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Am J Resp Cell Mol Biol. Role of Chemokines in the Pathogenesis of Acute Lung Injury
[Source: American Journal of Respiratory Cell and Molecular Biology, full text: (LINK). Abstract, edited.]
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Role of Chemokines in the Pathogenesis of Acute Lung Injury
Madhav Bhatia<SUP>1</SUP>,*, Rachel L. Zemans<SUP>2</SUP> and Samithamby Jeyaseelan<SUP>3</SUP>,<SUP>4</SUP>,*
Author Affiliations: <SUP>1</SUP>Department of Pathology, University of Otago, Christchurch, New Zealand <SUP>2</SUP>Department of Medicine, National Jewish Health and University of Colorado, Denver, Colorado <SUP>3</SUP>Pathobiological Sciences and Center for Experimental Infectious Disease Research, Louisiana State University, Baton Rouge, Louisiana; and <SUP>4</SUP>Pulmonary and Critical Care Medicine, Louisiana State University Health Sciences Center, New Orleans, Louisiana
Correspondence and requests for reprints should be addressed to Madhav Bhatia, Ph.D., Department of Pathology, University of Otago, 2 Riccarton Avenue, P.O. Box 4345, Christchurch 8140, New Zealand. E-mail: madhav.bhatia@otago.ac.nz
Abstract
Acute lung injury (ALI) is due to an uncontrolled systemic inflammatory response resulting from direct injury to the lung or indirect injury in the setting of a systemic process. Such insults lead to the systemic inflammatory response syndrome (SIRS), which includes activation of leukocytes?alveolar macrophages and sequestered neutrophils?in the lung. Although systemic inflammatory response syndrome is a physiologic response to an insult, systemic leukocyte activation, if excessive, can lead to end organ injury, such as ALI. Excessive recruitment of leukocytes is critical to the pathogenesis of ALI, and the magnitude and duration of the inflammatory process may ultimately determine the outcome in patients with ALI. Leukocyte recruitment is a well orchestrated process that depends on the function of chemokines and their receptors. Understanding the mechanisms that contribute to leukocyte recruitment in ALI may ultimately lead to the development of effective therapeutic strategies.
Keywords: acute lung injury ? inflammation ? leukocytes ? experimental ? clinical
Footnotes
-Madhav Bhatia<SUP>1</SUP>,*, Rachel L. Zemans<SUP>2</SUP> and Samithamby Jeyaseelan<SUP>3</SUP>,<SUP>4</SUP>,*
Author Affiliations: <SUP>1</SUP>Department of Pathology, University of Otago, Christchurch, New Zealand <SUP>2</SUP>Department of Medicine, National Jewish Health and University of Colorado, Denver, Colorado <SUP>3</SUP>Pathobiological Sciences and Center for Experimental Infectious Disease Research, Louisiana State University, Baton Rouge, Louisiana; and <SUP>4</SUP>Pulmonary and Critical Care Medicine, Louisiana State University Health Sciences Center, New Orleans, Louisiana
Correspondence and requests for reprints should be addressed to Madhav Bhatia, Ph.D., Department of Pathology, University of Otago, 2 Riccarton Avenue, P.O. Box 4345, Christchurch 8140, New Zealand. E-mail: madhav.bhatia@otago.ac.nz
Abstract
Acute lung injury (ALI) is due to an uncontrolled systemic inflammatory response resulting from direct injury to the lung or indirect injury in the setting of a systemic process. Such insults lead to the systemic inflammatory response syndrome (SIRS), which includes activation of leukocytes?alveolar macrophages and sequestered neutrophils?in the lung. Although systemic inflammatory response syndrome is a physiologic response to an insult, systemic leukocyte activation, if excessive, can lead to end organ injury, such as ALI. Excessive recruitment of leukocytes is critical to the pathogenesis of ALI, and the magnitude and duration of the inflammatory process may ultimately determine the outcome in patients with ALI. Leukocyte recruitment is a well orchestrated process that depends on the function of chemokines and their receptors. Understanding the mechanisms that contribute to leukocyte recruitment in ALI may ultimately lead to the development of effective therapeutic strategies.
Keywords: acute lung injury ? inflammation ? leukocytes ? experimental ? clinical
Footnotes
- ↵* Joint senior authors.
- This work was supported by in part by a University of Otago Establishment grant (M.B.), National Institutes of Health (NIH) grant K08-HL103772, a Flight Attendant Medical Research Institute (FAMRI) Young Clinical Scientist Award, a Parker B. Francis Fellowship (R.L.Z.), and by NIH grant R01-HL091958 (S.J.) and FAMRI grant YCSA_062466 (S.J.).
- Originally Published in Press as DOI: 10.1165/rcmb.2011-0392TR on February 9, 2012
- Author disclosures are available with the text of this article at www.atsjournals.org.
- Received November 11, 2011.
- Accepted February 2, 2012.
- Copyright ? 2012 by the American Thoracic Society
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