Lipopolysaccharide promotes and augments metal allergies in mice, dependent on innate immunity and histidine decarboxylase

Sato, Noriko; Kinbara, Masayuki; Kuroishi, Toshinobu; Kimura, Kiminori; Iwakura, Yoichiro; Ohtsu, Hiroshi; Sugawara, Shunji; Endo, Yasuo

doi:10.1111/j.1365-2222.2007.02705.x

Cited by 90 publications

(155 citation statements)

References 62 publications

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“…We previously suggested that the adjuvant effects of LPS and inflammatory substances on Ni-AD in mice depended on IL-1 and macrophages (Sato et al, 2007;Takahashi et al, 2011). So, here we examined the possible contributions made by IL-1 and macrophages to the adjuvant effects of RMs.…”

Section: Involvement Of Il-1 and Macrophages In The Adjuvant Effects mentioning

confidence: 99%

“…As yet, no one has succeeded in inducing RM-ACD in mice. We have reported that various bacterial components or ligands of Tolllike receptors (TLRs) act as potent adjuvants of the allergic dermatitis (AD) induced by intradermally injected Ni (Ni-AD) in mice, and this can occur at both the sensitization and elicitation steps (Sato et al, 2007;Kinbara et al, 2011;Takahashi et al, 2011;Huang et al, 2011). However, our attempts using these substances as adjuvants to produce RM-ACD in mice have all failed.…”

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confidence: 99%

“…Rustemeyer et al (1998) succeeded in sensitizing guinea pigs to RMs, but only by the drastic method of intradermally injecting mixtures of 1 M of RMs (10-20%) in water-Freund's complete adjuvant (1:1). In our experience with mice, 50% Freund's complete adjuvant alone (Sato et al, 2007) and such concentrations of RMs alone (unpublished observations) cause severe skin injuries. Thus, the above model may not reflect actual environmental situations that result in ACD in humans and suggest that unknown conditions or factors may be necessary for RM-ACD to occur.…”

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confidence: 99%

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Resin Monomers Act as Adjuvants in Ni-induced Allergic Dermatitis in vivo

Bando¹,

Takahashi

Kinbara³

et al. 2014

J Dent Res

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Resin monomers (RMs) are inflammatory agents and are thought to cause allergic contact dermatitis (ACD). However, mouse models are lacking, possibly because of the weak antigenicities of RMs. We previously reported that inflammatory substances can promote the allergic dermatitis (AD) induced by intradermally injected nickel (Ni-AD) in mice. Here, we examined the effects of RMs on Ni-AD. To sensitize mice to Ni, a mixture containing non-toxic concentrations of NiCl 2 and an RM [either methyl methacrylate (MMA) or 2-hydroxyethyl methacrylate (HEMA)] was injected intraperitoneally or into ear-pinnae intradermally. Ten days later, a mixture containing various concentrations of NiCl 2 and/or an RM was intradermally injected into earpinnae, and ear-swelling was measured. In adoptive transfer experiments, spleen cells from sensitized mice were transferred intravenously into non-sensitized recipients, and 24 h later NiCl 2 was challenged to ear-pinnae. Whether injected intraperitoneally or intradermally, RM plus NiCl 2 mixtures were effective in sensitizing mice to Ni. AD-inducing Ni concentrations were greatly reduced in the presence of MMA or HEMA (at the sensitization step from 10 mM to 5 or 50 µM, respectively, and at the elicitation step from 10 µM to 10 or 100 nM, respectively). These effects of RMs were weaker in IL-1-knockout mice and in macrophagedepleted mice. Cell-transfer experiments in IL-1-knockout mice indicated that both the sensitization and elicitation steps depended on IL-1. Challenge with an RM alone did not induce allergic ear-swelling in mice given the same RM + NiCl 2 10 days before the challenge. These results suggest that RMs act as adjuvants, not as antigens, to promote Ni-AD by reducing the AD-inducing concentration of Ni, and that IL-1 and macrophages are critically important for the adjuvant effects. We speculate that what were previously thought of as "RM-ACD" might include ACD caused by antigens other than RMs that have undergone promotion by the adjuvant effects of RMs.KEY WOrDs: methyl methacrylate, 2-hydroxyethyl methacrylate, dental material, macrophage, IL-1, allergy.

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Section: Involvement Of Il-1 and Macrophages In The Adjuvant Effects mentioning

confidence: 99%

mentioning

confidence: 99%

mentioning

confidence: 99%

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Resin Monomers Act as Adjuvants in Ni-induced Allergic Dermatitis in vivo

Bando¹,

Takahashi

Kinbara³

et al. 2014

J Dent Res

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“…How pathogenic T cells at the sites of allergic inflammation contribute to the development of metal allergy has not been explored because a suitable animal model has not been established. On the basis of previous reports [15][16][17], we generated a novel murine model of metal allergy, and have found the accumulation of the metal specific T cells in inflamed skin [16,17].…”

Section: Introductionmentioning

confidence: 99%

Accumulation of metal-specific T cells in inflamed skin in a novel murine model of Chromium-induced allergic contact dermatitis

Shigematsu¹,

Kumagai²,

Kobayashi³

et al. 2014

Journal of Oral and Maxillofacial Surgery

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Chromium (Cr) causes delayed-type hypersensitivity reactions possibly mediated by accumulating T cells into allergic inflamed skin, which are called irritants or allergic contact dermatitis. However, accumulating T cells during development of metal allergy are poorly characterized because a suitable animal model is not available. This study aimed to elucidate the skewing of T-cell receptor (TCR) repertoire and cytokine profiles in accumulated T cells in inflamed skin during elucidation of Cr allergy. A novel model of Cr allergy was induced by two sensitizations of Cr plus lipopolysaccharide solution into mouse groin followed by single Cr challenge into the footpad. TCR repertoires and nucleotide sequences of complementary determining region 3 were assessed in accumulated T cells from inflamed skin. Cytokine expression profiles and T-cell phenotypes were determined by qPCR. CD3+CD4+ T cells accumulated in allergic footpads and produced increased T helper 1 (Th1) type cytokines, Fas, and Fas ligand in the footpads after challenge, suggesting CD4+ Th1 cells locally expanded in response to Cr. Accumulated T cells included natural killer (NK) T cells and Cr-specific T cells with VA11-1/VB14-1 usage, suggesting metal-specific T cells driven by invariant NKT cells might contribute to the pathogenesis of Cr allergy.

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“…The mouse is not completely unresponsive to nickel though and it has proven possible to elicit responses if exposure is performed together with an adjuvant, or if there is some other source of local trauma or inflammation (Sato et al, 2007). It had been proposed also that, at least in part, the unresponsiveness of mice to nickel salts might be attributable to oral tolerance (resulting from oral ingestion of metallic nickel from cage material and drinking nipples).…”

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confidence: 99%