Sacramento, CA (PRWEB) April 28, 2014
The stress hormone epinephrine the source of the fight-or-flight response also heightens stresses at the cellular level, inhibiting wound healing and promoting a state of chronic inflammation that prohibits the bodys stem cells from migrating to a wound to encourage skin regeneration, UC Davis researchers have found.
The research, published in the April issue of the scientific journal Stem Cells Translational Medicine, is the first to show that epinephrine cross-activates other cellular pathways that feed off each other, generating inflammatory proteins in an exaggerated response that impedes wound healing. The research has important implications for the development of new treatments for chronic nonhealing wounds, conditions that affect more than 5 million Americans.
We have discovered that the pathways activated by the fight-or-flight hormone epinephrine and those activated by the presence of bacteria in wounds communicate with one another synergistically, greatly promoting inflammation, said Mohan R. Dasu, lead author of the study and an associate researcher in the UC Davis Department of Dermatology. The combination of stress and infection is a recipe for chronic infection.
Chronic infections are a major global health problem, with annual costs in the United States alone estimated to be more than $23 billion. Nonhealing wounds are particularly common in patients with diabetes, who often develop sores in the foot or leg that become chronic despite intensive antibiotic treatment and sometimes require amputation.
While chronic wounds are traditionally treated primarily with antibiotics, the findings open the way for enhancing therapy with agents that counteract stress hormones. Recent case studies have reported that topical treatment with beta blockers agents that block adrenergic receptors have improved chronic skin wounds, although until now, these outcomes have not been well explained.
Everyone knows that stress is harmful to the body, said Roslyn Isseroff, professor of dermatology at UC Davis and principal investigator of the study. Our findings provide a framework for systematically developing new therapeutic strategies that could selectively regulate inflammatory responses in nonhealing wounds. Isseroff is also chief of the dermatology service at the UC Davis-affiliated Department of Veterans Affairs Northern California Health Care System where she directs a multi-specialty wound clinic.
The biology of a nonhealing wound
Bacterial colonization produces in the body an inflammatory response mediated by Toll-like receptors on the cell membrane receptors that when activated, generate interleukin 6 (IL-6), a protein that plays an important role in fighting infection. Earlier work by lead author Dasu has demonstrated that activation of these receptors can contribute to nonhealing wounds in diabetic patients. In the current work, he provides an important advance to how this pathway works in the face of stress.
At the same time, wounds cause the release of stress hormones such as epinephrine that act on adrenergic receptors to also generate IL-6. Although IL-6 is essential to fighting infection, too much creates a state of chronic inflammation and actually impairs healing. Activation of adrenergic receptors also slows movement of the bodys stem cells that naturally migrate to a wound and promote healing and skin regeneration.
Continued here:
Recipe for Poor Wound Healing: Bacterial Infection Plus Stress
