Resin Monomers Act as Adjuvants in Ni-induced Allergic Dermatitis <i>in vivo</i>

Bando, Kanan; Takahashi, Hideo; Kinbara, Masayuki; Tanaka, Yukinori; Kuroishi, Toshinobu; Sasaki, Keiichi; Takano‐Yamamoto, Teruko; Sugawara, Shunji; Endo, Yasuo

doi:10.1177/0022034514552674

Cited by 18 publications

(27 citation statements)

References 39 publications

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“…1,5,31 In the present study, IL-1β exhibited an LPS-like adjuvant effect (see above), leading us to suppose that the adjuvant effect of IL-1β may be (at least partly) mediated by histamine newly formed via induction of HDC. 1,5,31 In the present study, IL-1β exhibited an LPS-like adjuvant effect (see above), leading us to suppose that the adjuvant effect of IL-1β may be (at least partly) mediated by histamine newly formed via induction of HDC.…”

Section: In Hdc-ko Mice Ni + Il-1β + Histamine At Sensitization Stsupporting

confidence: 57%

“…Like LPS, resin monomers and nitrogen-containing bisphosphonates exhibit adjuvant effects in the induction of Ni allergy, 3,5 and they also stimulate productions of IL-1α and IL-1β, 5 In the present study, the ear swelling induced by LPS 1 mg/mL alone was very small, although there were increases in IL-1β and HDC activity ( Figure 7B). It should be noted that the IL-1β antibody used in the method for measuring IL-1β cannot distinguish mature IL-1β (active) from pro-IL-1β (inactive).…”

Section: Adjuvant Effect Of Il-1supporting

confidence: 44%

“…As shown in Figure 3A, i.p. 5 As IL-1 has the ability to induce HDC, we examined the relationship between the adjuvant effect of IL-1 and the induction of HDC (ie newly formed histamine), as described in the following sections. Sensitization and challenge were carried out as indicated in WT C57BL/6 mice.…”

Section: In Il-1-ko Mice Il-1β Induces Hdc and Is Effective As An mentioning

confidence: 99%

“…[1][2][3][4][5] Among such adjuvants, lipopolysaccharide (LPS), a cell wall component of Gram-negative bacteria, exhibits the strongest adjuvant activity, and LPS markedly reduces the concentration of NiCl 2 needed to induce Ni allergy at both the sensitization and elicitation steps (Table 1), 6 Histamine is a well-known mediator of allergic inflammation. However, few adequate murine models exist of Ni-induced CHS or Ni allergy.…”

Section: Introductionmentioning

confidence: 99%

“…,33,41 although they have no adjuvant effects either in IL-1-KO mice or in macrophagedepleted mice 5. In addition, cell-transfer experiments in IL-1-KO mice have indicated that both sensitization and elicitation steps F I G U R E 7 In vivo (i.p.…”

mentioning

confidence: 99%

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Interleukin‐1 and histamine are essential for inducing nickel allergy in mice

Bando

Kuroishi

Sugawara

et al. 2019

Clin Experimental Allergy

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Background:We previously reported that (a) lipopolysaccharide (LPS) is a potent adjuvant for inducing Nickel (Ni) allergy in mice at both the sensitization and elicitation steps, (b) LPS induces Interleukin-1 (IL-1) and histidine decarboxylase (HDC, the histamine-forming enzyme), and IL-1 induces HDC, (c) Ni allergy is induced in mast cell-deficient, but not IL-1-deficient (IL-1-KO) or HDC-KO mice.Objective: To examine the roles of IL-1 and HDC (or histamine) and their interrelationship during the establishment of Ni allergy.Methods: Ni (NiCl 2 ) 1 mmol/L containing IL-1β and/or histamine was injected intraperitoneally (sensitization step). Ten days later, test substance(s) were intradermally injected into ear pinnas (elicitation step), and ear swelling was measured. Results:In wild-type mice, Ni + LPS or Ni + IL-1β injection at sensitization step followed by Ni alone at elicitation step induced Ni allergy. In IL-1-KO, injection of Ni + IL-1β (but not Ni + histamine) was required at both sensitization and elicitation steps to induce Ni allergy. In HDC-KO, Ni + IL-1β + histamine at sensitization step followed by Ni + histamine at elicitation step induced Ni allergy. In histamine H1 receptor-deficient mice, IL-1β induced HDC, but was ineffective as an adjuvant for inducing Ni allergy. In wild-type mice, injection into ear pinnas of Ni 10 mmol/L alone or Ni 1 mmol/L + LPS induced IL-1β, HDC and a prolonged swelling of ear pinnas. In non-sensitized mice, injection of IL-1β by itself into ear pinnas in IL-1-KO mice induced prolonged ear swelling. Ni augmented IL-1 production (both IL-1α and IL-1β) and HDC induction in wild-type mice sensitized to Ni. Conclusions:In mice: (a) for inducing Ni allergy, IL-1 is essential at both the sensitization and elicitation steps, and HDC induction is involved in the effect of IL-1, (b) stimulation of H1 receptor is also essential for inducing Ni allergy at both sensitization and elicitation steps, and (c) the 'sensitization to Ni' state may be a state where tissues are primed for augmented production of IL-1α and/or IL-1β in response to Ni.(within 300 words, now 300). K E Y W O R D Sallergic contact dermatitis, animal models, chemokines | 1363 BANDO et Al.

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Section: In Hdc-ko Mice Ni + Il-1β + Histamine At Sensitization Stsupporting

confidence: 57%

Section: Adjuvant Effect Of Il-1supporting

confidence: 44%

Section: In Il-1-ko Mice Il-1β Induces Hdc and Is Effective As An mentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

mentioning

confidence: 99%

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Interleukin‐1 and histamine are essential for inducing nickel allergy in mice

Bando

Kuroishi

Sugawara

et al. 2019

Clin Experimental Allergy

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The effects of the dental methacrylates TEGDMA, Bis‐GMA, and UDMA on neutrophils in vitro

Alizadehgharib

Östberg

Rudin

et al. 2020

Clinical & Exp Dental Res

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Objectives The prevalent usage of methacrylates in modern dentistry demands good knowledge of their biological impacts. While there have been several studies demonstrating the effects of different methacrylic monomers on mononuclear white blood cells, very little is known about the effects caused by these monomers on neutrophilic granulocytes. The objective of this study was to add novel knowledge about how neutrophils are affected by exposure to triethylene glycol dimethacrylate (TEGDMA), urethane dimethacrylate (UDMA), and bisphenol A glycol dimethacrylate (Bis‐GMA) alone or in combinations. Materials and Methods Isolated neutrophils were cultured in the presence or absence of methacrylates. The IL‐8 release was measured using a DuoSet ELISA development kit. Apoptosis and necrosis were analyzed using flow cytometry. The formation of neutrophil extracellular traps (NETs) was investigated using Sytox green DNA staining combined with microscopically examination of released DNA and myeloperoxidase (MPO). Results The release of IL‐8 was significantly increased after exposure to TEGDMA, Bis‐GMA, UDMA, or TEGDMA in combination with Bis‐GMA or UDMA compared to the unstimulated controls. Exposure to TEGDMA, UDMA, and Bis‐GMA for 24 hr separately or in combination did not affect apoptosis or necrosis of the exposed neutrophils. NET structures were formed by neutrophils after exposure to the different combinations of the methacrylates. Conclusion The combination of TEGDMA and Bis‐GMA had a synergistic proinflammatory effect on neutrophils by increasing the release of IL‐8 and the formation of NET structures. The changes in the normal functions of neutrophils caused by methacrylate exposure may lead to altered inflammatory response and relate to previously reported adverse immune reactions caused by these substances.

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The dental resin monomers HEMA and TEGDMA have inhibitory effects on osteoclast differentiation with low cytotoxicity

Inamitsu

Okamoto

Sakai

et al. 2017

J of Applied Toxicology

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The dental resin monomers 2-hydroxyethyl methacrylate (HEMA) and triethylene glycol dimethacrylate (TEGDMA) are released from the resin matrix due to unpolymerized monomers; once released, they influence various biological functions and the viability of cells in the oral environment. Although HEMA and TEGDMA have various effects on cells, including inflammation, inhibition of cell proliferation or differentiation, and apoptosis, the effects of these monomers on osteoclasts remain unknown. In this study, we investigated the effects of HEMA and TEGDMA on osteoclast differentiation of bone marrow-derived macrophages or murine monocytic cell line RAW-D. Both HEMA and TEGDMA inhibited osteoclast formation and their bone-resorbing activity at non-cytotoxic concentrations. Moreover, HEMA and TEGDMA decreased the expression of nuclear factor of activated T cells cytoplasmic-1 (NFATc1), a master regulator of osteoclast differentiation, and of osteoclast markers that are transcriptionally regulated by NFATc1, including Src and cathepsin K. Regarding their effects on signaling pathways involved in osteoclast differentiation, HEMA impaired the phosphorylation of extracellular signal-regulated kinase and Jun N-terminal kinase, whereas TEGDMA attenuated the phosphorylation of Akt and Jun N-terminal kinase. Thus, HEMA and TEGDMA inhibit osteoclast differentiation through different signaling pathways. This is the first report on the effects of the monomers HEMA and TEGDMA on osteoclasts. Copyright © 2017 John Wiley & Sons, Ltd.

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

Cited by 18 publications

References 39 publications

Interleukin‐1 and histamine are essential for inducing nickel allergy in mice

Interleukin‐1 and histamine are essential for inducing nickel allergy in mice

The effects of the dental methacrylates TEGDMA, Bis‐GMA, and UDMA on neutrophils in vitro

The dental resin monomers HEMA and TEGDMA have inhibitory effects on osteoclast differentiation with low cytotoxicity

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