A Urinary tract infection (UTI) is one reason many patients take a trip to visit their physician. Upon clearing of the infection, some individuals find that the annoyance has returned and rather quickly, leaving them questioning the effectiveness of the treatment. In a recent study published in the scientific journal known as PLOS Pathogens, a team of researchers sheds light on what could be going on.
A urinary tract infection is an infection in any part of your urinary system — kidneys, ureters, bladder, and urethra. Most infections involve the lower urinary tract — the bladder and the urethra.
Women are at higher risk of developing a UTI than are men. Infection limited to your bladder can be painful and annoying. However, serious consequences can occur if a UTI spreads to your kidneys.
Urinary tract infections are widespread and can be highly recurrent, with 1–2% of women suffering from six or more frequent episodes per year. The high incidence of recurrent UTI, including recurrent infections caused by the same bacterial strain that produced the first infection, suggests that at least some women do not mount a protective adaptive immune response to UTI.
Many patients suffer from highly recurrent urinary tract infections caused by Escherichia coli, which are genetically diverse bacteria. Recurrent episodes are often caused by the same E. coli strain that created the first infection, suggesting that some patients may not develop a protective immune response.
The researchers, making use of bladder infected mouse models, discover that two E. coli strains behave differently. One strain, known as UTI89, infects the bladder indefinitely, whereas another strain called CFT073 is cleared within eight weeks.
Interestingly, mice which had already been exposed to CFT073 and treated with antibiotics were henceforth protected from reinfection, however, remained susceptible to UTI89 infection. In contrast to this finding, mice with a UTI89 infection and antibiotics were susceptible to recurrent UTI when challenged with either strain.
“We found that depleting T cells, immune cells important for developing protection against infection prevented mice from clearing their CFT073 infections and made them susceptible to recurrent CFT073 UTI. Thus, while infection with one E. coli strain could trigger a protective immune response, another strain sidestepped this response” shares authors of the publication.
“Our findings demonstrate the complex interplay between the broad genetic diversity of UPEC and the host innate and adaptive immune responses during UTI. A better understanding of these host-pathogen interactions is urgently needed for effective drug and vaccine development in the era of increasing antibiotic resistance,” shares the authors of the study.
The findings to this study shed new light on immune responses to UTI and may be essential for drug and vaccine development.