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Effect of the interleukin‐1 genotype on monocyte IL‐1 β expression in subjects with adult periodontitis
Author(s) -
Mark Laura L.,
Haffajee Anne D.,
Socransky Sigmund S.,
Kent Ralph L.,
Guerrero Denise,
Kornman Kenneth,
Newman Michael,
Stashenko Philip
Publication year - 2000
Publication title -
journal of periodontal research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.31
H-Index - 83
eISSN - 1600-0765
pISSN - 0022-3484
DOI - 10.1034/j.1600-0765.2000.035003172.x
Subject(s) - prevotella intermedia , porphyromonas gingivalis , periodontitis , bacteroides , bacteroidaceae , biology , genotype , interleukin , microbiology and biotechnology , monocyte , immunology , medicine , cytokine , gene , genetics , bacteria
An association has been reported between polymorphisms in the genes encoding IL‐1α(−889) and IL‐1β(+3953)(periodontitis susceptibility trait, PST), and an increased severity of periodontitis (18). The IL‐1β polymorphism was reported to correlate with increased IL‐1β expression by monocytes in response to bacterial stimulants. In the present study, we determined if PST positive subjects with periodontitis exhibit elevated production of IL‐1β, compared to PST negative periodontitis patients. Peripheral blood monocytes were obtained from 10 PST+ and 10 PST− age‐ and disease‐balanced subjects with adult forms of periodontitis. Monocytes were cultured 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 results demonstrate that monocytes from PST+ and PST− patients showed no significant differences in IL‐1β production in response to any stimulant tested. In addition, the periodontal pathogens P. gingivalis , B. forsythus and P. intermedia failed to stimulate higher IL‐1β responses compared to health‐associated species V. parvula and S. sanguis . A marked interindividual variation in production of IL‐1β was seen, with high, low and intermediate responders present in both PST+ and PST− groups. We conclude that genetic loci other than the PST polymorphisms are also important regulators of monocyte IL‐1 responses.