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Articles in PresS, published online ahead of print August 21, 2001
Am J Physiol Renal Physiol, 10.1152/ajprenal.0163.2001
Submitted on May 25, 2001
Accepted on August 21, 2001
1 Physiology, Oklahoma University Health Sicences Center, OK City, OK, USA
2 Nephrology Section, Tulane University Medical Center, New Orelans, LA, USA
3 Quantum Dot Corporation, Hayward, CA, USA
4 Pathobiological Sciences, School of Veterinary Medicine, University of Wisconsin, Madison, WI, USA
5 Pfizer, Inc, Groton, CT, USA
6 Surgical Sciences, School of Veterinary Medicine, University of Wisconsin, Madison, WI, USA
* To whom correspondence should be addressed. E-mail: ricardo-saban{at}ouhsc.edu.
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 hours after exposure to LPS. In vitro studies determined the capacity of LPS and SP to induced 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 pre-treatment enhanced neutrophil-infiltration induced by SP, increased in vitro release of histamine, TNF
, and 
IFN, and significantly reduced TGFß1 release. These findings suggest that LPS amplifies neurogenic inflammation thereby playing a role in the pathogenesis of neurogenic cystitis.
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