Indistinguishable cellular changes in gastric mucosa between Helicobacter pylori infected asymptomatic tribal and duodenal ulcer patients

Table 1 Primers used in this study

Region(s) amplified	Primer	Nucleotide sequence	References
vacA s1 or vacA s2	VA1-F	5'-ATGGAAATACAACAAACACAC	[7]
	VA1-R	5'-CTGCTTGAATGCGCCAAAC
vacA m1 or vacA m2	VAG-F	5'-CAATCTGTCCAATCAAGCGAG	[28]
	VAG-R	5'-GCGTCAAAATAATTCCAAGG
cagA (5' end)	cag5c-F	5'-GTTGATAACGCTGTCGCTTC	[28]
	cag3c-R	5'-GGGTTGTATGATATTTTCCATAA
cag-PAI empty site	Luni 1	5'-ACATTTTGGCTAAATAAACGCTG	[7]
	R5280	5'-GGTTGCACGCATTTTCCCTTAATC
iceA1	IceA1F	5'-TATTTCTGGAACTTGCGCAACCTGAT	[7]
	M.Hpy1R	5'-GGCCTACAACCGCATGGATAT
IceA2	cycSF	5'-CGGCTGTAGGCACTAAAGCTA	[7]
	IceA2R	5'-TCAATCCTATGTGAAACAATGATCGTT

Table 2 Histological changes of gastric mucosa among H pylori associated symptomatic duodenal ulcer (DU) and asymptomatic tribal (TR) individuals n (%)

	Symptomatic DU (n = 50)	Asymptomatic TR (n = 36)	P-values	OR (95% CI)
Neutrophil infiltration	42 (84)	34 (94.4)	0.124	3.24 (0.57-23.76)
Lymphoid follicle/aggregates	20 (40)	15 (41.7)	0.876	1.07 (0.41-2.80)
Atrophy	30 (60)	10 (27.7)	0.0031	0.26 (0.10-2.67)
Metaplasia	7 (14)	3 (8.3)	0.325	0.56 (0.10-2.67)

¹Indicates statistically significant P-value.

Table 3 Genotypes of H pylori strains from duodenal ulcer (DU) and tribal (TR) subjects

	No. (%) of strain from
Genotype	DU patients (n = 50)	TRs (n = 36)
cagA positive only	47 (94)	36 (100)
cagA negative only	1 (2)	0 (0)
Both cagA+ and cagA-	2 (4)	0 (0)
vacA s1 only	47 (94)	36 (100)
vacA s2 only	1 (2)	0 (0)
vacA s1 and s2 mixed	2 (4)	0 (0)
vacA m1 only	31 (62)	26 (72.2)
vacA m2 only	17 (34)	7 (19.4)
vacA m1 and m2 mixed	2 (4)	3 (8.3)
ice A1 only	29 (58)	15 (41.7)
ice A2 only	18 (36)	14 (38.9)
ice A1 and ice A2 mixed	3 (6)	7 (19.4)