The Experts below are selected from a list of 168 Experts worldwide ranked by ideXlab platform
Shinichi Sato - One of the best experts on this subject based on the ideXlab platform.
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Inhibitory role of interleukin-10 in the cutaneous reverse Arthus Reaction.
The Journal of dermatology, 2020Co-Authors: Nobuko Ishiura, Koichi Yanaba, Kiyoko Nashiro, Mari Kudo, Taeko Goto, Hitoshi Okochi, Shinichi SatoAbstract:The formation and deposition of immune complexes (IC) containing immunoglobulin (Ig)G antibodies induces an acute inflammatory response with tissue injury. One of the experimental models of IC-related vasculitis is the cutaneous reverse passive Arthus Reaction, in which IgG antibodies are injected i.d., followed immediately by the i.v. application of the corresponding antigen. This Reaction is characterized by edema, hemorrhage and neutrophil infiltration. To assess the role of the anti-inflammatory cytokine interleukin (IL)-10 in IC-related vasculitis, we investigated the cutaneous Arthus Reaction using IL-10 knockout (IL-10KO) mice. Edema, which was quantified macroscopically by measuring the vascular leakage of Evans blue dye at 4 h after IC challenge, was significantly increased in IL-10KO mice compared with wild-type mice. In addition, hemorrhage, which was assessed by the average diameter of purpuric spots at 8 h after IC challenge, was enhanced significantly in IL-10KO mice compared with wild-type mice. Histological examination showed that the number of extravascular neutrophils was significantly increased in IL-10KO mice compared with wild-type mice at 4 and 8 h after IC challenge. Analysis of pro-inflammatory cytokine mRNA expression showed that IL-6 mRNA levels were significantly increased in IL-10KO mice compared with wild-type mice at 4 and 8 h after IC challenge. These results showed that IC-induced inflammation and vascular damage were significantly enhanced in the absence of IL-10. Thus, IL-10 may limit tissue disruption by suppressing the excessive infiltration of neutrophils and cytokine expression in a mouse model of type III vasculitis.
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exogenous application of hydrogen sulfide donor attenuates inflammatory Reactions through the l selectin involved pathway in the cutaneous reverse passive Arthus Reaction
Journal of Leukocyte Biology, 2013Co-Authors: Kazuhiro Shimizu, Toshihide Hara, Fumihide Ogawa, Koichi Yanaba, Eiji Muroi, Shinichi Sato, Ayumi Yoshizaki, Yuichiro Akiyama, Toshifumi YamaokaAbstract:H2S has been highlighted recently as an endogenous, gaseous signaling molecule, especially in inflammations. The deposition of IC induces an acute inflammatory response with tissue injury. To assess the roles of H2S in the IC-induced diseases, the cutaneous, reverse passive Arthus Reaction was conducted using NaHS as aH 2S donor. Furthermore, we conducted similar experiments using selectin / mice to determine the involvement of selectin molecules in the H2S-mediated pathway. Exogenous application of NaHS dramatically attenuated inflammatory Reactions in WT mice associated with Arthus Reaction. Namely, mRNA expressions of TNF-, IFN-, and neutrophil numbers were reduced significantly in the lesional skins of NaHS-treated WT mice relative to untreated ones. NaHS treatment significantly reduced these three parameters in the lesional skins of E- and P-selectin / mice but not in those of L-selectin / mice. Quite similar results were obtained in the blocking study using WT mice injected with mAb to E-, P-, and L-selectin. Our results indicated that the exogenous application of NaHS attenuates inflammatory responses in reverse passive Arthus Reaction through a L-selectin-involved pathway but not through E- or P-selectin pathways. J. Leukoc. Biol. 93: 000–000; 2013.
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Exogenous application of hydrogen sulfide donor attenuates inflammatory Reactions through the L‐selectin‐involved pathway in the cutaneous reverse passive Arthus Reaction
Journal of leukocyte biology, 2013Co-Authors: Kazuhiro Shimizu, Toshihide Hara, Fumihide Ogawa, Koichi Yanaba, Eiji Muroi, Ayumi Yoshizaki, Yuichiro Akiyama, Toshifumi Yamaoka, Shinichi SatoAbstract:H2S has been highlighted recently as an endogenous, gaseous signaling molecule, especially in inflammations. The deposition of IC induces an acute inflammatory response with tissue injury. To assess the roles of H2S in the IC-induced diseases, the cutaneous, reverse passive Arthus Reaction was conducted using NaHS as aH 2S donor. Furthermore, we conducted similar experiments using selectin / mice to determine the involvement of selectin molecules in the H2S-mediated pathway. Exogenous application of NaHS dramatically attenuated inflammatory Reactions in WT mice associated with Arthus Reaction. Namely, mRNA expressions of TNF-, IFN-, and neutrophil numbers were reduced significantly in the lesional skins of NaHS-treated WT mice relative to untreated ones. NaHS treatment significantly reduced these three parameters in the lesional skins of E- and P-selectin / mice but not in those of L-selectin / mice. Quite similar results were obtained in the blocking study using WT mice injected with mAb to E-, P-, and L-selectin. Our results indicated that the exogenous application of NaHS attenuates inflammatory responses in reverse passive Arthus Reaction through a L-selectin-involved pathway but not through E- or P-selectin pathways. J. Leukoc. Biol. 93: 000–000; 2013.
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involvement of gaseous low molecular monoxides in the cutaneous reverse passive Arthus Reaction cytoprotective action of carbon monoxide
Clinical and Experimental Immunology, 2008Co-Authors: Kazuhiro Shimizu, Fumihide Ogawa, Yohei Iwata, Eiji Muroi, Motoi Takenaka, Kazuhiro Komura, Toshifumi Yamaoka, S J Bae, Takeshi Hara, Shinichi SatoAbstract:The deposition of immune complexes (IC) induces an acute inflammatory response with tissue injury, for which the involvement of nitric oxide (NO) and carbon monoxide (CO) has been suggested. NO is induced by NO synthase (NOS) and CO is generated by haeme oxygenase (HO). Among HO isoenzymes, HO-1 is an induced type. To assess the role of NO and CO in the pathogenic process, the cutaneous reverse passive Arthus Reaction was examined using NOS inhibitor, HO-1 stimulator and HO-1 inhibitor. To evaluate the Reaction we considered oedema, tumour necrosis factor-α, interleukin-6, and neutrophil number. The values of these four parameters were significantly reduced in mice treated with HO-1 stimulator as compared with the positive control mice. Quite the reverse was observed in mice treated with HO-1 inhibitor. These results suggest that the HO-1/CO signalling pathway is a therapeutic target for human IC-mediated disease.
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role of c c chemokine receptors 1 and 5 and ccl3 macrophage inflammatory protein 1α in the cutaneous Arthus Reaction possible attenuation of their inhibitory effects by compensatory chemokine production
European Journal of Immunology, 2004Co-Authors: Kazuhiko Takehara, Koichi Yanaba, Naofumi Mukaida, Kouji Matsushima, Philip M Murphy, Shinichi SatoAbstract:The deposition of immune complexes induces an acute inflammatory response with tissue injury. Immune complex-induced tissue injury is mediated by inflammatory cell infiltration that is highly regulated by multiple chemokines. To assess the role of the chemokine receptors CCR1 and CCR5, and a ligand for these receptors CCL3/macrophage inflammatory protein-1α, in this pathogenic process, the reverse passive cutaneous Arthus Reaction was induced in mice lacking CCR1, CCR5, or CCL3. Edema was significantly attenuated in CCR1-deficient (CCR1–/–) and CCL3–/– mice but not CCR5–/– mice, compared with wild-type mice. Numbers of infiltrating neutrophils and mast cells were reduced in CCL3–/– and CCR1–/– mice, respectively, compared with wild-type mice. CCR1 and CCR5 were expressed on neutrophils and mast cells. Remarkably, the intradermal mRNA expression of CCL5/RANTES, another ligand for CCR1 and CCR5, was increased in CCR5–/– and CCL3–/– mice, compared with wild-type mice, while the cutaneous CCL3 mRNA expression was augmented in CCR1–/– and CCR5–/– mice. These results indicate that CCR1, CCR5, and CCL3 cooperatively contribute to the cutaneous Arthus Reaction, and also suggest that enhanced expression of CCL3 and CCL5 compensates for the loss of CCR1, CCR5, and CCL3 in the Reaction.
Koichi Yanaba - One of the best experts on this subject based on the ideXlab platform.
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Inhibitory role of interleukin-10 in the cutaneous reverse Arthus Reaction.
The Journal of dermatology, 2020Co-Authors: Nobuko Ishiura, Koichi Yanaba, Kiyoko Nashiro, Mari Kudo, Taeko Goto, Hitoshi Okochi, Shinichi SatoAbstract:The formation and deposition of immune complexes (IC) containing immunoglobulin (Ig)G antibodies induces an acute inflammatory response with tissue injury. One of the experimental models of IC-related vasculitis is the cutaneous reverse passive Arthus Reaction, in which IgG antibodies are injected i.d., followed immediately by the i.v. application of the corresponding antigen. This Reaction is characterized by edema, hemorrhage and neutrophil infiltration. To assess the role of the anti-inflammatory cytokine interleukin (IL)-10 in IC-related vasculitis, we investigated the cutaneous Arthus Reaction using IL-10 knockout (IL-10KO) mice. Edema, which was quantified macroscopically by measuring the vascular leakage of Evans blue dye at 4 h after IC challenge, was significantly increased in IL-10KO mice compared with wild-type mice. In addition, hemorrhage, which was assessed by the average diameter of purpuric spots at 8 h after IC challenge, was enhanced significantly in IL-10KO mice compared with wild-type mice. Histological examination showed that the number of extravascular neutrophils was significantly increased in IL-10KO mice compared with wild-type mice at 4 and 8 h after IC challenge. Analysis of pro-inflammatory cytokine mRNA expression showed that IL-6 mRNA levels were significantly increased in IL-10KO mice compared with wild-type mice at 4 and 8 h after IC challenge. These results showed that IC-induced inflammation and vascular damage were significantly enhanced in the absence of IL-10. Thus, IL-10 may limit tissue disruption by suppressing the excessive infiltration of neutrophils and cytokine expression in a mouse model of type III vasculitis.
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exogenous application of hydrogen sulfide donor attenuates inflammatory Reactions through the l selectin involved pathway in the cutaneous reverse passive Arthus Reaction
Journal of Leukocyte Biology, 2013Co-Authors: Kazuhiro Shimizu, Toshihide Hara, Fumihide Ogawa, Koichi Yanaba, Eiji Muroi, Shinichi Sato, Ayumi Yoshizaki, Yuichiro Akiyama, Toshifumi YamaokaAbstract:H2S has been highlighted recently as an endogenous, gaseous signaling molecule, especially in inflammations. The deposition of IC induces an acute inflammatory response with tissue injury. To assess the roles of H2S in the IC-induced diseases, the cutaneous, reverse passive Arthus Reaction was conducted using NaHS as aH 2S donor. Furthermore, we conducted similar experiments using selectin / mice to determine the involvement of selectin molecules in the H2S-mediated pathway. Exogenous application of NaHS dramatically attenuated inflammatory Reactions in WT mice associated with Arthus Reaction. Namely, mRNA expressions of TNF-, IFN-, and neutrophil numbers were reduced significantly in the lesional skins of NaHS-treated WT mice relative to untreated ones. NaHS treatment significantly reduced these three parameters in the lesional skins of E- and P-selectin / mice but not in those of L-selectin / mice. Quite similar results were obtained in the blocking study using WT mice injected with mAb to E-, P-, and L-selectin. Our results indicated that the exogenous application of NaHS attenuates inflammatory responses in reverse passive Arthus Reaction through a L-selectin-involved pathway but not through E- or P-selectin pathways. J. Leukoc. Biol. 93: 000–000; 2013.
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Exogenous application of hydrogen sulfide donor attenuates inflammatory Reactions through the L‐selectin‐involved pathway in the cutaneous reverse passive Arthus Reaction
Journal of leukocyte biology, 2013Co-Authors: Kazuhiro Shimizu, Toshihide Hara, Fumihide Ogawa, Koichi Yanaba, Eiji Muroi, Ayumi Yoshizaki, Yuichiro Akiyama, Toshifumi Yamaoka, Shinichi SatoAbstract:H2S has been highlighted recently as an endogenous, gaseous signaling molecule, especially in inflammations. The deposition of IC induces an acute inflammatory response with tissue injury. To assess the roles of H2S in the IC-induced diseases, the cutaneous, reverse passive Arthus Reaction was conducted using NaHS as aH 2S donor. Furthermore, we conducted similar experiments using selectin / mice to determine the involvement of selectin molecules in the H2S-mediated pathway. Exogenous application of NaHS dramatically attenuated inflammatory Reactions in WT mice associated with Arthus Reaction. Namely, mRNA expressions of TNF-, IFN-, and neutrophil numbers were reduced significantly in the lesional skins of NaHS-treated WT mice relative to untreated ones. NaHS treatment significantly reduced these three parameters in the lesional skins of E- and P-selectin / mice but not in those of L-selectin / mice. Quite similar results were obtained in the blocking study using WT mice injected with mAb to E-, P-, and L-selectin. Our results indicated that the exogenous application of NaHS attenuates inflammatory responses in reverse passive Arthus Reaction through a L-selectin-involved pathway but not through E- or P-selectin pathways. J. Leukoc. Biol. 93: 000–000; 2013.
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Platelets Control Leukocyte Recruitment in a Murine Model of Cutaneous Arthus Reaction
The American journal of pathology, 2009Co-Authors: Toshihide Hara, Kazuhiro Shimizu, Fumihide Ogawa, Koichi Yanaba, Yohei Iwata, Eiji Muroi, Motoi Takenaka, Kazuhiro Komura, Minoru Hasegawa, Manabu FujimotoAbstract:Platelets have been shown to be important in inflammation, but their role in the cutaneous Arthus Reaction remains unclear. To assess the role of platelets in this pathogenetic process, the cutaneous Arthus Reaction was examined in wild-type mice and mice lacking E-selectin, P-selectin, or P-selectin glycoprotein ligand-1 (PSGL-1) with or without platelet depletion by busulfan, a bone marrow precursor cell-specific toxin. Edema and hemorrhage induced by immune complex challenge significantly decreased in busulfan-treated wild-type mice compared with untreated mice. Busulfan treatment did not affect edema and hemorrhage in P-selectin- or PSGL-1-deficient mice, suggesting that the effect by busulfan is dependent on P-selectin and PSGL-1 expression. The inhibited edema and hemorrhage paralleled reduced infiltration of neutrophils and mast cells and reduced levels of circulating platelets. Increased cutaneous production of interleukin-6, tumor necrosis factor-α, and platelet-derived chemokines during Arthus Reaction was inhibited in busulfan-treated wild-type mice relative to untreated mice, which paralleled the reduction in cutaneous inflammation. Flow cytometric analysis showed that immune complex challenge generated blood platelet-leukocyte aggregates that decreased by busulfan treatment. In thrombocytopenic mice, the cutaneous inflammation after immune complex challenge was restored by platelet infusion. These results suggest that platelets induce leukocyte recruitment into skin by forming platelet-leukocyte aggregates and secreting chemokines at inflamed sites, mainly through the interaction of P-selectin on platelets with PSGL-1 on leukocytes.
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Establishment of Experimental Eosinophilic Vasculitis by IgE-Mediated Cutaneous Reverse Passive Arthus Reaction
The American journal of pathology, 2009Co-Authors: Takayuki Ishii, Takashi Matsushita, Kazuhiko Takehara, Kazuhiro Shimizu, Fumihide Ogawa, Koichi Yanaba, Minoru Hasegawa, Tomoyuki Fujita, Hiroko Nakashima, Thomas F. TedderAbstract:Prominent eosinophil infiltration is a characteristic of some forms of vasculitis, such as Churg-Strauss syndrome, also known as allergic granulomatous vasculitis. In the current study, we established a mouse model of cutaneous eosinophilic vasculitis by the cutaneous reverse passive Arthus Reaction using IgE injection instead of IgG. Wild-type C57BL/6 mice were injected with IgE anti-trinitrophenyl antibodies, followed immediately by intravenous administration of trinitrophenyl bovine serum albumin. IgE-mediated immune complex challenge induced substantial hemorrhage with marked infiltration of eosinophils in which neutrophils, mast cells, and macrophages were also mixed. This finding contrasted remarkably with the neutrophil-dominant infiltration pattern in IgG-mediated immune complex challenge. In the lesion, the expression level of monocyte chemotactic protein-3 was increased, and anti-monocyte chemotactic protein-3 treatment resulted in a significant but incomplete blockade of eosinophil recruitment. Furthermore, mice lacking E-selectin, P-selectin, L-selectin, or intercellular adhesion molecule-1, as well as wild-type mice that received anti-vascular cell adhesion molecule-1-blocking antibodies were assessed for the IgE-mediated Arthus Reaction. After 24 hours, the loss of P-selectin resulted in a significant reduction in eosinophil accumulation compared with both wild-type mice and other mouse mutants. Collectively, the Fc class of immunoglobulins, which forms these immune complexes, critically determines the disease manifestation of vasculitis. The IgE-mediated cutaneous reverse passive Arthus Reaction may serve as an experimental model for cutaneous eosinophilic infiltration in vasculitis as well as in other diseases.
Matthew Moyle - One of the best experts on this subject based on the ideXlab platform.
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The role of CD11/CD18 integrins in the reverse passive Arthus Reaction in rat dermal tissue.
Journal of leukocyte biology, 1996Co-Authors: William E. Rote, Erin Dempsey, Steve Maki, George P. Vlasuk, Matthew MoyleAbstract:The CD11/CD18 leukocyte integrins are necessary for tissue localization of neutrophils, an early requisite event in inflammation. We have analyzed the contribution of CD11a/CD18 and CD11b/CD18 to local neutrophil accumulation and tissue injury in the reverse passive Arthus Reaction in the rat dermis. Experimental groups comprised animals that received an intravenous infusion of (1) recombinant neutrophil inhibitory factor (NIF), a hookworm-derived antagonist of CD11b/CD18; (2) monoclonal antibody to CD11a/CD18 (TA-3); (3) a combination of these agents; (4) a monoclonal antibody to CD18 (WT.3); or (5) saline. Administration of recombinant NIF or anti-CD11a/CD18 monoclonal antibody alone produced a slight reduction in neutrophil accumulation but did not affect edema formation. In contrast, a combination of these antagonists yielded a significant reduction in neutrophil accumulation and a modest reduction in edema, equivalent to levels observed with either anti-CD18 antibodies or animals that were rendered neutropenic. These results indicate that neutrophil infiltration in rat dermal tissue in the reverse passive Arthus Reaction is dependent predominantly on the leukocyte integrins CD11a/CD18 and CD11b/CD18 and that either of these integrins is sufficient for neutrophil trafficking in this inflammatory setting.
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the role of cd11 cd18 integrins in the reverse passive Arthus Reaction in rat dermal tissue
Journal of Leukocyte Biology, 1996Co-Authors: William E. Rote, Erin Dempsey, Steve Maki, George P. Vlasuk, Matthew MoyleAbstract:The CD11/CD18 leukocyte integrins are necessary for tissue localization of neutrophils, an early requisite event in inflammation. We have analyzed the contribution of CD11a/CD18 and CD11b/CD18 to local neutrophil accumulation and tissue injury in the reverse passive Arthus Reaction in the rat dermis. Experimental groups comprised animals that received an intravenous infusion of (1) recombinant neutrophil inhibitory factor (NIF), a hookworm-derived antagonist of CD11b/CD18; (2) monoclonal antibody to CD11a/CD18 (TA-3); (3) a combination of these agents; (4) a monoclonal antibody to CD18 (WT.3); or (5) saline. Administration of recombinant NIF or anti-CD11a/CD18 monoclonal antibody alone produced a slight reduction in neutrophil accumulation but did not affect edema formation. In contrast, a combination of these antagonists yielded a significant reduction in neutrophil accumulation and a modest reduction in edema, equivalent to levels observed with either anti-CD18 antibodies or animals that were rendered neutropenic. These results indicate that neutrophil infiltration in rat dermal tissue in the reverse passive Arthus Reaction is dependent predominantly on the leukocyte integrins CD11a/CD18 and CD11b/CD18 and that either of these integrins is sufficient for neutrophil trafficking in this inflammatory setting.
Kazuhiro Shimizu - One of the best experts on this subject based on the ideXlab platform.
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exogenous application of hydrogen sulfide donor attenuates inflammatory Reactions through the l selectin involved pathway in the cutaneous reverse passive Arthus Reaction
Journal of Leukocyte Biology, 2013Co-Authors: Kazuhiro Shimizu, Toshihide Hara, Fumihide Ogawa, Koichi Yanaba, Eiji Muroi, Shinichi Sato, Ayumi Yoshizaki, Yuichiro Akiyama, Toshifumi YamaokaAbstract:H2S has been highlighted recently as an endogenous, gaseous signaling molecule, especially in inflammations. The deposition of IC induces an acute inflammatory response with tissue injury. To assess the roles of H2S in the IC-induced diseases, the cutaneous, reverse passive Arthus Reaction was conducted using NaHS as aH 2S donor. Furthermore, we conducted similar experiments using selectin / mice to determine the involvement of selectin molecules in the H2S-mediated pathway. Exogenous application of NaHS dramatically attenuated inflammatory Reactions in WT mice associated with Arthus Reaction. Namely, mRNA expressions of TNF-, IFN-, and neutrophil numbers were reduced significantly in the lesional skins of NaHS-treated WT mice relative to untreated ones. NaHS treatment significantly reduced these three parameters in the lesional skins of E- and P-selectin / mice but not in those of L-selectin / mice. Quite similar results were obtained in the blocking study using WT mice injected with mAb to E-, P-, and L-selectin. Our results indicated that the exogenous application of NaHS attenuates inflammatory responses in reverse passive Arthus Reaction through a L-selectin-involved pathway but not through E- or P-selectin pathways. J. Leukoc. Biol. 93: 000–000; 2013.
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Exogenous application of hydrogen sulfide donor attenuates inflammatory Reactions through the L‐selectin‐involved pathway in the cutaneous reverse passive Arthus Reaction
Journal of leukocyte biology, 2013Co-Authors: Kazuhiro Shimizu, Toshihide Hara, Fumihide Ogawa, Koichi Yanaba, Eiji Muroi, Ayumi Yoshizaki, Yuichiro Akiyama, Toshifumi Yamaoka, Shinichi SatoAbstract:H2S has been highlighted recently as an endogenous, gaseous signaling molecule, especially in inflammations. The deposition of IC induces an acute inflammatory response with tissue injury. To assess the roles of H2S in the IC-induced diseases, the cutaneous, reverse passive Arthus Reaction was conducted using NaHS as aH 2S donor. Furthermore, we conducted similar experiments using selectin / mice to determine the involvement of selectin molecules in the H2S-mediated pathway. Exogenous application of NaHS dramatically attenuated inflammatory Reactions in WT mice associated with Arthus Reaction. Namely, mRNA expressions of TNF-, IFN-, and neutrophil numbers were reduced significantly in the lesional skins of NaHS-treated WT mice relative to untreated ones. NaHS treatment significantly reduced these three parameters in the lesional skins of E- and P-selectin / mice but not in those of L-selectin / mice. Quite similar results were obtained in the blocking study using WT mice injected with mAb to E-, P-, and L-selectin. Our results indicated that the exogenous application of NaHS attenuates inflammatory responses in reverse passive Arthus Reaction through a L-selectin-involved pathway but not through E- or P-selectin pathways. J. Leukoc. Biol. 93: 000–000; 2013.
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Platelets Control Leukocyte Recruitment in a Murine Model of Cutaneous Arthus Reaction
The American journal of pathology, 2009Co-Authors: Toshihide Hara, Kazuhiro Shimizu, Fumihide Ogawa, Koichi Yanaba, Yohei Iwata, Eiji Muroi, Motoi Takenaka, Kazuhiro Komura, Minoru Hasegawa, Manabu FujimotoAbstract:Platelets have been shown to be important in inflammation, but their role in the cutaneous Arthus Reaction remains unclear. To assess the role of platelets in this pathogenetic process, the cutaneous Arthus Reaction was examined in wild-type mice and mice lacking E-selectin, P-selectin, or P-selectin glycoprotein ligand-1 (PSGL-1) with or without platelet depletion by busulfan, a bone marrow precursor cell-specific toxin. Edema and hemorrhage induced by immune complex challenge significantly decreased in busulfan-treated wild-type mice compared with untreated mice. Busulfan treatment did not affect edema and hemorrhage in P-selectin- or PSGL-1-deficient mice, suggesting that the effect by busulfan is dependent on P-selectin and PSGL-1 expression. The inhibited edema and hemorrhage paralleled reduced infiltration of neutrophils and mast cells and reduced levels of circulating platelets. Increased cutaneous production of interleukin-6, tumor necrosis factor-α, and platelet-derived chemokines during Arthus Reaction was inhibited in busulfan-treated wild-type mice relative to untreated mice, which paralleled the reduction in cutaneous inflammation. Flow cytometric analysis showed that immune complex challenge generated blood platelet-leukocyte aggregates that decreased by busulfan treatment. In thrombocytopenic mice, the cutaneous inflammation after immune complex challenge was restored by platelet infusion. These results suggest that platelets induce leukocyte recruitment into skin by forming platelet-leukocyte aggregates and secreting chemokines at inflamed sites, mainly through the interaction of P-selectin on platelets with PSGL-1 on leukocytes.
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Establishment of Experimental Eosinophilic Vasculitis by IgE-Mediated Cutaneous Reverse Passive Arthus Reaction
The American journal of pathology, 2009Co-Authors: Takayuki Ishii, Takashi Matsushita, Kazuhiko Takehara, Kazuhiro Shimizu, Fumihide Ogawa, Koichi Yanaba, Minoru Hasegawa, Tomoyuki Fujita, Hiroko Nakashima, Thomas F. TedderAbstract:Prominent eosinophil infiltration is a characteristic of some forms of vasculitis, such as Churg-Strauss syndrome, also known as allergic granulomatous vasculitis. In the current study, we established a mouse model of cutaneous eosinophilic vasculitis by the cutaneous reverse passive Arthus Reaction using IgE injection instead of IgG. Wild-type C57BL/6 mice were injected with IgE anti-trinitrophenyl antibodies, followed immediately by intravenous administration of trinitrophenyl bovine serum albumin. IgE-mediated immune complex challenge induced substantial hemorrhage with marked infiltration of eosinophils in which neutrophils, mast cells, and macrophages were also mixed. This finding contrasted remarkably with the neutrophil-dominant infiltration pattern in IgG-mediated immune complex challenge. In the lesion, the expression level of monocyte chemotactic protein-3 was increased, and anti-monocyte chemotactic protein-3 treatment resulted in a significant but incomplete blockade of eosinophil recruitment. Furthermore, mice lacking E-selectin, P-selectin, L-selectin, or intercellular adhesion molecule-1, as well as wild-type mice that received anti-vascular cell adhesion molecule-1-blocking antibodies were assessed for the IgE-mediated Arthus Reaction. After 24 hours, the loss of P-selectin resulted in a significant reduction in eosinophil accumulation compared with both wild-type mice and other mouse mutants. Collectively, the Fc class of immunoglobulins, which forms these immune complexes, critically determines the disease manifestation of vasculitis. The IgE-mediated cutaneous reverse passive Arthus Reaction may serve as an experimental model for cutaneous eosinophilic infiltration in vasculitis as well as in other diseases.
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involvement of gaseous low molecular monoxides in the cutaneous reverse passive Arthus Reaction cytoprotective action of carbon monoxide
Clinical and Experimental Immunology, 2008Co-Authors: Kazuhiro Shimizu, Fumihide Ogawa, Yohei Iwata, Eiji Muroi, Motoi Takenaka, Kazuhiro Komura, Toshifumi Yamaoka, S J Bae, Takeshi Hara, Shinichi SatoAbstract:The deposition of immune complexes (IC) induces an acute inflammatory response with tissue injury, for which the involvement of nitric oxide (NO) and carbon monoxide (CO) has been suggested. NO is induced by NO synthase (NOS) and CO is generated by haeme oxygenase (HO). Among HO isoenzymes, HO-1 is an induced type. To assess the role of NO and CO in the pathogenic process, the cutaneous reverse passive Arthus Reaction was examined using NOS inhibitor, HO-1 stimulator and HO-1 inhibitor. To evaluate the Reaction we considered oedema, tumour necrosis factor-α, interleukin-6, and neutrophil number. The values of these four parameters were significantly reduced in mice treated with HO-1 stimulator as compared with the positive control mice. Quite the reverse was observed in mice treated with HO-1 inhibitor. These results suggest that the HO-1/CO signalling pathway is a therapeutic target for human IC-mediated disease.
Rosa Carnuccio - One of the best experts on this subject based on the ideXlab platform.
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transcription factor decoy oligodeoxynucleotides to nuclear factor kappab inhibit reverse passive Arthus Reaction in rat
Naunyn-schmiedebergs Archives of Pharmacology, 2001Co-Authors: Fulvio Dacquisto, Angela Ianaro, Armando Ialenti, Pasquale Maffia, Maria Chiara Maiuri, Rosa CarnuccioAbstract:In the present study we investigated in the reverse passive Arthus Reaction elicited in the rat skin the anti-inflammatory effect of double-stranded oligodeoxynucleotides (ODN) with consensus nuclear factor-κB (NF-κB) sequence as transcription factor decoys (TFD) to inhibit NF-κB binding to native DNA sites. Local administration of wild-type-, but not mutant-decoy ODN, dose-dependently reduced both plasma leakage and neutrophil infiltration in rat skin. Molecular analysis performed on soft tissue obtained from rat skin demonstrated: (1) an inhibition of NF-κB/DNA binding activity; (2) a decreased nuclear level of p50 and p65 NF-κB subunits; (3) an inhibition of cyclooxygenase-2 (COX-2) and inducible nitric oxide synthase (iNOS) protein expression, two inflammatory enzymes transcriptionally controlled by NF-κB. Furthermore, SN-50, a cell-permeable peptide capable of inhibiting the nuclear translocation of NF-κB complexes, as well as ammonium pyrrolidine dithiocarbamate, an inhibitor of NF-κB activation, exhibited a similar profile of activity of decoy ODN. Our results indicate that decoy ODN, acting as an in vivo competitor for the transcription factor's ability to bind to cognate recognition sequence, may represent a novel strategy to modulate immune Reactions.
