scholarly journals Toll-like receptor 5 and the emerging role of bacteria in carcinogenesis

2013 ◽  
Vol 2 (4) ◽  
pp. e23620 ◽  
Author(s):  
Joonas H. Kauppila ◽  
Antti E. Mattila ◽  
Tuomo J. Karttunen ◽  
Tuula Salo
Keyword(s):  
Toll Like Receptor ◽  
Toll Like Receptor 5

scholarly journals The role of the C-terminal D0 domain of flagellin in activation of Toll like receptor 5

2017 ◽  
Vol 13 (8) ◽  
pp. e1006574 ◽  
Author(s):  
Vida Forstnerič ◽  
Karolina Ivičak-Kocjan ◽  
Tjaša Plaper ◽  
Roman Jerala ◽  
Mojca Benčina
Keyword(s):  
Toll Like Receptor ◽  
Toll Like Receptor 5

scholarly journals Toll-like receptor 5 in obesity: The role of gut microbiota and adipose tissue inflammation

Obesity ◽  
2015 ◽  
Vol 23 (3) ◽  
pp. 581-590 ◽  
Author(s):  
Satu Pekkala ◽  
Eveliina Munukka ◽  
Lingjia Kong ◽  
Eija Pöllänen ◽  
Reija Autio ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Gut Microbiota ◽  
Adipose Tissue Inflammation ◽  
Toll Like Receptor ◽  
Tissue Inflammation ◽  
Toll Like Receptor 5

scholarly journals Central role of liver in anticancer and radioprotective activities of Toll-like receptor 5 agonist

2013 ◽  
Vol 110 (20) ◽  
pp. E1857-E1866 ◽  
Author(s):  
L. G. Burdelya ◽  
C. M. Brackett ◽  
B. Kojouharov ◽  
I. I. Gitlin ◽  
K. I. Leonova ◽  
...  
Keyword(s):  
Toll Like Receptor ◽  
Toll Like Receptor 5

scholarly journals Toll-like receptor 5-mediated signaling enhances liver regeneration in mice

2021 ◽  
Vol 8 (1) ◽  
Author(s):  
Wen Zhang ◽  
Lei Wang ◽  
Xue-Hua Sun ◽  
Xian Liu ◽  
Yang Xiao ◽  
...  
Keyword(s):  
Liver Regeneration ◽  
Early Gene ◽  
Hepatocyte Proliferation ◽  
Toll Like Receptor ◽  
Hepatic Lipid ◽  
Growth Factor Production ◽  
Toll Like Receptor 5 ◽  
Oil Red O ◽  
Tlr5 Expression

Abstract Background Toll-like receptor 5 (TLR5)-mediated pathways play critical roles in regulating the hepatic immune response and show hepatoprotective effects in mouse models of hepatic diseases. However, the role of TLR5 in experimental models of liver regeneration has not been reported. This study aimed to investigate the role of TLR5 in partial hepatectomy (PHx)-induced liver regeneration. Methods We performed 2/3 PHx in wild-type (WT) mice, TLR5 knockout mice, or TLR5 agonist CBLB502 treated mice, as a model of liver regeneration. Bacterial flagellin content was measured with ELISA, and hepatic TLR5 expression was determined with quantitative PCR analyses and flow cytometry. To study the effects of TLR5 on hepatocyte proliferation, we analyzed bromodeoxyuridine (BrdU) incorporation and proliferating cell nuclear antigen (PCNA) expression with immunohistochemistry (IHC) staining. The effects of TLR5 during the priming phase of liver regeneration were examined with quantitative PCR analyses of immediate early gene mRNA levels, and with Western blotting analysis of hepatic NF-κB and STAT3 activation. Cytokine and growth factor production after PHx were detected with real-time PCR and cytometric bead array (CBA) assays. Oil Red O staining and hepatic lipid concentrations were analyzed to examine the effect of TLR5 on hepatic lipid accumulation after PHx. Results The bacterial flagellin content in the serum and liver increased, and the hepatic TLR5 expression was significantly up-regulated in WT mice after PHx. TLR5-deficient mice exhibited diminished numbers of BrdU- and PCNA-positive cells, suppressed immediate early gene expression, and decreased cytokine and growth factor production. Moreover, PHx-induced hepatic NF-κB and STAT3 activation was inhibited in Tlr5−/− mice, as compared with WT mice. Consistently, the administration of CBLB502 significantly promoted PHx-mediated hepatocyte proliferation, which was correlated with enhanced production of proinflammatory cytokines and the recruitment of macrophages and neutrophils in the liver. Furthermore, Tlr5−/− mice displayed significantly lower hepatic lipid concentrations and smaller Oil Red O positive areas than those in control mice after PHx. Conclusion We reveal that TLR5 activation contributes to the initial events of liver regeneration after PHx. Our findings demonstrate that TLR5 signaling positively regulates liver regeneration and suggest the potential of TLR5 agonist to promote liver regeneration.

scholarly journals Pathophysiological role of Toll-like receptor 5 engagement by bacterial flagellin in colonic inflammation

2005 ◽  
Vol 102 (38) ◽  
pp. 13610-13615 ◽  
Author(s):  
S. H. Rhee ◽  
E. Im ◽  
M. Riegler ◽  
E. Kokkotou ◽  
M. O'Brien ◽  
...  
Keyword(s):  
Toll Like Receptor ◽  
Colonic Inflammation ◽  
Pathophysiological Role ◽  
Toll Like Receptor 5

scholarly journals Critical Role of Innate Immunity to Flagellin in the Absence of Adaptive Immunity

2020 ◽  
Author(s):  
Jun Zou ◽  
Xu Zhao ◽  
Zhenda Shi ◽  
Zhan Zhang ◽  
Matam Vijay-Kumar ◽  
...  
Keyword(s):  
Adaptive Immunity ◽  
Critical Role ◽  
Fecal Microbiota ◽  
Innate Immune ◽  
Low Grade ◽  
Toll Like Receptor ◽  
Fecal Microbiota Transplant ◽  
Toll Like Receptor 5 ◽  
Immune Detection

Abstract Background Bacterial flagellin is a major target of innate and adaptive immunity, both of which can promote and/or compensate for deficiencies in each other’s function. Methods To investigate the role of innate immune detection of flagellin irrespective of adaptive immunity, we examined the consequences of loss of Toll-like receptor 5 (T5) and/or Nod-like receptor 4 (N4) upon a Rag1-deficient background. Results Mice lacking Toll-like receptor 5 and Rag1 (T5/Rag-DKO) exhibited frequent lethal Pasteurellaceae-containing abscesses that prevented breeding of these mice. Mice lacking Toll-like receptor 5, Nod-like receptor 4, and Rag1 (T5/N4/Rag-TKO) also resulted in sporadic lethal abdominal abscesses caused by similar Pasteurellaceae. In the absence of such infections, relative to Rag1-KO, T5/N4/Rag-TKO mice exhibited microbiota encroachment, low-grade inflammation, microbiota dysbiosis, and, moreover were highly prone to Citrobacter infection and developed severe colitis when adoptively transferred with colitogenic T cells. Relative proneness of T5/N4/Rag-TKO mice to T-cell colitis was ablated by antibiotics while fecal microbiota transplant from T5/N4/Rag-TKO mice to wild-type mice transferred proneness to Citrobacter infection, indicating that dysbiosis in T5/N4/Rag-TKO mice contributed to these phenotypes. Conclusions These results demonstrate a critical role for innate immune detection of flagellin, especially in the intestinal tract and particularly in hosts deficient in adaptive immunity.

Mo1342 ROLE OF TOLL-LIKE RECEPTOR 5 IN THE BRAIN-GUT-MICROBIOTA TRIALOGUE: A NEW PHARMACOLOGICAL TARGET FOR THE TREATMENT OF CHRONIC ABDOMINAL PAIN AND ASSOCIATED COMORBIDITIES

2020 ◽  
Vol 158 (6) ◽  
pp. S-857
Author(s):  
Geoffroy Mallaret ◽  
Amandine Lashermes ◽  
Al Mahdy Hamieh ◽  
Mathieu Meleine ◽  
Julie Barbier ◽  
...  
Keyword(s):  
Abdominal Pain ◽  
Gut Microbiota ◽  
Chronic Abdominal Pain ◽  
Toll Like Receptor ◽  
Pharmacological Target ◽  
Toll Like Receptor 5 ◽  
The Brain

scholarly journals Toll-Like Receptor 5-Deficient Mice Have Dysregulated Intestinal Gene Expression and Nonspecific Resistance to Salmonella-Induced Typhoid-Like Disease

2008 ◽  
Vol 76 (3) ◽  
pp. 1276-1281 ◽  
Author(s):  
Matam Vijay-Kumar ◽  
Jesse D. Aitken ◽  
Amrita Kumar ◽  
Andrew S. Neish ◽  
Satoshi Uematsu ◽  
...  
Keyword(s):  
Gene Expression ◽  
Salmonella Enterica ◽  
Host Recognition ◽  
Toll Like Receptor ◽  
Defense Gene Expression ◽  
Nonspecific Resistance ◽  
Serovar Typhimurium ◽  
Toll Like Receptor 5

ABSTRACT The recognition of flagellin by Toll-like receptor 5 (TLR5) is the dominant means by which model intestinal epithelia activate proinflammatory gene expression in response to Salmonella enterica. The role of the flagellin-TLR5 interaction in vivo has been addressed primarily via studies that use flagellar mutants. Such studies suggest that host recognition of flagellin promotes rapid neutrophil recruitment that protects the host from this pathogen. However, these works do not directly address the role of TLR5 and are subject to the caveat that flagellar mutations may broadly affect Salmonella gene expression. Thus, we examined the role of the flagellin-TLR5 interaction via the use of TLR5-deficient (TLR5KO) mice. We utilized both the traditional model of murine Salmonella infection, wherein low-dose oral infection of mice with Salmonella enterica subsp. enterica serovar Typhimurium results in systemic typhoid-like disease, and a more recently characterized model in which mice are pretreated with streptomycin to result in gut-restricted acute enteritis. In the enteritis model, TLR5KO mice had more severe gut pathology, thus “phenocopying” previous results obtained with Salmonella mutants. In contrast, TLR5KO mice were resistant to Salmonella-induced typhoid-like disease. However, such resistance was not specific for flagellated serovar Typhimurium, but rather, TLR5KO mice were also resistant to challenges by flagellin-deficient serovar Typhimurium. Such resistance associated with elevations in the microbiota was ablated by antibiotic pretreatment and correlated with basal elevations in intestinal host defense gene expression. All together, these results indicate that the resistance of TLR5KO mice to Salmonella-induced typhoid-like illness resulted from alterations in their basal phenotype rather than from the lack of TLR5 ligation during the infection per se.

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