Association between cag-pathogenicity island in Helicobacter pylori isolates from peptic ulcer, gastric carcinoma, and non-ulcer dyspepsia subjects with histological changes

doi:10.3748/wjg.v11.i43.6815

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World Journal of Gastroenterology

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1007-9327

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Baishideng Publishing Group Inc, 7041 Koll Center Parkway, Suite 160, Pleasanton, CA 94566, USA

Clinical Research

World J Gastroenterol. Nov 21, 2005; 11(43): 6815-6822
Published online Nov 21, 2005. doi: 10.3748/wjg.v11.i43.6815

Table 1 List of primers

Target	Primer	Sequence (5’- 3’)	Product
gene			size (bp)
	CagA-F1	AACAGGACAAGTAGCTAGCC
CagA1	CagA-R1	TATTAATGCGTGTGTGGCTG	701
	CagA-F2	GATAACAGGCAAGCTTTTGA
CagA2	CagA-R2	CTGCAAAAGATTGTTTGGCAGA	349
	CagAP-F1	GTGGGTAAAAATGTGAATCG
CagAP1	CagA-R1	TATTAATGCGTGTGTGGCTG	730
	CagAP-F2	CTACTTGTCCCAACCATTTT
CagAP2	CagA-R2	CTGCAAAAGATTGTTTGGCAGA	1 181
	CagE-F1	GCGATTGTTATTGTGCTTGTAG
CagE	CagE-R1	GAAGTGGTTAAAAAATCAATGCCCC	329
	CagT-F1	CCATGTTTATACGCCTGTGT
CagT	CagT-R1	CATCACCACACCCTTTTGAT	301
	LEC-F1	ACATTTTGGCTAAATAAACGCTG
LEC-1	LEC-R1	TCTCCATGTTGCCATTATGCT	384
	LEC-F2	ATAGCGTTTTGTGCATAGAA
LEC-2	LEC-R2	ATCTTTAGTCTCTTTAGCTT	877

Table 2 Relationship between the presence of cag-PAI and the clinical status

Clinical status (n)	Intact PAI (%)	cag-PAI type	Completely deleted
		Partially deleted	PAI (%)
		PAI (%)
DU (58)	4 (6.9)	54 (93.1)	0
GU (46)	45 (97.8)	1 (2.2)	0
NUD (56)	4 (7.1)	52 (92.9)	0
GC (14)	12 (85.7)	2 (14.3)	0
Total (174)	65 (37.4)	109 (62.6)	0

χ²=130.71 .

Table 3 cagA status of H pylori isolates

Clinical status (n)	cagA +ve (%)	*Partial cagA* +ve (%)**	cagA–ve (%)
DU (58)	8 (13.8)	46 (79.3)	4 (6.9)
GU (46)	45 (97.8)	1 (2.2)	0
NUD (56)	4 (7.1)	52 (92.9)	0
GC (14)	12 (85.7)	2 (14.3)	0
Total (174)	69 (39.7)	101 (58)	4 (2.3)

DU vs GU, DU vs GC, GU vs NUD and NUD vs GC combinations are highly significant at 0.1% level. DU vs NUD and GU vs GC combinations are not significant at 0.1% level.

Table 4 Distribution of cagA gene and cagA promoter in H pylori isolates

Clinical status (n)	A1+A2 (%)	AP1+AP2 (%)
DU (58)	43 (74.1)	8 (13.8)
GU (46)	45 (97.8)	46 (100)
NUD (56)	32 (57.1)	6 (10.7)
GC (14)	14 (100)	12 (85.7)
Total (174)	134 (77)	72 (41.4)

Table 5 Distribution of cagE, T, LEC1, and LEC2 in H pylori isolates

Clinical status (n)	cagE (%)	cagT (%)	LEC1 (%)	LEC2 (%)
DU (58)	47 (81)	56 (96.5)	44 (75.8)	33 (56.8)
GU (46)	46 (100)	46 (100)	46 (100)	46 (100)
NUD (56)	36 (64.2)	36 (64.2)	38 (67.8)	18 (32.1)
GC (14)	14 (100)	14 (100)	14 (100)	14 (100)
Total (174)	143 (82.1)	152 (87.3)	142 (81.6)	111 (63.7)

For cagE, GU vs NUD is highly significant at 0.1% level (P<0.001), DU vs GU, NUD vs GC combinations are significant at 1% level (P<0.01), DU vs NUD combination is significant at 5% level (P<0.05) and DU vs GC . For cagT, DU vs NUD, GU vs NUD combinations are highly significant at 0.1% level (P<0.001), NUD vs GC combination is significant at 1% level (P<0.01) and DU vs GU, DU vs GC, GU vs GC are not significant at 1% level. For LEC1, DU vs GU, GU vs NUD combinations are highly significant at 0.1% level (P<0.001), NUD vs GC is significant at 1% level (P<0.01), DU vs GC is significant at 5% level (P<0.05). For LEC2, DU vs GU, GU vs NUD, NUD vs GC combinations are highly significant at 0.1% level (P<0.001), DU vs NUD, DU vs GC combinations are significant at 1% level (P<0.01) and GU vs GC is not significant at 1% level.

Table 6 Frequency of atrophy, metaplasia, and dysplasia in chronic gastritis subjects

Clinical	Acute	Chronic gastritis
status (n)	gastritis (%)	Superficial	Gastritis with	Gastritis with	Gastritis with
		gastritis	atrophy (%)	metaplasia (%)	dysplasia (%)
DU (58)	0	52 (89.7)	2 (3.4)	4 (6.9)	0
GU (46)	0	9 (19.6)	13 (28.3)	14 (30.4)	10 (21.7)
NUD (56)	0	51 (91.1)	5 (8.9)	0	0
Total (160)	0	112 (70)	20 (12.5)	18 (11.25)	10 (6.25)

For atrophy, DU vs GU combination is highly significant at 0.1% level (P<0.001), GU vs NUD is significant at 1% level (P<0.01) and DU vs NUD combination is not significant at 1% level. For metaplasia, DU vs GU, GU vs NUD combinations are highly significant at 0.1% level (P<0.001) and DU vs NUD combination is significant at 5% level (P<0.05). For dysplasia, DU vs GU, GU vs NUD combinations are highly significant at 0.1% level (P<0.001) and DU vs NUD combination is not significant at any level.

Table 7 Histological status of subjects with intact cag-PAI (n = 65) and partial cag-PAI (n = 109)

Cag-type	Chronic gastritis							Gastric carcinoma
(n)	Superficial gastritis	Gastritis with atrophy	Gastritis with metaplasia (%)			Gastritis with dysplasia(%)		Intestinal (%)	Diffuse (%)
	(%)	(%)	Ty-1	Ty-2	Ty-3	Low grade	High grade
Intact (65)	8 (12.3)	17 (26.1)^b	0	0	18	0	10	12^b	0
					-27.7		-15.4	-18.5
Partial (109)	104 (95.4)	3 (2.8)	0	0	0	0	0	2 (1.8)	0

^bP<0. 001 vs others.

Table 8 Correlation of the histological status of the subjects with intact and partially deleted cag-PAI from varied disease status

Clinical status	Chronic gastritis								Gastric carcinoma
(n)	cag status	Superficial gastritis	Gastritis with atrophy (%)	Gastritis with metaplasia (%)			Gastritis with dysplasia (%)		Intestinal (%)	Diffuse (%)
	(n)	(%)		Ty-1	Ty-2	Ty-3	Low grade	High grade
DU (58)	Intact (4)	0	0	0	0	4 (100)	0	0	0	0
	Partial (54)	52 (96.3)	2 (3.7)	0	0	0	0	0	0	0
GU (46)	Intact (45)	8(17.8)^a	13 (28.9)	0	0	14 (31.1)	0	10 (22.2)	0	0
	Partial (1)	1 (100)	0	0	0	0	0	0	0	0
NUD (56)	Intact (4)	0	4(100)^a	0	0	0	0	0	0	0
	Partial (52)	51 (98.1)	1 (1.9)	0	0	0	0	0	0	0
GC (14)	Intact (12)	0	0	0	0	0	0	0	12 (100)^b	0
	Partial (2)	0	0	0	0	0	0	0	2 (100)	0

^aP <0.05, ^bP <0.001 vs others.

Citation: Ali M, Khan AA, Tiwari SK, Ahmed N, Rao LV, Habibullah C. Association between cag-pathogenicity island in Helicobacter pylori isolates from peptic ulcer, gastric carcinoma, and non-ulcer dyspepsia subjects with histological changes. World J Gastroenterol 2005; 11(43): 6815-6822
URL: https://www.wjgnet.com/1007-9327/full/v11/i43/6815.htm
DOI: https://dx.doi.org/10.3748/wjg.v11.i43.6815