Budget Amount *help |
¥2,200,000 (Direct Cost: ¥2,200,000)
Fiscal Year 1993: ¥1,100,000 (Direct Cost: ¥1,100,000)
Fiscal Year 1992: ¥1,100,000 (Direct Cost: ¥1,100,000)
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Research Abstract |
Chronic and latent infectious focus often causes or triggers the pathogenic process in distant part(s) of the body, being explained by a term "focal infection". Immunogenetically well-conserved proteins, heat shock proteins (HSPs), are inducied in cells after exposure to elevated temperature or others. This phenomenon has been investigated in relation to both host-defense to dacteria and induction of autoimmunity, since bacterial HSPs are immunogenic and targetted by immune surveilance, while mammalian HSPs induced after infectious stress are able to be recognized by the same immune mechanism. We started to investigate antibody production to mycobacterial HSP65 in various inflammatory skin diseases in order to correlate this so-called 'focal infection". In 1992, we obtained data from approximately 200 patients with various skin diseases. In comparison to normal group, patients with palmoplantar pustulosis (PPP), psoriasis (Pso), urticaria, and herpes zoster frequently showed elevated Ig
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G antibody to HSP65 from Mycobacterium leprae assayd on ELISA plates. In patients with anaphylactoid purpura the antibody level was not raised. In 1993, we further investigated correlation between antibody to HSP65 and skin inflammatory diseases triggered by bacterial infection. Patients with PPP were newly collected and divided into groups with and without chronic tonsilitis or periodontitis as infectious focus. OD at 492 nm in this ELISA technique revealed significant (p<0.01) difference between PPP with infectious focus (n=7,0.230(〕SY.+-.〔)0.065, mean(〕SY.+-.〔)SD) and PPP without it (n=12,0.139(〕SY.+-.〔)0.066). IN psoriasis, collected patients were divided into three groups according to types of psoriatic lesions : acute guttate psoriasis (PGA) that is a particular type of psoriasis induced often after steptococcal infection, plaque-type psoriasis (PV) and psutular-form psoasis (PP). The anti-HSP65IgG levels were 0.174(〕SY.+-.〔)0.032 for PGA (n=4), 0.101(〕SY.+-.〔)0.053 for PV (n=12) and 0.087(〕SY.+-.〔)0.025 for PP (n=6), showing significant changes between PGA and others (p=0.0165, PGA - PV ; p=0.001, PGA - PP). Elevation of anti-HSP65IgG was found in relation to bacterial infection-induced psoriatic and leukotactic inflammation in the skin. Less
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