Role of TLR4, NLRC1/NOD1 and NF-κB in Inflammation of Gastric Mucosa in Helicobacter pylori Infection in Children

O.Ye. Abaturov, O.M. Gerasymenko


The aim of the work was to study the role of TLR4, NLRC1/NOD1 and NF-κB in inflammation of gastric mucosa (GM) in children with chronic inflammatory H.pylori-associated gastroduodenal diseases of the intestinal tract.
Methods. We observed 128 children with chronic gastroduodenal diseases in the acute stage: 70 (54.7 %) children (mean age 14.04 ± 0.34 years) infected with H.pylori, and 58 (45.3 %) — in which H.pylori was not detected (mean age 14.12 ± 0.43 years). We used molecular genetic methods to determine the level of TLR4, NLRC1/NOD1 expression if biopsy material of GM and NF-κB in peripheral blood lymphocytes.
Results. It is shown that patients infected with H.pylori show increased level of both TLR4 gene and NLRC1/NOD1 expression in biopsy material of GM at reducing activity of transcription factor NF-κB expression in lymphocytes, unlike children, whose disease was not associated with H.pylori infection. In children infected with CagA(+)-strains of H.pylori we detected significantly lower activity of expression only of the transcription NF-κB in peripheral blood lymphocytes. We propose a model of participation of non-specific mechanisms of innate immunity in the development of chronic inflammation of the gastric mucosa of gasrtoduodenal part of the intestinal tract in children infected with CagA(+)- and CagA(–)-strains of H.pylori.


Helicobacter pylori; innate immunity; TLR4; NLRC1/NOD1; NF-κB; children


Абатуров А.Е., Волосовец А.П., Юлиш Е.И. Инициация воспалительного процесса при вирусных и бактериальных заболеваниях, возможности и перспективы медикаментозного управления. — Харьков: Новое слово, 2011. — 344 с.

Every A.L. Key host-pathogen interactions for designing novel interventions against Helicobacter pylori // Trends Microbiol. — 2013. — 21(5). — 253-9. doi:10.1016/j.tim.2013.02.007.

Ferrand J., Ferrero R.L. Recognition of Extracellular Bacteria by NLRs and Its Role in the Development of Adaptive Immunity // Front Immunol. — 2013. — 4. — 344. doi:10.3389/fimmu.2013.00344.

Ferrero R.L. Innate immune recognition of the extracellular mucosal pathogen, Helicobacter pylori // Mol. Immunol. — 2005. — 42(8). — 879-85.

He C. Helicobacter pylori-related host gene polymorphisms associated with susceptibility of gastric carcinogenesis: a two-stage case-control study in Chinese / C. He, H. Tu, L. Sun, Q. Xu, P. Li, Y. Gong, N. Dong, Y. Yuan // Carcinogenesis. — 2013. — 34(7). — 1450-7. doi:10.1093/carcin/bgt079.

Ihan A., Pinchuk I.V., Beswick E.J. Inflammation, immunity, and vaccines for Helicobacter pylori infection // Helicobacter. — 2012. — 17 Suppl. 1. — 16-21. doi: 10.1111/j.1523-5378.2012.00977.x.

Kim E.J. Association between genetic polymorphisms of NOD 1 and Helicobacter pylori-induced gastric mucosal inflammation in healthy Korean population / E.J. Kim, J.R. Lee, W.C. Chung, S.H. Jung, H.J. Sung, Y.W. Lee, Y.S. Oh, S.B. Kim, C.N. Paik, K.M. Lee, S.J. Noh // Helicobacter. — 2013. — 18(2). — 143-50. doi: 10.1111/hel.12020.

Lagunes-Servin H. Toll-like receptors and cytokines are upregulated during Helicobacter pylori infection in children / H. Lagunes-Servin, J. Torres, C. Maldonado-Bernal, M. Pérez-Rodríguez, S. Huerta-Yépez, A. Madrazo de la Garza, L. Muñoz-Pérez, L. Flores-Luna, G. Ramón-García, M. Camorlinga-Ponce // Helicobacter. — 2013. — 18(6). — 423-32. doi: 10.1111/hel.12067.

Posselt G., Backert S., Wessler S. The functional interplay of Helicobacter pylori factors with gastric epithelial cells induces a multi-step process in pathogenesis // Cell Commun Signal. — 2013. — 11. — 77. doi: 10.1186/1478-811X-11-77.

Sánchez-Zauco N.A., Giono-Cerezo S., Maldonado-Bernal C. Receptores tipo Toll, patogénesis y respuesta inmune a Helicobacter pylori // Salud. Publica Mex. — 2010. — 52(5). — 447-54.

Schmausser B. Expression and subcellular distribution of toll-like receptors TLR4, TLR5 and TLR9 on the gastric epithelium in Helicobacter pylori infection / B. Schmausser, M. Andrulis, S. Endrich, S.K. Lee, C. Josenhans, H.K. Müller-Hermelink, M. Eck // Clin. Exp. Immunol. — 2004. — 136(3). — 521-6. doi:10.1111/j.1365-2249.2004.02464.x.

Smith M.F. Toll-like receptor (TLR) 2 and TLR5, but not TLR4, are required for Helicobacter pylori-induced NF-kappa B activation and chemokine expression by epithelial cells / M.F. Smith Jr, A. Mitchell, G. Li, S. Ding, A.M. Fitzmaurice, K. Ryan, S. Crowe, J.B. Goldberg // J. Biol. Chem. — 2003 Aug 29. — 278(35). — 32552-60.

Watanabe T. Activation of type I IFN signaling by NLRC1/NOD1 mediates mucosal host defense against Helicobacter pylori infection / T. Watanabe, N. Asano, A. Kitani, I.J. Fuss, T. Chiba, W. Strober // Gut Microbes. — 2011. — 2(1). — 61-5. doi:10.4161/gmic.2.1.15162.

Yang Z.M., Chen W.W., Wang Y.F. Gene expression profiling in gastric mucosa from Helicobacter pylori-infected and uninfected patients undergoing chronic superficial gastritis // PLoS One. — 2012. — 7(3). — e33030. doi:10.1371/journal.pone.0033030.

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