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§§
From the Department of Internal Medicine,*
Division of
Gastroenterology and Hepatology, University of Texas Medical Branch,
Galveston, Texas; the Department of Surgery,
Division of Urology, University of Texas Medical Branch, Galveston,
Texas; the Pulmonary Division,
Beth Israel
Deaconess Medical Center, Harvard Medical School, and the Ina Sue
Pelmutter Laboratory,§
Children’s Hospital,
Harvard Medical School, Boston, Massachusetts; and the Tulane
Environmental Astrobiology Center and Nephrology
Section,¶
Tulane University Medical Center and VA
Medical Center, New Orleans, Louisiana
Interstitial cystitis (IC) is a debilitating disease that has been adversely affecting the quality of women’s lives for many years. The trigger in IC is not entirely known, and a role for the sensory nerves in its pathogenesis has been suggested. In addition to inflammation, increased mast cell numbers in the detrusor muscle have been reported in a subset of IC patients. Experimentally, several lines of evidence support a central role for substance P and neurokinin-1 (NK-1) receptors in cystitis. The availability of mice genetically deficient in neurokinin-1 receptor (NK-1R-/-) allows us to directly evaluate the importance of substance P in cystitis. An unexpected finding of this investigation is that NK-1R-/- mice present increased numbers of mast cells in the bladder when compared with wild-type control mice. Despite the increase in mast cell numbers, no concomitant inflammation was observed. In addition, bladder instillation of wild-type mice with a sensitizing antigen induces activation of mast cells and an acute inflammatory response characterized by plasma extravasation, edema, and migration of neutrophils. Antigen-sensitized NK-1R-/- mice also exhibit bladder mast cell degranulation in response to antigen challenge. However, NK-1R-/- mice are protected from inflammation, failing to present bladder inflammatory cell infiltrate or edema in response to antigen challenge. This work presents the first evidence of participation of NK-1 receptors in cystitis and a mandatory participation of these receptors on the chain of events linking mast cell degranulation and inflammation.
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