| Research Abstract |
2006: We found that endotoxin from gram-negative bacteria (or lipopolysaccharide, LPS) strongly promotes nickel (Ni)-allergy in the steps of both sensitization and elicitation, and we clarified the followings (published in Clin Exp Allergy 2007;37:743-751).
1. Inflammation was severer in Th1-dominant mice than in Th2-dominant mice.
2. Extent of inflammation in mice deficient in TNF or T cells was similar to that in control mice, while it was markedly weak in IL-1-deficient mice and in macrophage-depleted mice.
3. The activity of histamine-forming enzyme (HDC) increased in parallel with the progress of inflammation.
4. Inflammation tended to be augmented in mast cell-deficient mice, but markedly weak in HDC-deficient mice.
5. LPS also promoted the establishment of allergies to other metals (Cr, Co, Pd, Cu, and Ag).
2007: We found the followings (will be submitted after additional experiments)
1. In addition to macrophages, NK and/or basophiles may be involved in the development of Ni-allergy.
2. Ni-sensitized mice responded to Cr, Co, Pd, Cu, and Ag, too.
3. Histamine was involved in the process of elicitation.
4. In addition to LPS, other bacterial constituents or related inflammatory substances (MDP, mannan, polyI:polyC, or TLR2 ligands, concanavalin A, nitrogen-containing bisphosphonates) also promoted Ni-allergy in the steps of both sensitization and elicitation.
5. In the elicitation step, Ni, under the presence of LPS, induced inflammation at so low concentration as 1x10^<-12> M (i.e., inflammation may dramatically enhances the sensitivity to metal allergies).
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