scholarly journals Importance of the C-terminal histidine residues of Helicobacter pylori GroES for Toll-like receptor 4 binding and interleukin-8 cytokine production

2016 ◽  
Vol 6 (1) ◽  
Author(s):  
Haur Lee ◽  
Yu-Lin Su ◽  
Bo-Shih Huang ◽  
Feng-Tse Hsieh ◽  
Ya-Hui Chang ◽  
...  
Keyword(s):  
Helicobacter Pylori ◽  
Cytokine Production ◽  
Interleukin 8 ◽  
Toll Like Receptor ◽  
Toll Like Receptor 4 ◽  
Histidine Residues

Heat‐killed Helicobacter pylori upregulates NKG2D ligands expression on gastric adenocarcinoma cells via Toll‐like receptor 4

Helicobacter ◽  
2021 ◽  
Author(s):  
Carolina Hernández ◽  
Karen Toledo‐Stuardo ◽  
Paulina García‐González ◽  
Macarena Garrido‐Tapia ◽  
Karina Kramm ◽  
...  
Keyword(s):  
Helicobacter Pylori ◽  
Gastric Adenocarcinoma ◽  
Toll Like Receptor ◽  
Toll Like Receptor 4 ◽  
Nkg2d Ligands ◽  
Adenocarcinoma Cells

scholarly journals Association of toll-like receptor 4, 5 and 10 polymorphisms with Helicobacter pylori -positive peptic ulcer disease in a center in Jordan

2021 ◽  
Vol 41 (4) ◽  
pp. 206-215
Author(s):  
Laith AL-Eitan ◽  
Fouad Abdelaziz Almomani ◽  
Sohaib Mahmoud Al-Khatib ◽  
Hanan Abdulraheem Aljamal ◽  
Mohammed Nayef Al-Qusami ◽  
...  
Keyword(s):  
Helicobacter Pylori ◽  
Peptic Ulcer ◽  
Conflicts Of Interest ◽  
Care Center ◽  
Treatment Success ◽  
Tertiary Care ◽  
Genotype Distribution ◽  
Toll Like Receptor ◽  
Toll Like Receptor 4 ◽  
H Pylori

BACKGROUND: Helicobacter pylori infection is widespread, affecting about 50% of the global population. Polymorphisms in host genes such as the toll-like receptor 4 ( TLR4 ) might affect the susceptibility and severity of infection and treatment success. OBJECTIVE: Investigate the susceptibility and severity of H pylori infection with host TLR4 (rs11536889, rs4986790, rs200109652, rs10759932), TLR5 (rs5744174, rs2072493, rs746250566), TLR10 (rs559182335, rs10004195) polymorphisms. DESIGN: Analytical, cross-sectional. SETTING: Endoscopy clinic at tertiary care center. PATIENTS AND METHODS: Genomic DNA was extracted from formalin-fixed paraffin-embedded tissues collected from H pylori -infected patients and healthy individuals. The single nucleotide polymorphisms (SNPs) within the targeted TLR genes were genotyped to assess the genetic association of various SNPs with disease severity. MAIN OUTCOME MEASURES: Effect of genotype distribution on H pylori infection. SAMPLE SIZE: 250 peptic ulcer patients and 217 controls. RESULTS: The TLR10 genotype showed no significant association with H pylori infection except for rs10004195 (T>A) ( P =.002). The genotype frequency of Rs5744174 in TLR5 had a significant association with the presence of H pylori infection ( P =.046, OR=0.52). Except for gender (P=.022), there were no significant associations between clinical and demographic variables and SNPs relating to the severity of the H pylori infections. CONCLUSIONS: Our findings are consistent with differences in severity of H pylori infection due to TLR SNPs in different ethnic groups. Understanding differences in genetic susceptibility could help in classifying patients and matching patients with various treatment options on a genetic basis. LIMITATIONS: Lack of H pylori pathogenicity features assessment. CONFLICTS OF INTEREST: None.

scholarly journals Bacteroides fragilis-Derived Lipopolysaccharide Produces Cell Activation and Lethal Toxicity via Toll-Like Receptor 4

2005 ◽  
Vol 73 (9) ◽  
pp. 5620-5627 ◽  
Author(s):  
Giuseppe Mancuso ◽  
Angelina Midiri ◽  
Carmelo Biondo ◽  
Concetta Beninati ◽  
Maria Gambuzza ◽  
...  
Keyword(s):  
Cell Activation ◽  
Cytokine Production ◽  
Biological Activities ◽  
Endotoxic Shock ◽  
Intestinal Flora ◽  
Bacteroides Fragilis ◽  
Peritoneal Macrophages ◽  
Toll Like Receptor ◽  
Toll Like Receptor 4 ◽  
In Cells

ABSTRACT Bacteroides fragilis, which is part of the normal intestinal flora, is a frequent cause of serious disease, especially in diabetic and surgical patients. In these conditions, B. fragilis lipopolysaccharide (LPS) is likely to play a major pathophysiologic role. B. fragilis LPS is structurally different from classical enterobacterial LPS, whose biological activities are mediated by Toll-like receptor 4 (TLR4) activation. The ability of B. fragilis LPS to activate TLR4 and TLR2 was investigated here, since evidence on this issue is scarce and controversial. Each of four different protein-free B. fragilis LPS preparations could induce interleukin-8 responses in cells cotransfected with TLR4/CD14/MD2 but not TLR4/CD14 alone. Two of the preparations also induced cytokine production in cells cotransfected with TLR2/CD14 or in peritoneal macrophages from TLR4 mutant C3H/HeJ mice. Both of these activities, however, were lost after repurification with a modified phenol reextraction procedure. Importantly, all preparations could induce endotoxic shock in TLR2-deficient mice, but not in TLR4 mutant C3H/HeJ mice. Consistent with these findings, anti-TLR4 and anti-CD14, but not anti-TLR2, antibodies could inhibit B. fragilis LPS-induced cytokine production in human monocytes. Collectively, these results indicate that B. fragilis LPS signals via a TLR4/CD14/MD2-dependent pathway, and it is unable to activate TLR2. Moreover, our data document the occurrence of TLR2-activating contaminants even in highly purified B. fragilis LPS preparations. This may explain earlier contradictory findings on the ability of B. fragilis LPS to activate cells in the absence of functional TLR4. These data may be useful to devise strategies to prevent the pathophysiologic changes observed during B. fragilis sepsis and to better understand structure-activity relationships of LPS.

Safflower polysaccharides activate the transcription factor NF-κB via Toll-like receptor 4 and induce cytokine production by macrophages

2002 ◽  
Vol 2 (8) ◽  
pp. 1155-1162 ◽  
Author(s):  
Izuru Ando ◽  
Yoshinori Tsukumo ◽  
Tetsuya Wakabayashi ◽  
Sachiko Akashi ◽  
Kensuke Miyake ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Cytokine Production ◽  
Toll Like Receptor ◽  
Toll Like Receptor 4
Sign in / Sign up

Export Citation Format

Share Document