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The Use of Cystometry in Small Rodents: A Study of Bladder Chemosensation
Published on: August 21, 2012
LPS-sensory peptide communication in experimental cystitis.
M R Saban1, R Saban, T G Hammond
1Department of Physiology, The University Oklahoma Health Sciences Center, Oklahoma City, Oklahoma 73190, USA. ricardo-saban@ouhsc.edu
American Journal of Physiology. Renal Physiology
|January 15, 2002
Summary
Bacterial lipopolysaccharide (LPS) amplifies inflammation caused by substance P (SP) in the bladder. LPS pretreatment enhances inflammatory responses, suggesting a role in neurogenic cystitis development.
Area of Science:
- Urology
- Immunology
- Neuroscience
Background:
- Sensory nerve stimulation releases substance P (SP), leading to neurogenic inflammation.
- Bacterial lipopolysaccharide (LPS) is a key component of Gram-negative bacteria and a potent immune activator.
Purpose of the Study:
- To investigate the role of LPS in regulating SP-induced bladder inflammation.
- To determine if LPS exacerbates neurogenic inflammation.
Main Methods:
- Experimental cystitis induced in mice via intravesical instillation of SP and/or LPS.
- Fluorescein-labeled LPS uptake analyzed by confocal microscopy.
- Bladder inflammation assessed morphologically and via in vitro cytokine release assays.
Main Results:
- LPS was uptaken by urothelial cells and distributed systemically.
- LPS pretreatment enhanced SP-induced neutrophil infiltration and inflammatory mediator release (histamine, TNF-α, IFN-γ).
- LPS significantly reduced transforming growth factor-beta1 release.
Conclusions:
- LPS amplifies SP-induced neurogenic inflammation in the bladder.
- LPS may play a significant role in the pathogenesis of neurogenic cystitis.
