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The present study investigates a possible source of inflammatory mediators involved in the pathogenesis of bladder inflammation characteristics of interstitial cystitis disease. Our tested hypothesis is that in response to injury, tissues of the urinary bladder participate in the initiation of bladder inflammation by releasing inflammatory mediators such as neutrophil chemotactic factors. Bladders of anesthetized rabbits (n = 7) were instilled with an acidic solution (pH 4.5) for 15 minutes, then washed with saline and instilled with sterile phosphate buffered saline (PBS) (pH 7.2) for an additional 45 minutes prior to sacrificing the rabbits. Control rabbits (n = 7) were instilled with sterile PBS (pH 7.2) for 15 minutes, then 45 minutes. The levels of neutrophil chemotactic factors were measured using modified Boyden chambers and rabbit peritoneal neutrophils as indicator cells. Results indicated the release of high levels of neutrophil chemotactic factors (via a checkerboard analysis) from acid-treated bladders after 15 minutes (70 +/- 4% of standard) and 45 minutes (80 +/- 7%). Electron microscopy analysis of these acid-treated bladders revealed the infiltration of a large number of neutrophils, which correlates with the recovery of neutrophil chemotactic factors. Control rabbits, on the other hand, showed low levels of chemotactic activity (less than 10 percent) and exhibited normal bladder morphology with absence of neutrophils. The glycosaminoglycan (GAG) layer was intact in both acid-treated and control bladders. High levels of neutrophil chemotactic factors were also detected in urine samples from eleven patients with interstitial cystitis (113 +/- 25%) (not due to interleukin-1 or leukotriene B4) which were not detected in urine samples from healthy volunteers (n = 9) or from thirteen control patients with bladder diseases other than interstitial cystitis. These preliminary studies indicate the capability of injured bladder tissues to release neutrophil chemotactic factors which contribute to the initiation of bladder inflammation. The presence of neutrophil chemotactic factors in urine samples of interstitial cystitis patients suggests a possible role of these mediators in the pathogenesis of the disease.

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Surprisingly, little is known about host factors in cases of bladder carcinoma. We investigated 2 families prone to transitional cell carcinoma of the bladder. A high degree of pathology verification of cancer of all anatomic sites and a meticulous recording of genealogy, associated diseases and environmental exposures, when known, have allowed a more cogent appraisal of cancer etiology. It is reasonable to assume that members of the subject families may be more susceptible to variable carcinogenic exposures, a concept that is in accord with a genetic-environmental interaction hypothesis for cancer etiology. In addition to increased surveillance of high risk patients for earlier detection of bladder cancer, cancer control measures also should take into consideration preventive programs directed toward the avoidance of known carcinogenic exposures, such as cigarette smoking in high risk relatives of cancer-affected probands. We propose that the etiology of familial bladder cancer may be complex, involving possible other associated malignant neoplasms and/or certain non-neoplastic disorders, in addition to specific carcinogenic exposures. There is a serious need for the detailed reporting of families prone to bladder cancer wherein all of these potentially important associated factors are considered, so that a fuller appraisal of etiology might be achieved.