Year: 2011
Type: book-chapter
Abstract: IntroductionUrinary tract infection (UTI) is one of the most common infections in humans.It is estimated that 40% of women and 12% of men will experience a symptomatic UTI, with incidences peaking in their early 20s or after age 85, respectively (1).Approximately 25% of these women will experience recurrence within 6 to 12 months (1).Uropathogenic Escherichia coli (UPEC) is the most common etiological agent responsible for uncomplicated UTI.In the United States alone, the estimated annual societal cost of UTI is more than 3 billion dollars (1). Despite significant advances in the understanding of UPEC biology, mechanistic details regarding the host response to UTI and full comprehension of genetic loci that influence susceptibility require additional work.As new and intriguing details of how uropathogens initiate infections and persist within the urinary tract have emerged, so has important information regarding how the immune system functions within the urinary tract.The complex cross-linking for innate and adaptive immune response as well as humoral and cellular effectors is the key to the urinary tract immune system and to its defense against pathogenic microorganisms.As antibiotic therapy becomes increasingly ineffective, modulating the innate and adaptive immune system in the urinary tract using TLR4 ligands and other immunomodulators may become viable options to combat UTIs. Innate responses to urinary tract infections2.1 Host factors that prevent colonization of urinary tract with UPEC Uroepithelial adherence is critical for establishment of UTI.The urinary tract, comprised of the urethra, bladder, ureters and the kidneys, represents a formidable mechanical barrier to infection.In addition to the relative impregnability of the epithelium lining the tract, potential pathogens have to contend with the powerful flushing action of urine and the aggregating actions of urinary mucins (2;3).UPEC strains possess an impressive repertoire of adhesins that enable them to aggregate and adhere to cellular surfaces (4).Consequently, the first line of host defense against UTI is concentrated on preventing UPEC adherence to the bladder mucosa.The luminal surface of the bladder is lined with highly sulfated and anionic glycosaminoglycans (GAGs) that contribute to bladder wall impermeability and afford an antimicrobial anti-adherence property.Intuitively, urine flow seems to be a convenient defense mechanism; however, FimH binds to mannose moieties using "catch- www.intechopen.com
Source: InTech eBooks
DOI: 10.5772/21939
Author: Kelesidis Theodoros
Institution: University of California, Los Angeles
Language: English
Subfield: Epidemiology
Field: Medicine
Domain: Health Sciences
Open Access status: hybrid
OpenAlex ID: W1603436455