3): L540 - L545. [Abstract] [Full Text] [PDF] |
||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| Visit Other APS Journals Online |