TY - JOUR
T1 - Nickel allergy-promoting effects of microbial or inflammatory substances at the sensitization step in mice
AU - Takahashi, Harue
AU - Kinbara, Masayuki
AU - Sato, Naoki
AU - Sasaki, Keiichi
AU - Sugawara, Shunji
AU - Endo, Yasuo
N1 - Funding Information:
We are grateful to Dr. H. Takada of our institute for providing P. intermedia LPS and reviewing the manuscript, and to Dr. R. Timms for language editing the manuscript. This work was supported by Grants-in Aid from the Japan Society for the Promotion of Science (Nos. 18591995 and 21659442 ).
PY - 2011/10
Y1 - 2011/10
N2 - 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 1 mM NiCl 2 and a test solution was injected into BALB/c mice intraperitoneally (0.1 ml/10 g body weight), and 10 days later 5 mM 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 3Cys-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.
AB - 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 1 mM NiCl 2 and a test solution was injected into BALB/c mice intraperitoneally (0.1 ml/10 g body weight), and 10 days later 5 mM 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 3Cys-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.
KW - Adjuvant
KW - Allergy
KW - Infection
KW - Innate immunity
KW - Nickel
UR - http://www.scopus.com/inward/record.url?scp=80053280235&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=80053280235&partnerID=8YFLogxK
U2 - 10.1016/j.intimp.2011.05.010
DO - 10.1016/j.intimp.2011.05.010
M3 - Article
C2 - 21621645
AN - SCOPUS:80053280235
VL - 11
SP - 1534
EP - 1540
JO - International Immunopharmacology
JF - International Immunopharmacology
SN - 1567-5769
IS - 10
ER -