Effect of the interleukin-1 genotype on monocyte IL-1 beta expression in subjects with adult periodontitis

Citation
Ll. Mark et al., Effect of the interleukin-1 genotype on monocyte IL-1 beta expression in subjects with adult periodontitis, J PERIOD RE, 35(3), 2000, pp. 172-177
Citations number
26
Categorie Soggetti
da verificare
Journal title
JOURNAL OF PERIODONTAL RESEARCH
ISSN journal
00223484 → ACNP
Volume
35
Issue
3
Year of publication
2000
Pages
172 - 177
Database
ISI
SICI code
0022-3484(200006)35:3<172:EOTIGO>2.0.ZU;2-V
Abstract
An association has been reported between polymorphisms in the genes encodin g IL-1 alpha (-889) and IL-1 beta (+3953) (periodontitis susceptibility tra it, PST), and an increased severity of periodontitis (18). The IL-1 beta po lymorphism was reported to correlate with increased IL-1 beta expression by monocytes in response to bacterial stimulants. In the present study, we de termined if PST positive subjects with periodontitis exhibit elevated produ ction of IL-1 beta, compared to PST negative periodontitis patients. Periph eral blood monocytes were obtained from 10 PST + and 10 PST - age- and dise ase-balanced subjects with adult forms of periodontitis. Monocytes were cul tured with a panel of bacterial stimulants, including Escherichia coli and Porphyromonas gingivalis LPS, and whole formalinized periodontal pathogens P. gingivalis, Bacteroides forsythus and Prevotella intermedia, and health- associated organisms Veillonella parvula and Streptococcus sanguis. Our res ults demonstrate that monocytes from PST + and PST - patients showed no sig nificant differences in IL-1 beta production in response to any stimulant t ested. In addition, the periodontal pathogens P. gingivalis, B. forsythus a nd P. intel media failed to stimulate higher IL-1 beta responses compared t o health-associated species V. parvula and S, sanguis. A marked interindivi dual variation in production of IL-1 beta was seen, with high, low and inte rmediate responders present in both PST + and PST - groups. We conclude tha t genetic loci other than the PST polymorphisms are also important regulato rs of monocyte IL-1 responses.