The most common way of managing the pain that accompanies inflammation is to use drugs such as aspirin and ibuprofen. These work by selectively blocking the protein COX2, which functions to produce soluble molecules known as prostaglandins. Although it is known that blocking COX2 in the tissue and in the brain and spinal cord (the CNS) reduces the pain that accompanies inflammation, the relative contribution of COX2 at these two sites to the pain that accompanies inflammation has not been determined. However, a team of researchers, at Massachusetts General Hospital, Boston, and University of Pennsylvania, Philadelphia, have now shown that COX2 in mouse nerve cells in the CNS is crucial for some forms of pain associated with inflammation but not others. Specifically, hypersensitivity to pain caused by the heat associated with inflammation was normal in mice lacking COX2 in nerve cells in the CNS. By contrast, hypersensitivity to pain caused by the physical insult associated with inflammation was abolished in these mice. As pain caused by physical insult is a major symptom of postoperative and arthritic inflammation, it seems that COX2 in nerve cells in the CNS is central to the pain that accompanies these conditions.
TITLE: COX2 in CNS neural cells mediates mechanical inflammatory pain hypersensitivity in mice
AUTHOR CONTACT:
Clifford Woolf
Massachusetts General Hospital, Harvard Medical School, Charlestown, Massachusetts, USA.
Phone: (617) 724-3622; Fax: (617) 724-3632; E-mail: cwoolf@partners.org .
Garret A. FitzGerald
University of Pennsylvania, Philadelphia, Pennsylvania, USA.
Phone: (215) 898-1185; Fax: (215) 573-9135; E-mail: garret@spirit.gcrc.upenn.edu .
View the PDF of this article at: https://www.the-jci.org/article.php?id=37098
Journal of Clinical Investigation