Nickel allergy-promoting effects of microbial or inflammatory substances at the sensitization step in mice.

Abstract

Microbial components stimulate innate immunity via Toll-like receptors (TLRs), nucleotide-binding oligomerization domain (NOD)-like receptors (NLRs), and/or IL-1. We recently reported that in mice, Escherichia coli lipopolysaccharide (LPS, TLR4-ligand) promotes allergic responses to nickel (Ni) at both the sensitization and elicitation steps. Here, we examined in mice the effects of administering other microbial or inflammatory materials at the Ni-sensitization step. A mixture of 1mM NiCl(2) and a test solution was injected into BALB/c mice intraperitoneally (0.1 ml/10 g body weight), and 10 days later 5mM NiCl(2) was challenged intradermally into the ear pinnas of the mice (20 μl/ear). The following preparations or substances exhibited adjuvant activities: Prevotella intermedia LPS, Saccharomyces cerevisiae mannan, a synthetic muramyl dipeptide (NOD2-stimulating cell-wall component of bacteria), Pam(3)Cys-SKKKK (TLR2-stimulating synthetic peptide), poly I:C (TLR3-stimulating double-stranded RNA), concanavalin A (a typical T-cell mitogen and T-cell-mediated hepatitis-inducer), heat-killed Propionibacterium acnes (Gram-positive bacterium that causes pimples and induces macrophage-mediated experimental hepatitis), and nitrogen-containing bisphosphonates (chemicals stimulating IL-1 production). Unexpectedly, P. intermedia LPS, which displayed the most potent adjuvant activity among the tested preparations, was effective in TLR4-dysfunctional mutant mice, but not in TLR2-deficient mice, whereas the reverse was true for S. cerevisiae mannan. These results suggest that (i) for the establishment of Ni-allergy in mice, stimulation of innate immunity (including TLRs, NLRs, IL-1 production, and/or other factors) may be important at the sensitization step, and (ii) P. intermedia may produce a substance(s) that potently promotes Ni-allergy via stimulation of TLR2.

• Authors: Harue Takahashi, Masayuki Kinbara, Naoki Sato, Keiichi Sasaki, Shunji Sugawara, Yasuo Endo
• Journal: International immunopharmacology (Int Immunopharmacol) Vol. 11 Issue 10 Pg. 1534-40 (Oct 2011) ISSN: 1878-1705 [Electronic] Netherlands
• PMID: 21621645 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
• Copyright: Copyright © 2011 Elsevier B.V. All rights reserved.

Chemical References

• Adjuvants, Immunologic
• Dipeptides
• Inflammation Mediators
• Interleukin-1
• Lipopolysaccharides
• Lipoproteins
• Mannans
• Tlr2 protein, mouse
• Tlr4 protein, mouse
• Toll-Like Receptor 2
• Toll-Like Receptor 4
• Concanavalin A
• Acetylmuramyl-Alanyl-Isoglutamine
• Nickel
• 2,3-bis-(palmitoyloxy)-2-propyl-N-palmitoyl-cysteinylserine
• Poly I-C

Topics

• Acetylmuramyl-Alanyl-Isoglutamine (administration & dosage)
• Adjuvants, Immunologic (administration & dosage)
• Animals
• Concanavalin A (administration & dosage)
• Dipeptides (administration & dosage)
• Hypersensitivity, Delayed (chemically induced, immunology)
• Immunity, Innate (drug effects)
• Immunization
• Inflammation Mediators (administration & dosage)
• Interleukin-1 (genetics, immunology, metabolism)
• Lipopolysaccharides (administration & dosage)
• Lipoproteins (administration & dosage)
• Mannans (administration & dosage)
• Mice
• Mice, Inbred Strains
• Mice, Knockout
• Mutation (genetics)
• Nickel (administration & dosage)
• Poly I-C (administration & dosage)
• Prevotella intermedia (immunology)
• Propionibacterium acnes (immunology)
• Saccharomyces cerevisiae (immunology)
• Toll-Like Receptor 2 (agonists, genetics)
• Toll-Like Receptor 4 (agonists, genetics)