Journals / Turkish Journal of Gastroenterology / 2003 / Cilt: 14 - Sayı: 3

Aktif gastrit ve duodenal ülseri olan Helicobacter pylori-pozitif hastalarda klas I ve II MHC reseptörleri

Expression of class I and II MHC receptors in Helicobacter pylori-positive patients with active gastritis and duodenal ulcer

Pages
168–172
DOI
—
🏛️Bibliographic metadata and full text access for this article are provided via DergiPark.
DergiPark Record ↗
✨

AI Summary & Key Takeaways

AI Insight
⚡ TL;DR(Too Long; Didn't Read)

The increase in the number of cells expressing CD3/16/B6 in chronic antral gastritis and duodenal ulcer patients positive for Helicobacter pylori suggests a role for autoimmune events in these diseases.

📌 3 Key Takeaways

🎯
Objective & Hypothesis:Background/aims: Helicobacter pylori colonizes on the epithelial surface below the mucous membrane in the gastric antrum, causing chronic active gastritis and duodenal ulcer.
📊
Key Findings & Data:Methods: The study included a total of 124 cases (Helicobacter pylori-positive patients without prior treatment, 47 of whom had small-sized and 56 medium-sized duodenal ulcer, and 21 healthy individuals).
💡
Conclusion & Impact:The increase in the number of cells expressing CD3/16/B6 in chronic antral gastritis and duodenal ulcer patients positive for Helicobacter pylori suggests a role for autoimmune events in these diseases.
🔬Design:Research Article
📍Scope:Comprehensive Sample
⚙️Variables:Duodenum ülseri · Gastrit · Genler

Abstract

Background/aims: Helicobacter pylori colonizes on the epithelial surface below the mucous membrane in the gastric antrum, causing chronic active gastritis and duodenal ulcer. However, we know little about the response of the immune system, which is responsible for protecting the organism, to this bacteria and the duodenal tissue damage. The aims of our study were to examine the expression of class I and II MHC receptors in the immune cells in the peripheral venous blood of patients with chronic active gastritis and duodenal ulcer. Methods: The study included a total of 124 cases (Helicobacter pylori-positive patients without prior treatment, 47 of whom had small-sized and 56 medium-sized duodenal ulcer, and 21 healthy individuals). Immune cells carrying receptors CD3, CD4, CDS/4, CDS, CD3/8, CD14, CD45, CD14/45, HLA-DR, CD3/HLA-DR, CD16/66, and CDS 116156 by applying DAKO Dual Color Reagent, and non-specific indicators of reactivity, were investigated in the peripheral venous blood samples. Results: In both study groups, nonspecific indicators of reactivity in peripheral venous blood were not different from those in the healthy group irrespective of the ulcer size. It was detected that NK cells which express only CD3/16/56 receptor are more aggressive than class I MHC carriers, which were increased in both patient groups more markedly than in the control group (p<0.05). The number of CD14 cells in patient groups with small- and medium-sized duodenal ulcers was found to be lower than in the control group. This difference was more marked in the small-sized ulcer group than in the medium-sized ulcer group. While there was a similarity in the number ofCD45 cells in all three groups, the number of CD14/45 cells was reduced in the study group. This reduction was found statistically insignificant in the medium-sized ulcer group, but significant in the small-sized ulcer group (p<0.05). As compared to the control group, the number of HLA-DR cells was found to be increased in both study groups, and CD3/HLA-DR was found to be increased in the medium-sized ulcer group (p<0.05). Conclusions: The reduced number of CD14 cells may have been among the factors predisposing to the development of Helicobacter pylori infection. Such a deficit in cellular defense may be compensated through the upregulation of cells with HLA-DR and CDS IHLA-DR markers by the organism. The increase in the number of cells expressing CD3/16/B6 in chronic antral gastritis and duodenal ulcer patients positive for Helicobacter pylori suggests a role for autoimmune events in these diseases.

Özet

Amaç: Helicobacter Pylori, mide epiteline kolonize olarak kronik aktif gastrit duodenal ülser hastalığına naden olur. Ancak organizlayı koruyan immün sistemin Helicobacter Pylori'ye verdiği yanıt tam olarak bilinmemektedir. Bu çalışmanın amacı Helicobacter Pylori (+) kronik aktif gastritli ve duodenal ülserli hastaların venöz kanındaki immün hücrelerdeki class I ve II MHC reseptör ekspresyonunu araştrmaktır. Yöntem: Çalışmaya daha evvel tedavi görmemiş Helicobacter Pylori (+) 124 olgu alındı (47 küçük çaplı ülser, 56 orta çaplı ülser ve 21 sağlıklı ol-gu). Olguların periterik venöz kan örneklerinde CDS, CD4, CD3/4, CD8, CD3/8, CT>14, CD45, CD14/46, HLA-DR, CD3IHCA-DR, CD16/56 ve CD3/16/56 reseptörleri araştırıldı. Bulgular: CD3/16/56 reseptörlerini sunan NK hücreleri hasta grubunda kontrol grubuna göre daha fazla bulunmuştur. CD14 sunan hücrelerin sayısı hasta grubunda kontrol grubuna göre daha düşük bulunmuştur (p<0.005). Bu bulgu küçük çaplı ülser grubunda daha belirgin idi. CD45 eksprese eden hücrelerin sayısı 3 grupta da benzer iken, CD14/45 eksprese eden hücrelerin sayısı çalışma grubunda azalmıştır. Bu bulgu küçük çaplı ülser grubunda belirgindir (p<0.05). Kontrol grubu ile karşılaştırıldığında HLA-DR hücrelerinin sayısı çalışma grubunda artmıştır, CD3/HLA-DR sayısı ise orta çaplı ülser grubunda artmıştır (p<0.05). Sonuç: CD14 eksprese eden hücrelerin sayısında azalma Helicobakter Pylori infeksiyonu gelişmesine yol açan faktörler arasında olabilir. CD3/16/56 eksprese eden hücrelerin sayısınınHeyicobacter Pylori (+) aktif gastritve ülserli hastalarda artmış olması, bu hastalarda otoimmün olayların rolü düşündürmektedir.

🔖

Cite This Article

SÜLEYMANOV, Z. (2003). Aktif gastrit ve duodenal ülseri olan Helicobacter pylori-pozitif hastalarda klas I ve II MHC reseptörleri. Turkish Journal of Gastroenterology, Cilt: 14 - Sayı: 3, 168–172. https://ajindex.com/articles/410921

📄 Full Text PDF Viewer

📄

PDF görüntüleyici hazırlanıyor...

References (14)

  1. Özden A. İşte Helicobacter pylori gastrit peptik ülser. TGD yayini, 1995; p:166
  2. Ernst PB, Jin Y, Reyes VE, Growe SE. The role of the local immune response in the pathogenesis of peptic ulcer formation. Scand J Gastroenterology 1994; 29 (Suppl): 22-28
  3. Graham DY. Helicobacter pylori: its epidemiology and its role in duodenal ulcer disease. J Gastroenterol Hepatol 1991; 2: 105-113
  4. Graig PM, Territo MC, Karnes WE, et al. Helicobacter pylori secretes a chemotactic factor for monocytes and neutrophils. Gut 1992;33:1020-1023
  5. Wallase JL. Mucosal defense: new avenues for treatment of ulcer disease? Gastroenterol Clin North Am 1990; 19:87- 100
  6. Xiang Z, Bugnoli M, Rappuoli R, et al. Helicobacter pylori: host responses in peptic ulceration. Lancet 1993; 341:900- 1
  7. Gitnick G. Peptik Ülser Hastalığının Tanı ve Tedavisi. Turgut Yayıncılık. 1997; p:176
  8. Graham DY, Klein PD. Campylobacter pyloridis gastritis: the past, the present, and speculations about the future. Am J Gastroenterol 1987; 82: 283-6
  9. Kurose I, Granger DN, Doyle J, et al. Helicobacter pylori — induced microvascular protein leakage in rats: role of neutrophils, mast cells, and platelets. Gastroenterology 1994;107:70-9
  10. Cerf-Bensussan N, Guy-Grand D. Intestinal intraepithelial lymphocytes. Gastroenterol Clin North Am 1991;3: 549-75
  11. Playfair JHL. Immunology at a Glance. Blackwell Science; 1998: 95
  12. Ernst PB. Local immune and inflammatory responses following infection with H. pylori: a role in peptic ulcer formation. Syllabus for Conference on Hp and GI Disorders; April 24-25, 1995, IBC, Philadelphia, PA
  13. Kononov AV. Mestniy immunniy otvet na infeksiyu Helicobacter pylori. Materiali 7-y sessii Rossiyskoy gruppi po izuçeniyu Hp. Omsk. 1997; p: 14-19 (In Russian)
  14. MacDonald TT, Weinel A, Spencer J. HLA-DR expression in human fetal intestinal epithelium. Gut. 1988; 29; 1342- 8.