Can the TLR-4-Mediated Signaling Pathway Be “A Key Inflammatory Promoter for Sporadic TAA”?

Table 2

Allele frequencies of rs4986790 (+896A/G) TLR4, rs333 (Δ32) CCR5 deletion, rs2070744 (−786T/C) eNOs, rs1799752 (D/I) ACE, rs3918242 (−1562C/T) MMP-9, and rs2285053 (−735C/T) MMP-2 SNPs in 161 S-TAA patients and 128 matched controls (2×2 comparisons between the different groups with odd ratio (OR) and 95% confidence interval).

Candidate genes	Reference SNP number	Alleles	Patients; (𝑁=161)		Matched controls; (𝑁=128)		𝑃 (2×2 tables)	OR (95% CI)
TLR4	rs4986790	+896A	321	99.7%	245	96%	0.0008	14.4 (18.1–112.4); 𝑃=0.0008
		+896G	1	0.3%	11	4%
CCR5	rs333	WT	317	98%	238	93%	0.001	4.7 (1.7–13.1); 𝑃=0.001
eNOS	rs2070744	Δ32	5	2%	18	7%	0.00007	2.2 (1.5–3.2); 𝑃<0.0001
		−786T	207	64%	204	80%
		−786C	115	36%	52	20%
ACE	rs1799752	I	125	39%	141	55%	0.0001	1.9 (1.3–2.6); 𝑃=0.0001
		D	197	61%	115	45%
MMP-9	rs3918242	−1562C	282	88%	241	94%	0.011	2.27 (1.2–4.22); 𝑃=0.01
		−1562T	40	12%	15	6%
MMP-2	rs2285053	−735C	287	89%	251	98%	0.00005	6.1 (2.3–15.8); 𝑃<0.0001
		−735T	35	11%	5	2%

All genotypes were in Hardy-Weinberg equilibrium.