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Effect of whole oral bacteria and extracted lipopolysaccharides on peripheral blood leukocyte interleukin‐2 receptor expression
Author(s) -
Lindemann R.A.,
Kjeldsen Mette,
Cabret Michelle
Publication year - 1995
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 - 10.1111/j.1600-0765.1995.tb02132.x
Subject(s) - peripheral blood mononuclear cell , interleukin 2 , monocyte , interleukin , immune system , cytokine , receptor expression , receptor , biology , antigen , lipopolysaccharide , immunology , t cell , microbiology and biotechnology , chemistry , in vitro , biochemistry
Expression of the interleukin‐2 receptor (IL‐2R) on T cells is the molecular mechanism that initiates the G o to G 1 transition and is the critical first step for T cell proliferation in response to antigen. The effect of whole periodontal bacteria and lipopolysaccharides (LPS) on peripheral blood mononuclear cell (PBMC) IL‐2R expression was examined in vitro . LPS induced a modest but significant increase in high affinity lL‐2Rα/β (p55/p75 positive) expression on PBMC over untreated cells after 48 h culture. Addition of LPS to PBMC cultures depleted of monocytes had no effect on 1L‐2R expression compared to untreated cultures. Interleukin‐1 (IL‐1) caused a similar effect to LPS in 48 h PBMC cultures but IL‐1 also increased high affinity IL‐2R expression in cultures depleted of adherent mononuclear cells. When antibody to IL‐1 was simultaneously added with LPS to PBMC cultures, the high affinity IL‐2R inductive effect was reversed at 48 h, suggesting that the LPS effect on PBMC IL‐2R was indirect, via monocytes. Whole pathogenic oral bacteria cultured with PBMC at high (100:1), but not low (10:1) bacteria:PBMC ratios had a similar effect to LPS, inducing high affinity IL‐2R expression at 48 h. Increases in soluble IL‐2Rα were also measured in supernatants of PBMC incubated with periodontal bacteria compared to untreated controls. In this system, a critical threshold of bacteria was required to activate PBMC perhaps related to the quantity of cell‐surface LPS presented to adherent mononuclear cells.