Prevalence of tumor necrosis factor alpha inducing protein (tipα) gene of Helicobacter pylori and its association with upper gastrointestinal diseases in India

3 Biotech ◽  
2021 ◽  
Vol 11 (5) ◽  
Author(s):  
Shweta Mahant ◽  
Shubham Mehra ◽  
Ayushi Chhawchharia ◽  
Bipul Chandra Karmakar ◽  
Sangita Paul ◽  
...  
2020 ◽  
Author(s):  
Shweta Mahant ◽  
Shubham Mehra ◽  
Ayushi Chhawchharia ◽  
Bipul Chandra Karmakar ◽  
Sangita Paul ◽  
...  

Abstract Background: Helicobacter pylori (H. pylori) is known to cause several gastro-duodenal diseases including chronic Gastritis, Peptic Ulcer disease and Gastric Cancer. Virulent genes of H. pylori like cagA, vacA are known to be responsible for the disease pathogenesis. But these virulence genes are not always found to be associated with disease outcome in all populations around the world. Relationship of H. pylori with Gastro Esophageal Reflux Diseases is controversial and uncertain. Tumor necrosis factor alpha inducing protein tipα is a new discovered virulent gene of H. pylori and is an inducer of certain cytokines and chemokines that are responsible for causing stomach cancer. Therefore, we conducted a study which aims to find the prevalence of tipα gene in the Indian population and its association with H. pylori related upper gastrointestinal diseases.Results: 267 clinical H. pylori isolates are included in our study for finding the prevalence of tipα gene and its association with cagA and vacA gene using PCR assay. The current study shows the prevalence rate of tipα gene in the Indian population to be 59.9%. Our study has found a significant association (p < 0.05) of tipα gene with Non Ulcer Dyspepsia (NUD) and also an association of cagA and vacA s1m1 with Gastritis and Duodenal Ulcer.Conclusion: Our study demonstrates for the first time the presence of tipα as virulent factor of H. pylori strain in Indian population isolated from patients suffering from upper gastrointestinal diseases. Further, tipα is significantly associated with NUD but not with other upper gastrointestinal diseases in India.


2020 ◽  
Author(s):  
Shweta Mahant ◽  
Shubham Mehra ◽  
Ayushi Chhawchharia ◽  
Bipul Chandra Karmakar ◽  
Sangita Paul ◽  
...  

Abstract Background: Helicobacter pylori (H. pylori) is known to cause several gastro-duodenal diseases including chronic Gastritis, Peptic Ulcer disease and Gastric Cancer. Virulent genes of H. pylori like cagA, vacA are known to be responsible for the disease pathogenesis. But these virulence genes are not always found to be associated with disease outcome in all populations around the world. Relationship of H. pylori with Gastro Esophageal Reflux Diseases is controversial and uncertain. Tumor necrosis factor alpha inducing protein tipα is a new discovered virulent gene of H. pylori and is an inducer of certain cytokines and chemokines that are responsible for causing stomach cancer. Therefore, we conducted a study which aims to find the prevalence of tipα gene in the Indian population and its association with H. pylori related upper gastrointestinal diseases.Results: The current study shows the prevalence rate of tipα gene in the Indian population to be 59.9%. Our study has found a significant association (p < 0.05) of tipα gene with Non Ulcer Dyspepsia (NUD) and also an association of cagA and vacAs1m1 with Gastritis and Duodenal Ulcer.Conclusion: Our study demonstrates for the first time the presence of tipα as virulent factor of H. pylori strain in Indian population isolated from patients suffering from upper gastrointestinal diseases. Further, tipα is significantly associated with NUD but not with other upper gastrointestinal diseases in India.


2001 ◽  
Vol 69 (11) ◽  
pp. 6749-6754 ◽  
Author(s):  
Kazushige Uchida ◽  
Kazuichi Okazaki ◽  
Andras Debrecceni ◽  
Toshiki Nishi ◽  
Hirosi Iwano ◽  
...  

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.


2007 ◽  
Vol 190 (3) ◽  
pp. 1146-1151 ◽  
Author(s):  
Mohammed Rizwan ◽  
Ayesha Alvi ◽  
Niyaz Ahmed

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.


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