Evaluation of serum levels of Proinflammatory Cytokines IL-8, IL-17, and IL-22 in Helicobacter pylori infection and their association with the degree of gastritis histopathology in a sample of Iraqi patients

Main Article Content

Miriam Jasim Shehab
https://orcid.org/0000-0001-7333-1669
Batool Mutar Mahdi
https://orcid.org/0000-0001-6637-8936
Reem Husam Al-Tabra
https://orcid.org/0000-0002-0402-9631
Dhuha Salim Namaa
https://orcid.org/0000-0001-5223-4843

Abstract

Gastritis can be defined as histological inflammation of the gastric mucosa. It can be classified according to the time course of the disease as acute or chronic, histological findings, anatomic location, and pathological mechanisms. The objective of this study was to evaluation of serum levels of the proinflammatory cytokines IL-8, IL-17 and IL-22 in Helicobacter pylori infection and their association with the degree of gastritis histopathology in a sample of Iraqi patients. The case-control prospective study consists of 60 patients who attended the Gastrointestinal Tract Center at Al-Kindy Teaching Hospital during the period from December 2019 to April 2020. In addition, the control group included 60 apparently healthy individuals. Biopsies from the gastric antrum and/or body mucosa were used to assess the severity of chronic inflammation, neutrophil infiltration, atrophy, intestinal metaplasia. Serum samples were obtained to determine H. pylori infection, circulating interleukin (IL)-8, IL-17, and IL-22. Results showed that the Patients’ ages with gastritis ranged from 18-75 years. The body mass index revealed that 33.33% of the patients were obese and 35% of them were overweight. Most of the patients with active chronic gastritis and superficial chronic gastritis had positive titers for anti-H. pylori IgG antibody (167.89 ± 3.18 IU/ml) and (150.74± 1.45 IU/ml) respectively, which was significantly different from the control group (4.36 ± 0.29 IU/ml) (P=0.0001). Histopathological analysis showed that all subjects experienced chronic inflammation, while neutrophil infiltration was found 36.66% and there was significant association between serum levels of IL-8, IL-17, and IL-22 with a degree of chronic inflammation and neutrophils infiltration. In conclusion, the most common cause of gastritis was H. pylori with histopathological lesions, showing neutrophils infiltration and chronic gastric mucosal inflammation associated with increased levels of IL-8, IL-17, and IL-22 in serum.

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Evaluation of serum levels of Proinflammatory Cytokines IL-8, IL-17, and IL-22 in Helicobacter pylori infection and their association with the degree of gastritis histopathology in a sample of Iraqi patients. Baghdad Sci.J [Internet]. 2023 Jun. 20 [cited 2024 Nov. 6];20(3(Suppl.):0937. Available from: https://bsj.uobaghdad.edu.iq/index.php/BSJ/article/view/8621
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How to Cite

1.
Evaluation of serum levels of Proinflammatory Cytokines IL-8, IL-17, and IL-22 in Helicobacter pylori infection and their association with the degree of gastritis histopathology in a sample of Iraqi patients. Baghdad Sci.J [Internet]. 2023 Jun. 20 [cited 2024 Nov. 6];20(3(Suppl.):0937. Available from: https://bsj.uobaghdad.edu.iq/index.php/BSJ/article/view/8621

References

Azer SA, Akhondi H. Gastritis. In: StatPearls. Treasure Island (FL): Stat Pearls Publishing; July 4, 2022. PMID: 31334970, Bookshelf ID: NBK544250.

Raza M, Bhatt H. Atrophic Gastritis. In: StatPearls. Treasure Island (FL): Stat Pearls Publishing; August 8, 2021.

Sharndama HC, Mba IE. Helicobacter pylori: an up-to-date overview on the virulence and pathogenesis mechanisms. Braz J Microbiol. 2022;53(1):33-50. https://doi.org/10.1007/s42770-021-00675-0

Ruggiero P. Helicobacter pylori and inflammation. Curr Pharm Des. 2010;16(38):4225-4236. https://doi.org/10.2174/138161210794455117.

Bagheri N, Razavi A, Pourgheysari B, et al. Up-regulated Th17 cell function is associated with increased peptic ulcer disease in Helicobacter pylori-infection. Infect Genet Evol. 2018;60:117-125. https://doi.org/10.1016/j.meegid.2018.02.020

Eyerich K, Dimartino V, Cavani A. IL-17 and IL-22 in immunity: driving protection and pathology. Eur J Immunol. 2017;47(4):607-614. https://doi.org/10.1002/eji.201646723.

Dixon MF, Genta RM, Yardley JH, Correa P. Classification and grading of gastritis. The updated Sydney System. International Workshop on the Histopathology of Gastritis, Houston 1994. Am J Surg Pathol. 1996;20(10):1161-81.

Kako S, Iwaya Y, Nagaya T, et al. Clinicopathological features of nodular gastritis in three classes of age. Helicobacter. 2021;26(6):e12845. https://doi.org/10.1111/hel.12845

Pilotto A and Franceschi M. Helicobacter pylori infection in older people. World J Gastroenterol.2014; 20:6364-73.

Alsamarai AM, Thegeal F and Alobaidi AHM. Frequency of Biomarkers Positivity in Iraqi Subject with Gastritis. Sci. Int. 2017; 5 (2): 68-83.

Bionda M, Kapoglou I, Wiest R. H. pylori-assoziierte Gastritis: Diagnostik, Therapie und Nachsorge [H. pylori-associated gastritis: diagnostic, treatment and surveillance]. Ther Umsch. 2020;77(4):127-131. https://doi.org/10.1024/0040-5930/a001167

Pandya HB, Patel JS, Agravat HH, Singh NKR. Non-Invasive Diagnosis of Helicobacter pylori: Evaluation of Two Enzyme Immunoassays, Testing Serum IgG and IgA Response in the Anand District of Central Gujarat, India. J Clin Diagn Res. 2014; 8(6): 12-15.

Leja M, Grinberga-Derica I, Bilgilier C, Steininger C. Review: Epidemiology of Helicobacter pylori infection. Helicobacter. 2019 Sep;24 Suppl 1:e12635. https://doi.org/10.1111/hel.12635. PMID: 31486242

Al-Thuwaini TM. Body mass indexand shortened telomere length in middle-aged female and male Running Head : Middle-aged and shortened telomere length. Baghdad Sic J. 2022;19(2):246-254. http://dx.doi.org/10.21123/bsj.2022.19.2.0246

Al-Zubaidi AM, Alzobydi AH, Alsareii SA, Al-Shahrani A, Alzaman N, Kassim S. Body Mass Index and Helicobacter pylori among Obese and Non-Obese Patients in Najran, Saudi Arabia: A Case-Control Study. Int J Environ Res Public Health. 2018;15(11):2586. Published 2018 Nov 19. https://doi.org/10.3390/ijerph15112586

Mustaf AJ and Ismail PA. Association of potent inflammatory Cytokine and Oxidative DNA Damage Biomarkers in Stomach cancer patients. Baghdad Sic J. 2022, 19(6): 1313-1325. https://dx.doi.org/10.21123/bsj.2022.6589

Siregar GA, Halim S and Sitepu RR. Serum TNF-α, IL-8, VEGF Levels in Helicobacter pylori Infection and Their Association with Degree of Gastritis. Acta Med Indones-Indones J Intern Med. 2015; 47(2):120-126.

Goldenring JR, Mills JC. Cellular Plasticity, Reprogramming, and Regeneration: Metaplasia in the Stomach and Beyond. Gastroenterology. 2022;162(2):415-430. https://doi.org/10.1053/j.gastro.2021.10.036

Dixon BR, Radin JN, Piazuelo MB, Contreras DC, Algood HM. IL-17a and IL-22 Induce Expression of Antimicrobials in Gastrointestinal Epithelial Cells and May Contribute to Epithelial Cell Defense against Helicobacter pylori. PLoS One. 2016;11(2):e0148514. https://doi.org/10.1371/journal.pone.0148514

Della Bella C, Antico A, Panozzo MP, Capitani N, Petrone L, Benagiano M, et al. Gastric Th17 Cells Specific for H+/K+-ATPase and Serum IL-17 Signature in Gastric Autoimmunity. Front Immunol. 2022;13:952674. https://doi.org/10.3389/fimmu.2022.952674. PMID: 35911678; PMCID: PMC9328118.

Nguyen PM, Putoczki TL. Could the inhibition of IL-17 or IL-18 be a potential therapeutic opportunity for gastric cancer?. Cytokine. 2019;118:8-18. https://doi.org/10.1016/j.cyto.2018.01.008

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