AJP - Regulatory, Integrative and Comparative Physiology, Vol 261, Issue 3 543-R547, Copyright © 1991 by American Physiological Society
Bradykinin-induced prostaglandin synthesis is enhanced in keratinocytes and fibroblasts by UV injury
A. P. Pentland and S. C. Jacobs
Division of Dermatology, Washington University School of Medicine, St. Louis, Missouri 63110.
Ultraviolet (UV) light exposure substantially modifies the host immune
response, in part through the synthesis of prostaglandins. Work examining
the mechanisms by which UV irradiation stimulates prostaglandin synthesis
has focused on mediators that increase in quantity after irradiation. The
present work demonstrates that UV irradiation injury increases the
sensitivity and maximum response of keratinocytes to bradykinin, suggesting
that agonist quantities need not increase in injured tissue to contribute
to inflammation. The ability of UV injury to increase bradykinin-stimulated
prostaglandin synthesis is not limited to keratinocytes, as irradiation
produced a similar response in fibroblasts. Receptor binding studies
demonstrate that the enhanced response of irradiated cells is not due to
increased bradykinin binding. These data suggest that UV irradiation may
cause cells to increase their response to an array of inflammatory
mediators present in injured tissue, whether or not the quantity of the
mediator increases.
