Mysorekar Vijaya V, Dandekar Chitralekha P, Prakash B S Satya
Department of Pathology, M.S. Ramaiah Medical College, M.S. Ramaiah Medical Teaching Hospital, Bangalore.
Indian J Pathol Microbiol. 2003 Oct;46(4):605-9.
Mast cells are known to be effector cells in various inflammatory reactions, but their role in gastritis is unclear. The present study was undertaken to investigate the extent of mast cell involvement in antral gastritis with and without Helicobacter pylori (H. pylori) infection and thus evaluate the possible role of mast cells in the pathogenesis of H. pylori-associated gastritis. Antral mucosal biopsies were taken from 212 subjects with symptoms suggestive of acid peptic disease. Sections were assessed for inflammation. Modified Giemsa stain was used to detect H. pylori infection and 1% toluidine blue to count mast cells. Mast cell counts were significantly higher in the antral mucosa even in H. pylori-negative gastritis (68.4 +/- 6.7/mm2), as compared to normal non-inflamed mucosa (45.7 +/- 5.8/mm2) (P < 0.05). However, with H. pylori infection, the mucosal mast cell count were markedly increased (123.8 +/- 4.7/mm2) as compared to normal mucosa (P < 0.01). and H. pylori-negative gastritis (P < 0.01) this increase was noticed uniformly in patients with H. pylori-positivity, irrespective of the presence or absence of a peptic ulcer. After cure of H. pylori infection, the mast cell density decreased significantly (44.9 +/- 4.6/mm2) to reach levels that were similar to those in normal mucosa. There was a positive correlation between the antral mucosal mast cell density and polymorphonuclear and mononuclear cell infiltration (rs = 0.61). H. pylori infection, and 0.73 respy. It was concluded that could be responsible for increasing the mast cell density in the gastric antrum. Probably by inducing castain mucosal cytokine.
肥大细胞是各种炎症反应中的效应细胞，但其在胃炎中的作用尚不清楚。本研究旨在调查肥大细胞在有无幽门螺杆菌（H. pylori）感染的胃窦炎中的参与程度，从而评估肥大细胞在幽门螺杆菌相关性胃炎发病机制中的可能作用。从212例有酸相关性疾病症状的受试者中获取胃窦黏膜活检组织。对切片进行炎症评估。采用改良吉姆萨染色检测幽门螺杆菌感染，用1%甲苯胺蓝计数肥大细胞。即使在幽门螺杆菌阴性的胃炎中，胃窦黏膜中的肥大细胞计数（68.4±6.7/mm²）也显著高于正常非炎症黏膜（45.7±5.8/mm²）（P<0.05）。然而，与正常黏膜相比（P<0.01），幽门螺杆菌感染时黏膜肥大细胞计数显著增加（123.8±4.7/mm²），与幽门螺杆菌阴性胃炎相比（P<0.01），无论有无消化性溃疡，幽门螺杆菌阳性患者均出现这种增加。幽门螺杆菌感染治愈后，肥大细胞密度显著降低（44.9±4.6/mm²），达到与正常黏膜相似的水平。胃窦黏膜肥大细胞密度与多形核细胞和单核细胞浸润之间存在正相关（rs = 0.61），与幽门螺杆菌感染分别为0.73。得出的结论是，幽门螺杆菌感染可能通过诱导胃窦黏膜细胞因子，导致胃窦肥大细胞密度增加。
