Relationship between mucosal levels of interleukin 8 and toxinogenicity of Helicobacter pylori.
OBJECTIVE
To investigate if an association exists between in-vivo mucosal levels of IL-8 and bacterial expression of cytotoxin and cagA gene of H. pylori.


METHODS
Seventy-two dyspeptic patients referred for endoscopy were studied, including 36 patients with peptic ulcer (PU) and 36 with non-ulcer dyspepsia (NUD). Biopsies were taken for histology, H. pylori culture and measurement of IL-8 by ELISA. To test the ability of H. pylori to produce cytotoxin (VacA), broth culture supernatants were assayed on Vero cells and vacuolation measured. PCR was used to detect the cagA gene of H. pylori.


RESULTS
H. pylori was isolated in 52 of 72 patients studied. Among the 52 strains, 25 (49%) were VacA+ve/cagA+ve; 12 (23%) were VacA-ve/cagA-ve; the remaining 15 strains (28%) were either VacA+ve/cagA-ve or VacA-ve/cagA+ve. IL-8 levels (median (interquartile) pg/mg) in patients infected with VacA+ve (1.5 (0.64, 2.84)) or cagA+ve strains (1.25 (0.72, 2.34) were significantly higher than in those with VacA-ve (0.76 (0.4, 1.0)) or cagA-ve strains (0.5 (0.4, 1.5); p<0.05). The neutrophil infiltration score was also higher in patients infected with VacA+ve or cagA+ve strains than in those infected with VacA-ve or cagA-ve strains (p<0.05).


CONCLUSIONS
VacA+ve/cagA+ve strains were associated with an enhanced production of mucosal IL-8 in vivo and correlated with a stronger infiltration of neutrophils. Enhanced mucosal production of IL-8 and its role in neutrophil chemotaxis and activation could be important in H. pylori-induced gastroduodenal inflammation and in the development of peptic ulcer disease.
Zhang
Q B
QB
Department of Gastroenterology, Bacteriology, University of Glasgow NHS Trust, Glasgow, UK.
Etolhi
G
G
Dawodu
J B
JB
Husain
A
A
Gemmell
C G
CG
Russell
R I
RI
Scand J Gastroenterol. 1994 May;29(5):419-24
8036457
Gastroenterology. 1992 Feb;102(2):720-7
1732141
J Clin Invest. 1989 Oct;84(4):1045-9
2677047
Lancet. 1991 Aug 10;338(8763):332-5
1677696
Eur J Gastroenterol Hepatol. 1994 Dec;6 Suppl 1:S33-8
7735932
J Clin Pathol. 1995 Oct;48(10):967-9
8537502
Gut. 1996 Jun;38(6):841-5
8984021
Lancet. 1990 May 26;335(8700):1233-5
1971318
Scand J Immunol. 1993 Jan;37(1):65-70
8418474
Clin Sci (Lond). 1997 Jan;92(1):69-73
9038594
Lab Invest. 1995 Dec;73(6):760-70
8558837
Infect Immun. 1991 Apr;59(4):1264-70
2004808
Gut. 1992 Mar;33(3):289-92
1568643
Proc Natl Acad Sci U S A. 1993 Jun 15;90(12):5791-5
8516329
J Clin Pathol. 1995 Jan;48(1):41-5
7706517
Infect Immun. 1995 Jan;63(1):94-8
7806390
J Clin Pathol. 1994 Oct;47(10):945-50
7962609
J Clin Invest. 1994 Jul;94(1):4-8
8040281
Infect Immun. 1995 May;63(5):1732-8
7729879
J Clin Pathol. 1995 Feb;48(2):133-6
7745112
Lancet. 1984 Jun 16;1(8390):1311-5
6145023
Gastroenterology. 1996 Sep;111(3):638-47
8780568
Gastroenterology. 1997 Jan;112(1):92-9
8978347
J Med Microbiol. 1988 Jun;26(2):93-9
3385767
Proc Natl Acad Sci U S A. 1996 Dec 10;93(25):14648-53
8962108
Infect Immun. 1995 May;63(5):1681-87
7729872
Annu Rev Med. 1992;43:135-45
1580578
Am J Gastroenterol. 1987 Mar;82(3):192-9
3826027
J Clin Microbiol. 1989 Jan;27(1):225-6
2913034
J Biol Chem. 1995 Jul 28;270(30):17771-7
7629077