Urinary Tract Infection, UTI - Host immunity

Host immunity of Urinary Tract Infection (UTI)

Many individuals, mostly women are colonized in the vaginal or periurethral area with microorganisms originating from the GI tract yet Urinary Tract Infection (UTI) is not developed in major cases. Whether the colonized microorganisms cause infection or not, depends upon a complex interplay of host and microbial factors.

Host defense mechanisms are able to eliminate the organisms. Urine itself is inhibitory to some urethral flora such as anaerobes. Organisms able to grow in the urinary tract may be inhibited if urine has low pH, high or low osmolality, high urea concentration, or high organic acid content.

If bacteria do get to the bladder, constant flushing eliminates microorganisms from the colonized area of their number is maintained at low levels.

Mechanical obstructions resulting from kidney stones or strictures will interfere with the normal voiding of their number maintained at low levels.

Bladder mucosal surfaces have antimicrobial properties. If colonies are not eradicated, the site of infection remains restricted to the superficial mucosa. Deep layers of the bladder are rarely involved.

Between ureters and bladder, a valve-like mechanism is present which prevents reflux (backflow) of urine up to the kidneys. If in any case, this mechanism is compromised either by obstruction or congenital reasons, urine reflux can be possible. In such patients, microorganisms can easily reach up to the kidney and can cause infection.

During pregnancy, hormonal changes and their effects can increase the chance of urine reflux to the upper urinary tract. Uropathogens help in fending off infection by activating the host's immune response. Eg: bacterial contact with urothelial cells initiates an immune response via a variety of signaling pathways.

1. Bacterial lipopolysaccharides (LPS) activate host cells to ultimately release cytokines such as Tumor necrosis factor (TNF) and interferon-gamma.

2. Bacteria can activate complement cascade leading to the production of biologically active components such as osmosis as well as augment (increase/intensify) the host’s adaptive immune response.

3. Host factors that lead to host susceptibility or resistance to uropathogens have been identified. Eg. In a specific anatomic location of the kidney, epithelial cells synthesize glycoprotein known as Tamm-Horsfall protein or uromodulin, which serves as an anti-adherence factor by binding to E. coli expressing type I fimbriae

4. A group of small antimicrobial peptides and defensins produced by a variety of host cells such as macrophages, neutrophils, and cells in the urinary tract adheres to the bacterial cell, eventually causing its death.

Urinary Tract Infection (UTI) is caused by many microorganisms but in most cases, Urinary Tract Infection (UTI) is the result of a few organisms. Eg: E. coli. Only a number of serotypes of E.coli can cause Urinary Tract Infection (UTI), these serotypes termed UPEC (Uropathogenic E. coli) possess virulence factors that enhance their ability to colonize and invade the urinary tract.