Prostaglandin E2 production and cyclooxygenase-2 induction in human urinary tract infections and bladder cancer

Marcia A Wheeler1, Derek A Hausladen, Jeong H Yoon

  • 1Department of Urology, Yale University School of Medicine, New Haven, Connecticut, USA.

The Journal of Urology
|September 28, 2002
PubMed
Abstract

Related Concept Videos

Drugs for Peptic Ulcer Disease: Prostaglandin Analogs as Mucosal Protective Agents01:20

Drugs for Peptic Ulcer Disease: Prostaglandin Analogs as Mucosal Protective Agents

The gastric mucosa produces prostaglandins E2 (PGE2) and prostacyclin (PGI2), crucial in maintaining gastric health. They exert cytoprotective effects, including increasing bicarbonate secretion, releasing protective mucin, reducing gastric acid output, and preventing harmful vasoconstriction. These effects are mediated through various receptors, such as EP1, EP2, EP3, and EP4.
Non-steroidal anti-inflammatory drugs (NSAIDs) can induce peptic ulcers by inhibiting cyclooxygenase, decreasing...
Urinary Tract Infection II: Pathophysiology01:25

Urinary Tract Infection II: Pathophysiology

The pathophysiology of urinary tract infections (UTIs) encompasses several progressive stages, beginning with bacterial colonization and culminating in potential systemic complications if untreated. UTIs are primarily initiated by bacteria, such as Escherichia coli, which often originate from the gastrointestinal tract and migrate to the urinary system through the periurethral area. This migration can occur via several routes, including improper hygiene practices, sexual activity, or...
Peptic Ulcer Disease II: Pathophysiology01:24

Peptic Ulcer Disease II: Pathophysiology

Peptic ulcer disease develops when protective mechanisms of the gastrointestinal mucosa are overwhelmed by harmful factors, leading to localized erosions in the stomach or proximal duodenum. The main causes are Helicobacter pylori infection and chronic use of nonsteroidal anti-inflammatory drugs (NSAIDs).Helicobacter pylori–Induced InjuryBacterial Adaptation and Colonization:H. pylori is a spiral, Gram-negative bacterium adapted to the acidic stomach. and transmitted through oral-oral or...
Gastritis-II: Pathophysiology01:17

Gastritis-II: Pathophysiology

Gastritis is marked by disruption of the mucosal barrier that usually protects the stomach tissue from digestive juices and manifests in acute and chronic forms.
In acute gastritis, the gastric mucosa becomes swollen and red and undergoes superficial erosion. Superficial ulceration may lead to bleeding.
In chronic gastritis, persistent or repeated insults lead to chronic inflammatory changes and, eventually, thinning or atrophy of the gastric tissue.
Gastritis can stem from various causes, each...
Microbiota of the Urogenital Tract01:28

Microbiota of the Urogenital Tract

The human urogenital system, once thought to be sterile in healthy individuals, is now recognized as a complex microbial habitat. Advancements in molecular sequencing techniques have revealed that even in healthy adults, the kidneys and bladder harbor microbial populations similar to those found in the distal urethra, albeit in much lower abundance. These resident microorganisms, while generally innocuous, can become opportunistic pathogens under conditions that alter the urogenital...
Urinary Tract Infection I: Introduction01:26

Urinary Tract Infection I: Introduction

Urinary tract infections (UTIs) impact various parts of the urinary system, including the kidneys, ureters, bladder, and urethra. These infections are generally bacterial, with Escherichia coli being the most common causative agent, often originating from the gastrointestinal tract. However, other bacteria, such as Staphylococcus saprophyticus, Klebsiella pneumoniae, and Proteus mirabilis, are also known to cause UTIs. The type, location, and underlying complexity of the UTI guide both...