Extracellular and Intracellular Pattern Recognition Receptors Cooperate in the Recognition of Helicobacter pylori

Rad, Roland; Ballhorn, Wibke; Voland, Petra; Eisenächer, Katharina; Mages, Jörg; Rad, Lena; Ferstl, Ruth; Lang, Roland; Wagner, Hermann; Schmid, Roland M.; Bauer, Stefan; Prinz, Christian; Kirschning, Carsten J.; Krug, Anne

doi:10.1053/j.gastro.2009.02.066

Cited by 158 publications

(194 citation statements)

References 34 publications

Supporting

Mentioning

183

Contrasting

Unclassified

Order By: Relevance

“…It is also clear, however, that host cells express surface receptors other than Muc1 that serve as adhesion sites for H. pylori. Some of these that have been reported in the literature include Toll-like receptors, integrins, and CD74 (52)(53)(54). On the basis of the data presented in this report, we hypothesize that, in the context of expression of the Muc1 intracellular COOH terminus, downstream signaling initiated by H. pylori is suppressed through the ability of the Muc1 cytoplasmic domain to interact with IKK␥.…”

Section: Discussionmentioning

confidence: 55%

Muc1 Cell Surface Mucin Attenuates Epithelial Inflammation in Response to a Common Mucosal Pathogen

Guang

Ding

Czinn

et al. 2010

Journal of Biological Chemistry

View full text Add to dashboard Cite

show abstract

Section: Discussionmentioning

confidence: 55%

Muc1 Cell Surface Mucin Attenuates Epithelial Inflammation in Response to a Common Mucosal Pathogen

Guang

Ding

Czinn

et al. 2010

Journal of Biological Chemistry

View full text Add to dashboard Cite

show abstract

“…Along the same lines, B. burgdorferi extracts depleted enzymatically for nucleic acids showed dependency on TLR7 with respect to IFNs, yet they also induced NF-kB-dependent genes (37). Using murine DCs, Helicobacter pylori RNA induced proinflammatory cytokines (71), and phagocytosis of H. pylori activated TLR8 in human monocytes (72). Mycobacterium bovis bacillus Calmette-Guérin upregulated TLR8 in differentiated macrophages, and TLR8 gene variants were associated with susceptibility to pulmonary tuberculosis, arguing for a contribution of TLR8 signaling in mycobacteria infection (73).…”

Section: Significance Of Bacterial Rna Recognition For Innate Immune mentioning

confidence: 80%

Bacterial RNA: An Underestimated Stimulus for Innate Immune Responses

Eigenbrod

Dalpke

2015

The Journal of Immunology

View full text Add to dashboard Cite

Although DNA of bacterial and viral origin, as well as viral RNA, have been intensively studied as triggers of innate immune responses, the stimulatory properties of bacterial RNA and its role during infections have just begun to be deciphered. Bacterial RNA is a strong inducer of type I IFN and NF-κB–dependent cytokines, and it also can activate the Nlrp3 inflammasome. In this review, we focus on the receptors and signaling pathways involved in innate immune activation by bacterial RNA and analyze the physiological relevance of bacterial RNA recognition during infections. Furthermore, we present the concept that RNA modifications can impair RNA-dependent immune activation. RNA modifications differ between eukaryotes and prokaryotes; thus, they can serve to define the innate pattern that is recognized. In this regard, we discuss the role of ribose 2′-O-methylation as a potential immune-escape mechanism.

show abstract

“…Stimulation of the TLR pathway induces NF-kB activation and transcription of immune response genes such as cytokines and chemokines, leading to the activation of innate immunity and regulation of acquired immunity (9). To date, 10 members of the TLR family have been identified in humans (10), in which TLR2, 4, 5, and 9 are reported to be involved in H. pylori recognition (11)(12)(13)(14)(15)(16)(17)(18). TLR2 was shown to recognize H. pylori lipopolysaccharide (LPS) (11).…”

Section: Introductionmentioning

confidence: 99%

“…H. pylori flagellin is a TLR5 agonist in vitro (11,16), whereas some conflicting reports show that H. pylori flagellin evades TLR5 recognition, which may contribute to its long-term persistence in hosts (19,20). TLR9 could recognize H. pylori CpG DNA, leading to the induction of cytokine secretion (17,18).…”

Section: Introductionmentioning

confidence: 99%

Genetic Variants of Toll-Like Receptor 2 and 5, Helicobacter Pylori Infection, and Risk of Gastric Cancer and Its Precursors in a Chinese Population

Zeng

Pan

Zhang

et al. 2011

Cancer Epidemiology, Biomarkers &Amp; Prevention

View full text Add to dashboard Cite

Background: Genetic polymorphisms of Toll-like receptors (TLR) may influence the outcome of Helicobacter pylori infection and play important roles in gastric carcinogenesis. To screen the genetic variants of TLR2 and TLR5, and evaluate their associations with gastric cancer (GC) and its precursors, a population-based study was conducted in Linqu County, Shandong Province, China.Methods: Genetic variants were identified by PCR-based denaturing high-performance liquid chromatography and PCR-restriction fragment length polymorphism analysis in 248 GC cases, 846 subjects with advanced gastric lesions including 350 dysplasia and 496 intestinal metaplasia, and 496 superficial gastritis/mild chronic atrophic gastritis controls.Results: Nine allelic variants each were detected within the promoter and exons of TLR2 and TLR5. Among those, TLR2 c. À196 to À174 del carriers (ins/delþdel/del) showed a significantly decreased risk of GC (adjusted OR, 0.66; 95% CI: 0.48-0.90), whereas TLR5 rs5744174 C carriers (TCþCC) had an increased risk of GC (OR, 1.43; 95% CI: 1.03-1.97). Further analysis indicated an elevated risk of GC in subjects with the TLR5 rs5744174 TCþCC genotype and H. pylori infection (OR, 3.35; 95% CI: 2.13-5.26), and a significant interaction between rs5744174 and H. pylori infection was observed (OR, 2.15; 95% CI: 1.12-4.16).Conclusion: These findings suggest that TLR2 c. À196 to À174 ins>del, TLR5 rs5744174 and interaction between rs5744174 and H. pylori infection were associated with the development of GC.Impact: TLR2 and TLR5 polymorphisms may play important roles in the process of H. pylori-related gastric carcinogenesis. Cancer Epidemiol Biomarkers Prev; 20(12); 2594-602. Ó2011 AACR.

show abstract

Extracellular and Intracellular Pattern Recognition Receptors Cooperate in the Recognition of Helicobacter pylori

Cited by 158 publications

References 34 publications

Muc1 Cell Surface Mucin Attenuates Epithelial Inflammation in Response to a Common Mucosal Pathogen

Muc1 Cell Surface Mucin Attenuates Epithelial Inflammation in Response to a Common Mucosal Pathogen

Bacterial RNA: An Underestimated Stimulus for Innate Immune Responses

Genetic Variants of Toll-Like Receptor 2 and 5, Helicobacter Pylori Infection, and Risk of Gastric Cancer and Its Precursors in a Chinese Population

Contact Info

Product

Resources

About