A possible role for tumor necrosis factor alpha (TNFa) in the balance between cellular proliferation and death in helicobacter pylori (Hp) related gastric lesions

2001 ◽  
Vol 33 ◽  
pp. A87
Author(s):  
E. Ierardi ◽  
S. Marangi ◽  
O. Bwattini ◽  
A. Pansrese ◽  
C. Panella ◽  
...  
Keyword(s):  
Helicobacter Pylori ◽  
Tumor Necrosis Factor ◽  
Tumor Necrosis Factor Alpha ◽  
Tumor Necrosis ◽  
Cellular Proliferation ◽  
Gastric Lesions ◽  
Necrosis Factor Alpha ◽  
Factor Alpha ◽  
Necrosis Factor

scholarly journals Analysis of Cytokines in the Early Development of Gastric Secondary Lymphoid Follicles in Helicobacter pylori-Infected BALB/c Mice with Neonatal Thymectomy

2001 ◽  
Vol 69 (11) ◽  
pp. 6749-6754 ◽  
Author(s):  
Kazushige Uchida ◽  
Kazuichi Okazaki ◽  
Andras Debrecceni ◽  
Toshiki Nishi ◽  
Hirosi Iwano ◽  
...  
Keyword(s):  
Immune Response ◽  
Helicobacter Pylori ◽  
Tumor Necrosis Factor ◽  
Tumor Necrosis Factor Alpha ◽  
Tumor Necrosis ◽  
Necrosis Factor Alpha ◽  
Factor Alpha ◽  
H Pylori ◽  
Lymphotoxin Α ◽  
Necrosis Factor

ABSTRACT Immunological interaction between the host and Helicobacter pylori seems to play a critical role in follicular formation in gastric mucosa. We reported H. pylori-induced follicular gastritis model using neonatally thymectomized mice. In this study, we investigated the involvement of various cytokines in this model. BALB/c mice were thymectomized on the third day after birth (nTx). At 6 weeks old, these mice were orally infected with H. pylori. Histological studies showed that follicular formation occurred from 8 weeks after the infection and that most of the infiltrating lymphocytes were CD4+ and B cells. Neutrophils increased transiently at 1 week after the infection. Gamma interferon, interleukin-7 (IL-7), and IL-7 receptor were expressed in the stomach of the nTx mice irrespective of the infection. In contrast, expressions of the tumor necrosis factor alpha, IL-4 and lymphotoxin-α genes were remarkably upregulated by the infection. Our findings suggest that follicular formation may require cooperative involvement of a Th2-type immune response, tumor necrosis factor alpha and lymphotoxin-α in addition to the Th1-type immune response in H. pylori-induced gastritis in nTx mice.

scholarly journals Novel Protein Antigen (JHP940) from the Genomic Plasticity Region of Helicobacter pylori Induces Tumor Necrosis Factor Alpha and Interleukin-8 Secretion by Human Macrophages

2007 ◽  
Vol 190 (3) ◽  
pp. 1146-1151 ◽  
Author(s):  
Mohammed Rizwan ◽  
Ayesha Alvi ◽  
Niyaz Ahmed
Keyword(s):  
Gastric Cancer ◽  
Helicobacter Pylori ◽  
Tumor Necrosis Factor ◽  
Tumor Necrosis Factor Alpha ◽  
Tumor Necrosis ◽  
Necrosis Factor Alpha ◽  
Human Macrophages ◽  
Plasticity Region ◽  
Factor Alpha ◽  
Necrosis Factor

ABSTRACT The plasticity region of the Helicobacter pylori genome comprises strain-specific gene loci. We performed genotyping and functional biology analysis of one such locus (jhp940) that was previously found to be functionally unknown but present in gastric cancer-associated strains from many different countries. We found its geographic prevalence to be independent of cagA presence and disease status. Cloning, expression, and purification of JHP940 revealed a novel, ∼36-kDa protein in a biologically active form which elicited strong and significant levels of tumor necrosis factor alpha and interleukin-8 in human macrophages. Also, JHP940 was able to induce enhanced translocation of the transcription factor NF-κB complex in cultured macrophages. The induction of the proinflammatory cytokines by JHP940, therefore, points to its putative role in chronic gastric inflammation and, possibly, the various other outcomes of H. pylori infection, including gastric cancer.

scholarly journals Tumor necrosis factor alpha gene polymorphism in Serbian patients with sarcoidosis

2013 ◽  
Vol 141 (3-4) ◽  
pp. 169-172 ◽  
Author(s):  
Tatjana Radjenovic-Petkovic ◽  
Tatjana Pejcic ◽  
Jelica Videnovic-Ivanov ◽  
Tatjana Jevtovic-Stoimenov ◽  
Irena Jankovic ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Tumor Necrosis Factor Alpha ◽  
Tumor Necrosis ◽  
Cellular Proliferation ◽  
Unknown Etiology ◽  
Control Group ◽  
Allele Frequency Distribution ◽  
Necrosis Factor Alpha ◽  
Factor Alpha ◽  
Necrosis Factor

Introduction. Sarcoidosis is a multisystemic disease of unknown etiology. Genetic factors play a considerable role in the onset of the disease. Tumor necrosis factor alpha (TNF-?) is a proinflammatory cytokine which plays an important role in the pathogenesis of the disease and the formation of granuloma by regulating cellular proliferation and apoptosis. Objective. The aim of this study was to investigate the role of TNF-?-308 G/A polymorphism in the development of sarcoidosis and to evaluate the association between the aforementioned type of polymorphism and the clinical course of the disease. Methods. Seventy patients with sarcoidosis and 50 healthy volunteers were genotyped for the TNF-?-308G/A polymorphism. Polymorphism variants were examined by PCR-RFLP (polymerase chain reaction-restriction fragment length polymorphism) on the DNA isolated from blood leukocytes. Results. There were no significant differences in TNF-?-308A allele frequency distribution between sarcoidosis patients and the control group, but the TNF-?-308A allele was observed significantly more frequently in the sarcoidosis patients with L?fgren?s syndrome when compared with non-L?fgren?s patients. Conclusion. We have found that the TNF-?-308A variant is associated with L?fgren?s syndrome in Serbian patients with sarcoidosis.

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