Chemokines: Attractive Targets in the Sunburn Reaction

The chemokine CXCL5 is a peripheral mediator of pain induced by UVB irradiation to the skin.


Injudicious exposure to ultraviolet B (UVB) radiation can cause very uncomfortable sunburns. Although several soluble mediators have been associated with the sunburn response in general, those responsible for pain have not been identified. To investigate this issue, researchers exposed 1-cm2 areas of forearm skin of 10 healthy volunteers to UVB radiation at 3 times the minimal erythemal dose.

In biopsy samples taken 40 hours after exposure — when sunburned sites had maximal hyperalgesia to mechanical and thermal stimuli — polymerase chain reaction (PCR) array analysis revealed elevated RNAs of a large number of molecules, including cyclooxygenase-2; the cytokines interleukin (IL)-1?, IL-6, and IL-24; and the chemokines CXCL5 and CXCL2. The investigators focused on CXCL5, which had the largest increase. Piroxicam, a nonsteroidal anti-inflammatory drug used to treat sunburn, reduced the increase in CXCL5 expression. CXCL5 is a potent chemoattractant for neutrophils and monocytes. In further explorations in UVB-irradiated rats, antibodies to CXCL5 attenuated hypersensitivity to mechanical pain and also reduced the number of neutrophils and macrophages that migrated into the skin.


Citation(s):

Dawes JM et al. CXCL5 mediates UVB irradiation–induced pain. Sci Transl Med 2011 Jul 6; 3:90ra60.