In particular, IL1A and PTGS2 played central roles in the interaction network characterizing the gene expression signature associated with benzene in this study.
5-fold at all four doses relative to unexposed controls, including five genes [PTX3 (pentraxin-related gene), CD44 (CD44 antigen), PTGS2 (prostaglandin-endoperoxide synthase 2), IL1A (interleukin 1, alpha), and SERPINB2 (serpin peptidase inhibitor, clade B, member 2) with FDR-adjusted p-values [less than or equal to] 0.
000 factor, alpha-induced protein 6 6590338 IL1A (b) interleukin 1, 2.
The frequencies of the IL1A variants [(-889)C/T and (+4845)G/T] as well as the polymorphisms within the IL1B gene [(-511)C/T, (-31)C/T, and (+3954)C/T] did not differ significantly between the patient group and the control population (Table 1) or between survivors and nonsurvivors.
Controls All patients Genotype (n = 481) (n = 285) P (a) IL1A (-889), n (%) C/C 248 (51.
The IL1A (-889)C/T, IL1A (+4845)G/T, IL1B (-511)C/T, IL1B (-31)C/T, IL1B (+3954)C/T, and IL1RA (+2018)C/T single-nucleotide polymorphisms were genotyped by a multiplexed mutagenic separated-PCR assay.
The allele-specific PCR products [305 by for IL1A (-889)C, 317 by for IL1A (-889)T, 170 by for IL1A (+4845)T, 183 by for IL1A (+4845)G, 279 by for IL1B (-511)C, 289 by for IL1B (-511)T, 252 by for IL1B (-31)C, 262 by for IL1B (-31)T, 230 by for IL1B (+3954)C, 240 by for IL1B (+3954)T, 204 by for IL1RA (+2018)C, and 212 by for IL1RA (+2018)T] were separated on PolyNAT 12% S-50 Wide Mini Gels (Elchrom Scientific) by electrophoresis for 2.
Cluster 1 genes (ZBTB1, PML, ZNF44, SIX1, BCL6, ZNF450) were down-regulated by V and involved in gene transcription, whereas cluster 2 genes (IL8, IL1A, PTGS2, DTR, TNFAIP3, CXCL3) were up-regulated and linked to inflammatory response and cell proliferation.
Cluster 2 contained IL8, IL1A, PTGS2, DTR, TNFAIP3, and CXCL3 that were up-regulated and linked primarily to inflammatory response and cell proliferation.
The stimulatory effects of V on IL1A and TNFAIP3 gene expression, however, have not been reported.
Five genes (IL8, IL1A
, CXCR4, RALBP1, and SCYE1) have been implicated in chemotaxis of the early inflammatory response, especially IL8, which is a critical mediator for neutrophil-dependent acute inflammation (Mukaida 2000, 2003).
This review and meta-analysis show that IL1A
and IL1B genetic variations are significant contributors to chronic periodontitis in Caucasians," said Dr.