Impact of Toll-like receptor signalling on urinary tract infection

Scherberich, J E; Hartinger, A.

doi:10.1016/j.ijantimicag.2007.07.032

Cited by 25 publications

(22 citation statements)

References 31 publications

(48 reference statements)

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“…Epithelial cells are the first line of host defense against invading pathogens [9]. In addition, epithelial cells contribute to the initiation of host innate and adaptive immune responses by producing chemokines, cytokines, and antimicrobial peptides [23]. The immune response to UPEC is initiated by bacterial invasion of bladder epithelial cells, which induces the production of proinflammatory cytokines such as IL-6 and IL-8 and recruits neutrophils to the infection Fig.…”

Section: Discussionmentioning

confidence: 99%

Characterization and Zoonotic Potential of Uropathogenic Escherichia coli Isolated from Dogs

Nam

Ko²,

Chae³

et al. 2013

J. Microbiol. Biotechnol.

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The aim of this study was to investigate the characteristics of canine uropathogenic Escherichia coli (UPEC) and the interaction between canine UPEC and human bladder epithelial cells. Ten E. coli isolates collected from dogs with cystitis were analyzed for antimicrobial resistance patterns, the presence of virulence factors, and biofilm formation. The ability of these isolates to induce cytotoxicity, invade human bladder epithelial cells, and stimulate an immune response was also determined. We observed a high rate of antimicrobial resistance among canine UPEC isolates. All virulence genes tested (including adhesins, iron acquisition, and protectin), except toxin genes, were detected among the canine UPEC isolates. We found that all isolates showed varying degrees of biofilm formation (mean, 0.26; range, 0.07 to 0.82), using a microtiter plate assay to evaluate biofilm formation by the isolates. Cytotoxicity to human bladder epithelial cells by the canine UPEC isolates increased in a time-dependent manner, with a 56.9% and 36.1% reduction in cell viability compared with the control at 6 and 9 h of incubation, respectively. We found that most canine UPEC isolates were able to invade human bladder epithelial cells. The interaction between these isolates and human bladder epithelial cells strongly induced the production of proinflammatory cytokines such as IL-6 and IL-8. We demonstrated that canine UPEC isolates can interact with human bladder epithelial cells, although the detailed mechanisms remain unknown. The results suggest that canine UPEC isolates, rather than dogspecific pathogens, have zoonotic potential.

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Section: Discussionmentioning

confidence: 99%

Characterization and Zoonotic Potential of Uropathogenic Escherichia coli Isolated from Dogs

Nam

Ko²,

Chae³

et al. 2013

J. Microbiol. Biotechnol.

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“…Pharmacological agents (TLR agonists) contain synthetic lipopeptide derivatives from bacterial lipoproteins, ssRNA, CpG motifcontaining oligonucleotides or CpG oligodeoxynucleotides. Patients who are susceptible to UTI, in which defective TLR mutants might be responsible for increased infection rates, could be treated with specific TLR-modulating drugs to conquer impaired immune defense systems, particularly in chronic recurrent UTI [40].…”

Section: Tlr-based Drug Developmentmentioning

confidence: 99%

“…Stimulation of TLR-related antimicrobial signaling of target cells (monocytes, DCs, lymphocytes) via immunoadjuvants may reflect an innovative form of immunization, similar to-or even more effective than-the conventional vaccination that targets the pathogen [41]. In a similar method, recent pre-clinical studies used TLR ligands to treat viral diseases and to improve antitumor treatment (e.g., ligands that play as agonists for TLR7 activation against cancer cells) [40].…”

Section: Tlr Agonistsmentioning

confidence: 99%

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Clinical Significance of Toll-Like Receptor and Toll-Like Receptor Blocker

Choi

Song

2016

Urogenit Tract Infect

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“…When TLR4 and TLR5 are bound by ligand they are phosphorylated on the cytoplasmic domain. Activation of the TLRs initiates signaling of immune and inflammation responses [22][23][24][25][26]. TLR4 activation by LPS or P fimbriae binding results in secretion of IL-6 and IL-8.…”

Section: Toll-like Receptorsmentioning

confidence: 99%

Innate Immune Response to Urinary Tract Infections Involving Escherichia coli

Reygaert¹

2014

J Clin Cell Immunol

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The innate immune system responds in a rapid, initially nonspecific manner to infection in the urinary tract. There are many molecules and cells involved in this response. These include: antimicrobial peptides, toll-like receptors, chemokines, cytokines, and neutrophils. The most common cause of urinary tract infections (UTIs) are uropathogenic Escherichia coli (UPEC). The innate immune system responds to the presence of flagella, fimbriae, and the lipopolysaccharide outer membrane of these bacteria. Antimicrobial peptides are used to lyse the bacteria and also prevent the bacteria from binding to epithelial cells in the urinary tract. The toll-like receptors sense the presence of the bacteria and signal for the production of molecules that cause immune and inflammation responses. The various chemokines and cytokines such as CXCL8, CCL2, interleukins (IL-6, IL-8, IL-10, IL-17A), and granulocyte colony stimulating factor (G-CSF), are used for much of the signaling in innate immunity. In addition, neutrophils play a major role in rapid removal of invading bacteria. The rapid innate immune response is designed to remove most of the bacteria within 24 hours in an uncomplicated UTI. This review presents an overview of the innate immune response to UTIs caused by UPEC and the host molecules and cells involved.

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Impact of Toll-like receptor signalling on urinary tract infection

Cited by 25 publications

References 31 publications

Characterization and Zoonotic Potential of Uropathogenic Escherichia coli Isolated from Dogs

Characterization and Zoonotic Potential of Uropathogenic Escherichia coli Isolated from Dogs

Clinical Significance of Toll-Like Receptor and Toll-Like Receptor Blocker

Innate Immune Response to Urinary Tract Infections Involving Escherichia coli

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