Analysis Of Inflammatory Cell Profile In Helicobacter Pylori Positive Gastrit Cases

Öz

Introduction: Being the most frequent and important factor in the etiology of chronic active gastritis Helicobacter pylori can make up the basis for several diseases like peptic ulcer, adenocarcinoma, and MALT lymphoma. It is important to determined the profile of inflammatory cell in Helicobacter pylori gastritis for lightening the pathogenesis of the diseases the Helicobacter pylori may cause. In this study the inflammatory cell profile of the cases with Helicobacter pylori gastritis was investigated. 

Methods: 100 cases with Helicobacter pylori positive gastritis and 20 cases with Helicobacter pylori negative gastritis were included in the study. In addition to these CD3, CD4, CD5, CD8, CD10, CD20, CD68, CD79 α and CD138 immunohistochemical stains, H&E and Giemsa stains were performed and detailed inflammatory cell analyse was done.

Results: In immunohistochemical investigation, considering the CD3, CD20, CD68 and CD79α positivities, a significant difference was not determined between the groups. It was established that while the number of inflammatory cells positively reacted with CD10 and CD138 was increasing, the number of inflammatory cells positively reacted with CD4, CD5 and CD8 was decreasing significantly with the increasing amounts of Helicobacter pylori. Additionally CD138 positive plasma cells were the most densely seen cell type in all the cases.

Discussion and Conclusion: It is considered that in HP gastrits, the obvious increase of plasma cells and the decrease of CD5 positive lymphocytes in the group which has the most HP intensity might be playing a role in HP related stomach disease.

Anahtar Kelimeler

• Helicobacter pylori,Inflammation,Immunohistochemistry

Helikobakter Pylori Pozitif Gastrit Vakalarında İnflamatuar Hücre Analizi

Öz

Amaç: Helikobakter pylori kronik aktif gastrit etiyolojisinde en sık ve en önemli faktör olup, peptik ülser, adenokarsinoma ve MALT Lenfoma gibi çeşitli hastalıklara da zemin hazırlayabilmektedir.Helikobakter pylori gastriti olgularında inflamatuar hücre profilinin ortaya konması Helikobakter pylorinin neden olabileceği hastalıkların patogenezine ışık tutabilmek için önemlidir. Bu çalışmada Helikobakter pylori gastritli olgulardaki inflamatuar hücre profili araştırıldı.

Yöntem ve Gereçler: Çalışmaya 100 adet Helikobakter pylori pozitif kronik gastrit ve 20 adet Helikobakter pylori negatif gastrit vakası dahil edildi. Tüm guruplarda H&E ve giemsa boyaması yanında ayrıca immünohistokimyasal olarak CD3, CD4, CD5, CD8, CD10, CD20, CD68, CD79α ve CD138 boyamaları uygulandı ve detaylı inflamatuar hücre analizi yapıldı.

Bulgular: İmmünohistokimyasal incelemede, Helikobacter pylori negatif ve pozitif olgular arasında CD3, CD20, CD68 ve CD79α pozitiflikleri açısından anlamlı bir farklılık saptanmadı. Helikobakter pylori miktarı arttıkça CD10 ile ve CD138 ile pozitif reaksiyon veren inflamatuar hücre sayısı anlamlı derecede artarken, CD4, CD5 ve CD8 pozitif olanların sayılarının ise anlamlı derecede azaldığı tesbit edildi. Ayrıca CD138 pozitif plazma hücreleri tüm olgularda en yüksek yoğunluktaki hücre tipiydi.

Tartışma ve Sonuç: HP gastritlerinde HP’nin en yoğun olduğu grupta plazma hücrelerinin belirgin biçimde artması ve CD5 pozitif lenfositlerin azalmasının HP ilişkili mide hastalıklarının patogenezinde rol oynuyor olabileceği düşünülmüştür.

Anahtar Kelimeler

• Helikobakter pylori,İnflamasyon,İmmünohistokimya

Kaynakça

1. Referans1 Marshall BJ, Warren JR. Unidentified curved bacilli in the stomach of patients with gastritis and peptic ulceration. Lancet, 1984;1:1311-1315.
2. Referans2 Dunn BE, Cohen B, Blaser MJ. Helicobacter pylori. Clin Microbiol Rev, 1997; 10:720-741.
3. Referans3 Forman D. The prevalence of Helicobacter pylori infection in gastric cancer. Aliment Pharmacol Ther, 1995; 9:71-76.
4. Referans4 Chuan X, Nonghua L. Kyoto global consensus report for treatment of Helicobacter pylori and its implications for China. Zhejiang Da Xue Xue Bao Yi Xue Ban. 2016; 45:1-4.
5. Referans5 Dixon MF, Genta RM, Yardley JH, et al: Classification and grading of gastritis. The updates Sydney system Am J Surg Pathol. 1996;20:1161-1181.
6. Referans6 Owen DA: Gastritis and carditis. Mod. Pathol, 2003; 16:325.
7. Referans7 Kumar V, Abbas K, Fausto N, Aster C, Robbins and Cotran Pathologic Basis of Disease, 8.ed, Philedelphia: Elsevier, 2010; p.774,775.
8. Referans8 Cecilia MF-Preiser et al: The non-neoplastic Stomach in Gastrointestinal Pathology Plus: An atlas and text. 3.ed, Philedelphia:Lippincott William Wilkins, 2008; p. 190-192.

9. Referans9 Genta R, Segura AM; Will Curing Helicobacter Pylori Eliminate Gastric Cancer? Adv Anat Pathol1999; 3: 228-232.
10. Referans10 Hoshi T, Sasano H, Kato K: Cell Damage and Proliferation in Human Gastric Mucosa Infected by Helicobacter pylori-A Comparison Before and After H. Pylori Eradication in Non-Atrophic Gastritis; Hum Pathol 1999; 30: 1412-1417.
11. Referans11 Hatz RA, Meimarakis G, Bayerdörffer E, et al. Characterization of Lymphocytic Infiltrates in Helicobacter pylori-Associated Gastritis. Scand J Gastroenterol 1996; 31:222-228.
12. Referans12 Broide E, Sandbank J, Scapa E, et al. The Immunohistochemistry Profile of Lymphocytic Gastritis in Celiac Disease and Helicobacter Pylori Infection: Interplay between Infection and Inflammation. Mediators Inflamm 2007;2007:81838.
13. Referans13 Rossi G, Fortuna D, Pancotto L, et al. Immunohistochemical Study of Lymphocyte Populations Infiltrating the Gastric Mucosa of Beagle Dogs Experimentally Infected with Helicobacter pylori. Infect Immun 2000; 68: 4769-4772.
14. Referans14 Oksanen A, Sankila A, Boguslawski K, et al. Inflammation and cytokeratin 7/20 staining of cardiac mucosa in young patients with and without Helicobacter pylori infection. J Clin Pathol 2005;58:376–381.
15. Referans15 Soo Won Hong, Mee Yon Cho, Chanil Park. Expression of eosinophil chemotactic factors in stomach cancer. Yonsei Medical Journal, 1999; 40: 131-136.
16. Referans16 Santra A, Chowdhury A, Chawdhuri S, et al. Oxidative stress in gastric mucosa in Helicobacter pylori infection. Indian J Gastroenterol 2000; 19:21-23.
17. Referans17 Kim H. Oxidative stress in Helicobacter pylori-induced gastric cell injury. Inflammopharmacology 2005;13:63-74.
18. Referans18 Witteman EM, Mravunac M, Becx MJ, et al . Improvement of gastric inflammation and resolution of epithelial damage one year after eradication of Helicobacter pylori. J Clin Pathol 1995; 48: 250-256.
19. Referans19 Öztürk S, Serinsöz E, Kuzu I, et al. The Sydney System in the assessment of gastritis: Inter-observer agreement. Turkish Journal of Gastroenterology 2001;12:36-39.
20. Referans20 Genta RM, Hamner HW, Graham DY. Gastric Lymphoid Follicles in Helicobacter pylori Infection: Frequency, Distribution, and Response to Triple Therapy. Hum Pathol 1993;24: 557-583.
21. Referans21 Eidt S, Stolte M: Prevalance of lymphoid follicles and aggregates in Helicobacter pylori gastritis in antral andy body mucosa. J Clin Pathol 1993; 22: 9-15.
22. Referans22 Fritscher-Ravens A, Petrash S, Tiemann M, et al. Antigenic phenotyping of lymphoid cell and B cell gene rearrangement in type B gastritis and in gastritis not associated with h. pylori colonization. Acta hematology 1999;102:77-82.
23. Referans23 Wotherspoon AC, Doglioni C, Diss TC, et al. Regression of primary lowgrade B-cell gastric lymphoma of mucosa-associated lymphoid tissue type after eradication of Helicobacter pylori.Lancet 1993;342:575-577.
24. Referans24 Sackmann M, Morgner A, Rudolph B, et al. Regression of gastric MALT lymphoma after eradication of Helicobacter pylori is predicted by endosonographic staging. MALT Lymphoma Study Group. Gastroenterology 1997; 113:1087-1090.
25. Referans25 Thiede C, Morgner A, Alpen B, et. al. What role does Helicobacter pylori eradication play in gastric MALT and gastric MALT lymphoma? Gastroenterology 1997 ;113: 61-64.
26. Referans26 Wotherspoon AC, Ortiz-Hidalgo C, Falzon MR, et al. Helicobacter pylori-associated gastritis and primary B-cell gastric lymphoma. Lancet. 1991; 338:1175-1176.
27. Referans27 Cecilia MF-Preiser et al: Lymphoproliferative Disorders of the gastrointestinal tract in Gastrointestinal Pathology Plus: An atlas and text. 3.baskı, Philedelphia, Lippincott William Wilkins, 2008; 1170.
28. Referans28 Terres AM, Pajares JM. An increased number of follicles containing activated CD69+ helper T cells and proliferating CD71+ B cells are found in h. pylori-infected gastric mucosa. Am J Gastroenterol 1998; 93:579-583.
29. Referans29 Furuta GT. Emerging questions regarding eosinophil's role in the esophagogastrointestinal tract. Curr Opin Gastroenterol 2006;22:658–663.
30. Referans30 Nakajima S, Bamba N, Hattori T. Histological aspects and role of mast cells in Helicobacter pyloriinfected gastritis. Aliment Pharmacol Ther 2004; 20:165–170.
31. Referans31 Moorchung N, Srivastava AN, Gupta NK, et al. The role of mast cells and eosinophils in chronic gastritis. Clin Exp Med 2006; 6:107–114.
32. Referans32 Radin MJ, Eaton KA, Krakowka S, et al. Helicobacter pylori Gastric Infection in Gnotobiotic Beagle Dogs. Infection And Immunity 1990; 58: 2606-2612.
33. Referans33 Handt LK, Fox JG, Stalis HG, et al. Characterization of Feline Helicobacter pylori Strains and Associated Gastritis in a Colony of Domestic Cats. J of Clin. Microbiol. 1995; 33: 2280-2289.
34. Referans34 Aydemir S, Tekin İÖ, Numanoğlu G, et al. Eosinophil infiltration, gastric juice and serum eosinophil cationic protein levels in Helicobacter pylori-associated chronic gastritis and gastric ulcer. Mediators Inflamm 2004; 13: 369-372.
35. Referans35 Kalebi A, Rana F, Mwanda W, et al. Histopathological profile of gastritis in adult patients seen at a referral hospital in Kenya. World J Gastroenterol 2007; 13: 4117-4121.
36. Referans36 Sulik A, Kemona A: Mast cell in chronic gastritis of children. Pol Merkuriuzc Lek 2001;10:156-160.