Epidemiology of Bladder Cancer in 2023: A Systematic Review of Risk Factors.

Urinary tract infections (UTIs) are among the most common bacterial infections worldwide, occurring in both community and healthcare settings. Although the clinical symptoms of UTIs are heterogeneous and range from uncomplicated (uUTIs) to complicated (cUTIs), most UTIs are usually treated empirically. Bacteria are the main causative agents of these infections, although more rarely, other microorganisms, such as fungi and some viruses, have been reported to be responsible for UTIs. Uropathogenic Escherichia coli (UPEC) is the most common causative agent for both uUTIs and cUTIs, followed by other pathogenic microorganisms, such as Klebsiella pneumoniae, Proteus mirabilis, Enterococcus faecalis, and Staphylococcus spp. In addition, the incidence of UTIs caused by multidrug resistance (MDR) is increasing, resulting in a significant increase in the spread of antibiotic resistance and the economic burden of these infections. Here, we discuss the various factors associated with UTIs, including the mechanisms of pathogenicity related to the bacteria that cause UTIs and the emergence of increasing resistance in UTI pathogens.

/pdf/urinary-tract-infections-the-current-scenario-and-future-1fffla37.pdf

Urinary Tract Infections: The Current Scenario and Future Prospects

The vaginal microbiome is a distinct component of the human microbiome that is colonized by a wide variety of microorganisms. Lactobacilli are the most frequently identified microorganisms in the healthy human vagina. These Gram-positive bacilli can acidify the vaginal microenvironment, inhibit the proliferation of other pathogenic microorganisms, and promote the maintenance of a eubiotic vaginal microbiome. However, a vaginal flora with a reduced proportion or abundance of lactobacilli is associated with various vaginal infections that have been linked to serious health consequences such as infertility, preterm birth, pelvic inflammatory disease, premature rupture of membranes, and miscarriage. Due to their “Generally Recognized as Safe” classification and critical role in vaginal health, probiotic lactobacilli have been widely used as an alternative or adjunct to traditional antibiotic therapy for the treatment of vaginal infections and restoration of the vaginal microbiome. This review focuses on the significant role of probiotic lactobacilli in the vaginal microenvironment and discusses the use of probiotic lactobacilli in the treatment of female vaginal infections in vitro and in vivo.

/pdf/use-of-probiotic-lactobacilli-in-the-treatment-of-vaginal-228uaion.pdf

Use of probiotic lactobacilli in the treatment of vaginal infections: In vitro and in vivo investigations

SUMMARYThe general stress response (GSR) is a widespread strategy developed by bacteria to adapt and respond to their changing environments. The GSR is induced by one or multiple simultaneous stresses, as well as during entry into stationary phase and leads to a global response that protects cells against multiple stresses. The alternative sigma factor RpoS is the central GSR regulator in E. coli and conserved in most γ-proteobacteria. In E. coli, RpoS is induced under conditions of nutrient deprivation and other stresses, primarily via the activation of RpoS translation and inhibition of RpoS proteolysis. This review includes recent advances in our understanding of how stresses lead to RpoS induction and a summary of the recent studies attempting to define RpoS-dependent genes and pathways. 

RpoS and the bacterial general stress response

Commensal microbes have increasingly been found to be involved in the development and progression of cancer. The recent discovery of the urinary microbiome bolstered the notion that microbes might play a role in bladder cancer. Although microbial involvement in bladder neoplastic transformation and metastatic progression, except schisto somiasis, has not been established, accumulating research suggests that dysbiosis of the urinary microbiome can produce a chronically inflammatory urothelial microenvironment and lead to bladder cancer. In this review, we describe how the urinary microbiome might facilitate the development of bladder cancer by altering the host immune system and the kind of cytokines that are directly involved in these responses. We investigated the therapeutic possibilities of modulating the urinary microbiome, including immune checkpoint therapy. The responsiveness of patients to intravesical Bacillus Calmette-Guerin therapy was evaluated with respect to microbiome composition. We conclude by noting that the application of microbes to orchestrate the inflammatory response in the bladder may facilitate the development of treatments for bladder cancer.

/pdf/the-urinary-microbiome-role-in-bladder-cancer-and-treatment-dlingiok.pdf

The Urinary Microbiome: Role in Bladder Cancer and Treatment

Significance The urinary bladder, which was previously believed to be a sterile environment, is actually a habitat for commensal microbes. However, the presence of the bladder microbiome and its functional relationship with the underlying uroepithelial cells have remained a mystery. In this work, we have shown that Lactobacilli, the most abundant commensal bacteria in human bladders, promote type I interferon production in bladder epithelial cells, resulting in mature phagolysosomes with enhanced cathepsin D and acidification. Functionally, Lactobacilli create a microenviroment that protects the host from infection by uropathogenic Escherichia coli. These findings provide compelling evidence that Lactobacilli can modulate innate immunity in the urinary bladder and exert therapeutic effects against urinary tract infection.

Lactobacillus crispatus Limits Bladder Uropathogenic E. coli Infection by Triggering a Host Type I Interferon Response

Manganese Transporter Proteins in Salmonella enterica serovar Typhimurium

Among the AAA+ proteases in bacteria, FtsH is a membrane-bound ATP-dependent metalloprotease, which is known to degrade many membrane proteins as well as some cytoplasmic proteins. In the intracellular pathogen Salmonella enterica serovar Typhimurium, FtsH is responsible for the proteolysis of several proteins including MgtC virulence factor and MgtA/MgtB Mg2+ transporters, the transcription of which is controlled by the PhoP/PhoQ two-component regulatory system. Given that PhoP response regulator itself is a cytoplasmic protein and also degraded by the cytoplasmic ClpAP protease, it seems unlikely that FtsH affects PhoP protein levels. Here we report an unexpected role of the FtsH protease protecting PhoP proteolysis from cytoplasmic ClpAP protease. In FtsH-depleted condition, PhoP protein levels decrease by ClpAP proteolysis, lowering protein levels of PhoP-controlled genes. This suggests that FtsH is required for normal activation of PhoP transcription factor. FtsH does not degrade PhoP protein but directly binds to PhoP, thus sequestering PhoP from ClpAP-mediated proteolysis. FtsH's protective effect on PhoP can be overcome by providing excess ClpP. Because PhoP is required for Salmonella's survival inside macrophages and mouse virulence, these data implicate that FtsH's sequestration of PhoP from ClpAP-mediated proteolysis is a mechanism ensuring the amount of PhoP protein during Salmonella infection.

Membrane-Bound Protease FtsH Protects PhoP from the Proteolysis by Cytoplasmic ClpAP Protease in Salmonella Typhimurium.

Pathogenic bacteria that colonize the human intestinal tract have evolved strategies to overcome acidic conditions when they pass through the gastrointestinal tract. Amino acid-mediated acid resistance systems are effective survival strategies in a stomach that is full of amino acid substrate. The amino acid antiporter, amino acid decarboxylase, and ClC chloride antiporter are all engaged in these systems, and each one plays a role in protecting against or adapting to the acidic environment. The ClC chloride antiporter, a member of the ClC channel family, eliminates negatively charged intracellular chloride ions to avoid inner membrane hyperpolarization as an electrical shunt of the acid resistance system. In this review, we will discuss the structure and function of the prokaryotic ClC chloride antiporter of amino acid-mediated acid resistance system.

ClC Chloride Channels in Gram-Negative Bacteria and Its Role in the Acid Resistance Systems.

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Lactobacillus crispatus Limits Bladder Uropathogenic E. coli Infection by Triggering a Host Type I Interferon Response

Manganese Transporter Proteins in Salmonella enterica serovar Typhimurium

Membrane-Bound Protease FtsH Protects PhoP from the Proteolysis by Cytoplasmic ClpAP Protease in Salmonella Typhimurium.

ClC Chloride Channels in Gram-Negative Bacteria and Its Role in the Acid Resistance Systems.