David Klumpp

I received a Ph.D. in Biochemistry, Molecular Biology and Cell Biology from Northwestern University in 1994, studying retinal neuron physiology. After postdoctoral studies in HPV pathogenesis and epithelial biology at Northwestern’s Feinberg School of Medicine, I joined the Department of Urology in 1998. I am an Associate Professor of Urology and Microbiology-Immunology in the Feinberg School of Medicine and the Anthony J. Schaeffer MD Professor of Urology.

Our team studies diverse aspects of neuro-immune and bacterial mechanisms of bladder inflammation and pelvic pain as well as the influence of microbiota on pain and cognition. Pain modulation by bacteria. Urinary tract infections due to colonization by uropathogenic E. coli are characterized by inflammatory and symptomatic responses. In contrast, asymptomatic bacteriuria associated with E. coli are asymptomatic by definition, pointing to distinct bacterial pain phenotypes in the bladder. We are exploring the mechanisms underlying bacterial pain phenotypes in the bladder using murine models that recapitulate key clinical findings. We find that E. coli exhibit distinct pain phenotypes independent of inflammation and that specific strains possess analgesic properties amenable for development as therapies for urologic disease. Genetic modulation of pain. We have recently identified the gene encoding acyloxyacyl hydrolase, Aoah, as a genetic modulator of pelvic pain. AOAH protein is expressed along the bladder-brain axis, and we are working to define the mechanisms by which Aoah modulates pain and urinary function. Pain and the microbiome. Our current clinical studies include characterizing changes in gut microbiota associated with interstitial cystitis/bladder pain syndrome. Supported by mechanistic studies in mice, we are working to define the influence of microbiota on pelvic pain and urologic and cognitive functions.