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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 
 
 
 
 

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

An association has been reported between polymorphisms in the genes encoding IL-1alpha (-889) and IL-1beta (+3953) (periodontitis susceptibility trait, PST), and an increased severity of periodontitis (18). The IL-1beta polymorphism was reported to correlate with increased IL-1beta 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-1beta, 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-1beta production in response to any stimulant tested. In addition, the periodontal pathogens P. gingivalis, B. forsythus and P. intermedia failed to stimulate higher IL-1beta responses compared to health-associated species V. parvula and S. sanguis. A marked interindividual variation in production of IL-1beta 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.[1]

References

  1. Effect of the interleukin-1 genotype on monocyte IL-1beta expression in subjects with adult periodontitis. Mark, L.L., Haffajee, A.D., Socransky, S.S., Kent, R.L., Guerrero, D., Kornman, K., Newman, M., Stashenko, P. J. Periodont. Res. (2000) [Pubmed]
 
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