Organ-specific inflammation following acute ethanol and burn injury

Melanie D. Bird^*^,^, and Elizabeth J. Kovacs^*^,^,^,^,1

^* Departments of Surgery and
Cell Biology, Neurobiology and Anatomy,
Burn and Shock Trauma Institute,
Alcohol Research Program, Loyola University Medical Center, Maywood, Illinois, USA

¹ Correspondence: Loyola University Medical Center, 2160 South First Avenue, Maywood, IL 60153, USA. E-mail: ekovacs{at}lumc.edu

ABSTRACT

Clinical and experimental evidence demonstrates that ethanolexposure prior to injury alters local and systemic inflammatoryresponses, increasing morbidity and mortality. Moreover, theaberrant inflammatory responses can directly and indirectlylead to the poor prognosis after injury by altering leukocyteinfiltration into the wound site and remote organs and by suppressingimmunity leading to increased susceptibility to opportunisticinfections. Recent studies from our laboratory have focusedon inflammatory responses at the wound site and in other distalorgans after exposure to acute ethanol and burn injury. Thiscombined insult leads to increased mortality after dermal orintratracheal pseudomonas infection, relative to infected micegiven ethanol or burn injury alone. The increased mortalityin mice given ethanol and burn injury parallels elevated serumlevels of proinflammatory cytokines, IL-6 and TNF- ${alpha}$ , marked infiltrationof leukocytes into the lung and gut, as well as immunosuppressionat the sites of infection. Bacterial translocation from thegut is likely to be responsible, in part, for the aberrant accumulationof leukocytes in the lungs of ethanol-exposed, burn-injuredmice. Additionally, other factors, such as expression of adhesionmolecules, increased chemokine production, and leakiness ofthe vascular endothelium, may also be involved.

Key Words: neutrophils • T cells • cytokines • immunosuppression • lungs • gut