الفهرس 
TitleOnly 14 pages are availabe for public view
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Abstract
Helicobacter pylori (H. pylori) is a Gram-negative microaerophilic curved rod bacterium colonize in roughly 50% of the human gut worldwide and infection levels reach over 70% in developing countries(136). In Egypt, it ranks the first among bacterial infections with prevalence of 70% in the general population.
The clinical outcome of the infection ranges from an asymptomatic illness at one end of the spectrum to life-threatening peptic ulceration, gastric carcinoma and mucosa-associated lymphoid tissue (MALT) B-cell lymphoma at the other end(52). In addition, serological evidence for H. pylori infection was found to be associated with the development of several extra-gastric complications such as ischemic heart disease, neurodegenerative diseases, and hematological disorders. (32)However, many researchers suggested the protective role of H. pylori infection against various diseases.
Once infection is established, H. pylori colonizes in specific locations such as the antrum and corpus where it is well adapted to establish persistent infection. In reality, it is no exaggeration to conclude that smart and sophisticated strategies are contributing to adaptation of the bacterium to its permanent environment. However, understanding of these governing strategies will improve the identification of increased risk of H. pylori induced diseases.
Our study aimed to high light the importance of IL-22 and Mincle in elucidating the evasion strategies used by H. pylori in despite of strong immune responses, and their impacts on the clinical outcome of H. pylori induced gastritis (virulent versus avirulent strains).
The current study was conducted on 45 subjects who were divided into three groups; fifteen normal healthy individuals, fifteen symptomatic H. pylori positive patients and fifteen asymptomatic H. pylori positive individuals. Fresh stool samples were obtained in order to assess the current infection as well as fresh blood and serum samples were obtained to evaluate IL-22 and Mincle levels in relation with virulent versus avirulent strains.
Our results reveal that there was a statistical significant increase in IL-22 levels in both symptomatic and asymptomatic H. pylori positive individuals in comparison with normal healthy individuals(p=0.01). However, there was no significant variation between symptomatic and asymptomatic groups. In addition, there was an increase in the percentage of Mincle in both symptomatic and a symptomatic groups by 38% and 30.4% relative to control group, respectively.
H. pylori line IgG(immunoblot) was applied for serum samples obtained from H. pylori positive individuals in order to evaluate virulent strains (cag A+ and vac A strains).
Our results revealed that there was a significant association of cag A+ and/or vac A+ strains with the clinical outcome of H. pylori induced gastritis. Furthermore, the results show significant association between both virulent strains and IL-22 level. However there was a reduction of percentage of Mincle in both cag A+ and vac A+ in symptomatic and asymptomatic groups, respectively.
Conclusion
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CONCLUSION
According to our study findings, we can conclude that:
Elevated IL-22 seems to reflect a state of pro-inflammatory environment created in response to H. pylori infections since it was significantly elevated in all patients as compared to healthy controls.
IL-22 is obviously higher in all H. pylori positive subjects irrespective of symptom severity since no significant difference was recorded among symptomatic and a-symptomatic subjects.
IL-22 can be used as a determinant of the severity of H. pylori-induced gastritis since it showed significant positive correlation with positivity for stool antigen
IL-22 does not seem to be influenced by H. pylori virulence since it did not correlate with VacA/CagA sero-prevalence.
Mincle, supposed to be an essential player in H. pylori-induced gastritis, did not show a significant variation in H. pylori infected subjects as compared with healthy controls; although it showed higher median and was percentually elevated among patients.
Interestingly, the Mincle response seems to be H. pylori strain-dependent since it showed higher levels among CagA-/VacA- in comparison to CagA+/VacA+ patients. However, it did not correlate with either antigen in stool or other disease manifestations indicating lower relevance as a reliable monitor of symptom severity and/or gastric complications.