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Am J Physiol Renal Physiol 282: F202-F210, 2002. First published August 21, 2001; doi:10.1152/ajprenal.0163.2001
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Vol. 282, Issue 2, F202-F210, February 2002

LPS-sensory peptide communication in experimental cystitis

M. R. Saban1, R. Saban1, T. G. Hammond2, M. Haak-Frendscho3, H. Steinberg4, M. W. Tengowski5, and D. E. Bjorling6

1 Department of Physiology, The University Oklahoma Health Sciences Center, Oklahoma City, Oklahoma 73190; 2 Nephrology Section, Tulane University Medical Center, Tulane Environmental Astrobiology Center, and Veterans Affairs Medical Center, New Orleans, Louisiana 70112; 3 Quantum Dot Corporation, Hayward, California 94545; Departments of 4 Surgical Sciences and 6 Pathobiological Sciences, School of Veterinary Medicine, University of Wisconsin, Madison, Wisconsin 53706; and 5 Pfizer, Incoporated, Groton, Connecticut 06340-8014

Stimulation of sensory nerves can lead to release of peptides such as substance P (SP) and consequently to neurogenic inflammation. We studied the role of bacterial lipopolysaccharide (LPS) in regulating SP-induced inflammation. Experimental cystitis was induced in female mice by intravesical instillation of SP, LPS, or fluorescein-labeled LPS. Uptake of fluorescein-labeled LPS was determined by confocal analysis, and bladder inflammation was determined by morphological analysis. SP was infused into the bladders of some mice 24 h after exposure to LPS. In vitro studies determined the capacity of LPS and SP to induce histamine and cytokine release by the bladder. LPS was taken up by urothelial cells and distributed systemically. Twenty-four hours after instillation of LPS or SP, bladder inflammation was characterized by edema and leukocytic infiltration of the bladder wall. LPS pretreatment enhanced neutrophil infiltration induced by SP, increased in vitro release of histamine, tumor necrosis factor-alpha , and interferon-gamma , and significantly reduced transforming growth factor-beta 1 release. These findings suggest that LPS amplifies neurogenic inflammation, thereby playing a role in the pathogenesis of neurogenic cystitis.

disease animal model; interstitial cystitis; neurogenic inflammation


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