The relationship between persistent secretion of RANTES and residual infiltration of eosinophils and memory T lymphocytes after Helicobacter pylori eradication

Citation
T. Kikuchi et al., The relationship between persistent secretion of RANTES and residual infiltration of eosinophils and memory T lymphocytes after Helicobacter pylori eradication, J PATHOLOGY, 192(2), 2000, pp. 243-250
Citations number
35
Categorie Soggetti
Research/Laboratory Medicine & Medical Tecnology","Medical Research Diagnosis & Treatment
Journal title
JOURNAL OF PATHOLOGY
ISSN journal
00223417 → ACNP
Volume
192
Issue
2
Year of publication
2000
Pages
243 - 250
Database
ISI
SICI code
0022-3417(200010)192:2<243:TRBPSO>2.0.ZU;2-1
Abstract
Helicobacter pylori (HP)-infected gastric mucosa displays a conspicuous inf iltration of mononuclear cells as well as neutrophils. RANTES is a potent c hemoattractant peptide for memory T lymphocytes and eosinophils. RANTES pro tein concentration and the numbers of RANTES-, CD45RO-, and major basic pro tein (MBP)-positive cells were therefore evaluated in the gastric mucosa fr om 51 patients with HP-positive chronic gastritis before and after HP eradi cation and from 22 HP-negative healthy volunteers. RANTES protein concentra tion was significantly elevated in HP-positive cases and remained high afte r HP eradication. The numbers of RANTES-, CD45RO-, and MBP-positive cells w ere significantly increased in HP-positive cases and were well correlated w ith RANTES protein levels. All tended to decrease after HP eradication, but did not reach the level of HP-negative cases, even at 24 months after HP e radication. It was concluded that persistent expression and secretion of RA NTES mere closely related to residual infiltration of memory T lymphocytes and eosinophils, for a prolonged period after HP eradication. This seems to be an important mechanism of prolonged gastric mucosal immune response aga inst HP infection, even after HP eradication, and of persistent mucosal dam age and atrophy. Copyright (C) 2000 John Wiley & Sons, Ltd.