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Kovacs EJ, Grabowski KA, Duffner LA, et al. Survival and cell mediated immunity after burn injury in aged mice. J Am Aging Assoc. 2002;25(1):3-9doi: 10.1007/s11357-002-0001-4.
Kovacs, E. J., Grabowski, K. A., Duffner, L. A., Plackett, T. P., & Gregory, M. S. (2002). Survival and cell mediated immunity after burn injury in aged mice. Journal of the American Aging Association, 25(1), 3-9. https://doi.org/10.1007/s11357-002-0001-4
Kovacs, Elizabeth J, et al. "Survival and cell mediated immunity after burn injury in aged mice." Journal of the American Aging Association vol. 25,1 (2002): 3-9. doi: https://doi.org/10.1007/s11357-002-0001-4
Kovacs EJ, Grabowski KA, Duffner LA, Plackett TP, Gregory MS. Survival and cell mediated immunity after burn injury in aged mice. J Am Aging Assoc. 2002 Jan;25(1):3-9. doi: 10.1007/s11357-002-0001-4. PMID: 23604885; PMCID: PMC3455289.
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J Am Aging Assoc. 2002 Jan;25(1):3-9. doi: 10.1007/s11357-002-0001-4.

Survival and cell mediated immunity after burn injury in aged mice.

Journal of the American Aging Association

Elizabeth J Kovacs, Kristy A Grabowski, Lisa A Duffner, Timothy P Plackett, Meredith S Gregory

Affiliations

  1. Immunology and Aging Program, Loyola University Chicago, Maywood, IL ; Department of Cell Biology, Neurobiology, and Anatomy, Loyola University Chicago, Stritch School of Medicine, Building 110, Room 4221, 2160 South First Avenue, Maywood, IL 60153 ; Burn and Shock Trauma Institute, Loyola University Chicago, Maywood, IL ; Department of Surgery, Loyola University Chicago, Stritch School of Medicine, Building 110, Room 4221, 2160 South First Avenue, Maywood, IL 60153.

PMID: 23604885 PMCID: PMC3455289 DOI: 10.1007/s11357-002-0001-4

Abstract

The elderly are less able to survive burn injury than young healthy individuals. Regardless of age, burn victims often succumb to secondary infections rather than the primary injury. Since immune responses diminish with age, it is likely that aged individuals are predisposed to a poor outcome by virtue of their weak immune system. Elevated production of macrophage-derived mediators, including interleukin-6 (IL-6), may lead to post-injury immunosuppression in young adults. Healthy aged individuals produce high circulating levels of these mediators; therefore, the combination of the age and burn trauma could further suppress immune responses and contribute to the rapid demise of aged burn patients. Herein, the effects of age and burn trauma using a murine scald injury model were examined. After injury, aged mice are less likely to survive, are unable to mount immune responses, and produce more IL-6 when compared to young adult mice given the same size injuries. Enhancing our understanding of the mechanisms responsible for regulating cell-mediated immune responses after injury could lead to the development of therapies designed to treat aged burn patients.

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