The Experts below are selected from a list of 198 Experts worldwide ranked by ideXlab platform

Naohito Ohno - One of the best experts on this subject based on the ideXlab platform.

  • Induction of IFN-γ by a highly branched 1,3-β-d-glucan from Aureobasidium pullulans in Mouse-derived splenocytes via dectin-1-independent pathways.
    Biochemical and biophysical research communications, 2010
    Co-Authors: Rui Tada, Masashi Yoshikawa, Takao Kuge, Asuka Tanioka, Ken-ichi Ishibashi, Yoshiyuki Adachi, Kazufumi Tsubaki, Futoshi Ikeda, Yuya Kato, Naohito Ohno
    Abstract:

    We have previously elucidated the precise structure of a unique type of 1,3-β-D-glucan, AP-FBG (Aureobasidium pullulans-fermented β-D-glucan), from the fungus A. pullulans and found that AP-FBG strongly induced the production of various cytokines in DBA/2 Mouse-derived splenocytes in vitro. However, the mechanism(s) of action of AP-FBG on in vitro Mouse primary cells have not been characterized in detail. Herein, we report that the production of IFN-γ in DBA/2 Mouse-derived splenocytes by AP-FBG was not inhibited following treatment with an anti-dectin-1 neutralizing antibody. In addition, AP-FBG not only failed to activate dectin-1-mediated signaling pathways, examined by a reporter gene assay but also failed to bind to dectin-1, a pivotal receptor for 1,3-β-D-glucan. Taken together, AP-FBG induced cell activation via dectin-1-independent pathways.

  • a highly branched 1 3 β d glucan extracted from aureobasidium pullulans induces cytokine production in DBA 2 Mouse derived splenocytes
    International Immunopharmacology, 2009
    Co-Authors: Rui Tada, Masashi Yoshikawa, Takao Kuge, Asuka Tanioka, Ken-ichi Ishibashi, Yoshiyuki Adachi, Kazufumi Tsubaki, Naohito Ohno
    Abstract:

    We recently elucidated the structure of a highly branched 1,3-beta-D-glucan with 6-monoglucopyranosyl side chains, extracted from Aureobasidium pullulans (AP-FBG). Although the biological effects of beta-D-glucans are known to depend on their structures, the effects of a highly branched 1,3-beta-D-glucan on the production of cytokines by leukocytes in mice have not yet been elucidated. In this study, we found that AP-FBG strongly induced the production of various cytokines, especially Th1 cytokines (e.g., IFN-gamma and IL-12p70) and Th17 cytokines (e.g., IL-17A), but did not induce the production of IL-4, IL-10, and TNF-alpha in DBA/2 Mouse-derived splenocytes in vitro.

  • A highly branched 1,3-β-D-glucan extracted from Aureobasidium pullulans induces cytokine production in DBA/2 Mouse-derived splenocytes
    International immunopharmacology, 2009
    Co-Authors: Rui Tada, Masashi Yoshikawa, Takao Kuge, Asuka Tanioka, Ken-ichi Ishibashi, Yoshiyuki Adachi, Kazufumi Tsubaki, Naohito Ohno
    Abstract:

    We recently elucidated the structure of a highly branched 1,3-beta-D-glucan with 6-monoglucopyranosyl side chains, extracted from Aureobasidium pullulans (AP-FBG). Although the biological effects of beta-D-glucans are known to depend on their structures, the effects of a highly branched 1,3-beta-D-glucan on the production of cytokines by leukocytes in mice have not yet been elucidated. In this study, we found that AP-FBG strongly induced the production of various cytokines, especially Th1 cytokines (e.g., IFN-gamma and IL-12p70) and Th17 cytokines (e.g., IL-17A), but did not induce the production of IL-4, IL-10, and TNF-alpha in DBA/2 Mouse-derived splenocytes in vitro.

  • Histopathological examination and analysis of mortality in DBA/2 Mouse vasculitis induced with CAWS, a water-soluble extracellular polysaccharide fraction obtained from Candida albicans
    Yakugaku zasshi : Journal of the Pharmaceutical Society of Japan, 2006
    Co-Authors: Naoto Hirata, Ken-ichi Ishibashi, Shin Ohta, Satoru Hata, Hiroyasu Shinohara, Mio Kitamura, Noriko Miura, Naohito Ohno
    Abstract:

    CAWS, a water-soluble extracellular polysaccharide fraction obtained from the culture supernatant of Candida albicans, is one of the fungal pathogen-associated molecular patterns (PAMPs). It has been reported to show potent activity inducing arteritis and coronaritis in mice. Especially, CAWS-induced arteritis has a 100% incidence and severe mortality in the DBA/2 Mouse strain. This artificial vasculitis was reported to provide a good murine model of Kawasaki disease and other inflammatory vascular disease. However, severe mortality was observed only in DBA/2 mice, which is a CAWS-sensitive strain. In this study, to clarify the mechanisms of CAWS-induced arteritis and mortality, we investigated microscopic histopathological changes in cardiovascular tissues in DBA/2 mice. Severe inflammatory infiltration was observed from the external elastic lamina in the aorta and proximal coronary arteries within 1 week after CAWS administration. Severe stenosis of the aorta and coronary arteries was observed more than 3 weeks after CAWS administration. Fibrinoid necrosis was observed in these vessel walls. All CAWS-treated mice died between the fifth and twelfth week after administration. Severe inflammatory change with aortic valve transformation suggested that CAWS-treated mice died of valvular endocarditis or cardiac dysfunction. Based on the simple induction method and complete incidence, these data suggest that CAWS-induced arteritis is a good model of not only Kawasaki disease but also other cardiovascular diseases such as valvular endocarditis.

  • histopathological examination and analysis of mortality in DBA 2 Mouse vasculitis induced with caws a water soluble extracellular polysaccharide fraction obtained from candida albicans
    Yakugaku Zasshi-journal of The Pharmaceutical Society of Japan, 2006
    Co-Authors: Naoto Hirata, Ken-ichi Ishibashi, Shin Ohta, Satoru Hata, Hiroyasu Shinohara, Mio Kitamura, Noriko Miura, Naohito Ohno
    Abstract:

    CAWS, a water-soluble extracellular polysaccharide fraction obtained from the culture supernatant of Candida albicans, is one of the fungal pathogen-associated molecular patterns (PAMPs). It has been reported to show potent activity inducing arteritis and coronaritis in mice. Especially, CAWS-induced arteritis has a 100% incidence and severe mortality in the DBA/2 Mouse strain. This artificial vasculitis was reported to provide a good murine model of Kawasaki disease and other inflammatory vascular disease. However, severe mortality was observed only in DBA/2 mice, which is a CAWS-sensitive strain. In this study, to clarify the mechanisms of CAWS-induced arteritis and mortality, we investigated microscopic histopathological changes in cardiovascular tissues in DBA/2 mice. Severe inflammatory infiltration was observed from the external elastic lamina in the aorta and proximal coronary arteries within 1 week after CAWS administration. Severe stenosis of the aorta and coronary arteries was observed more than 3 weeks after CAWS administration. Fibrinoid necrosis was observed in these vessel walls. All CAWS-treated mice died between the fifth and twelfth week after administration. Severe inflammatory change with aortic valve transformation suggested that CAWS-treated mice died of valvular endocarditis or cardiac dysfunction. Based on the simple induction method and complete incidence, these data suggest that CAWS-induced arteritis is a good model of not only Kawasaki disease but also other cardiovascular diseases such as valvular endocarditis.

Ken-ichi Ishibashi - One of the best experts on this subject based on the ideXlab platform.

  • Induction of IFN-γ by a highly branched 1,3-β-d-glucan from Aureobasidium pullulans in Mouse-derived splenocytes via dectin-1-independent pathways.
    Biochemical and biophysical research communications, 2010
    Co-Authors: Rui Tada, Masashi Yoshikawa, Takao Kuge, Asuka Tanioka, Ken-ichi Ishibashi, Yoshiyuki Adachi, Kazufumi Tsubaki, Futoshi Ikeda, Yuya Kato, Naohito Ohno
    Abstract:

    We have previously elucidated the precise structure of a unique type of 1,3-β-D-glucan, AP-FBG (Aureobasidium pullulans-fermented β-D-glucan), from the fungus A. pullulans and found that AP-FBG strongly induced the production of various cytokines in DBA/2 Mouse-derived splenocytes in vitro. However, the mechanism(s) of action of AP-FBG on in vitro Mouse primary cells have not been characterized in detail. Herein, we report that the production of IFN-γ in DBA/2 Mouse-derived splenocytes by AP-FBG was not inhibited following treatment with an anti-dectin-1 neutralizing antibody. In addition, AP-FBG not only failed to activate dectin-1-mediated signaling pathways, examined by a reporter gene assay but also failed to bind to dectin-1, a pivotal receptor for 1,3-β-D-glucan. Taken together, AP-FBG induced cell activation via dectin-1-independent pathways.

  • a highly branched 1 3 β d glucan extracted from aureobasidium pullulans induces cytokine production in DBA 2 Mouse derived splenocytes
    International Immunopharmacology, 2009
    Co-Authors: Rui Tada, Masashi Yoshikawa, Takao Kuge, Asuka Tanioka, Ken-ichi Ishibashi, Yoshiyuki Adachi, Kazufumi Tsubaki, Naohito Ohno
    Abstract:

    We recently elucidated the structure of a highly branched 1,3-beta-D-glucan with 6-monoglucopyranosyl side chains, extracted from Aureobasidium pullulans (AP-FBG). Although the biological effects of beta-D-glucans are known to depend on their structures, the effects of a highly branched 1,3-beta-D-glucan on the production of cytokines by leukocytes in mice have not yet been elucidated. In this study, we found that AP-FBG strongly induced the production of various cytokines, especially Th1 cytokines (e.g., IFN-gamma and IL-12p70) and Th17 cytokines (e.g., IL-17A), but did not induce the production of IL-4, IL-10, and TNF-alpha in DBA/2 Mouse-derived splenocytes in vitro.

  • A highly branched 1,3-β-D-glucan extracted from Aureobasidium pullulans induces cytokine production in DBA/2 Mouse-derived splenocytes
    International immunopharmacology, 2009
    Co-Authors: Rui Tada, Masashi Yoshikawa, Takao Kuge, Asuka Tanioka, Ken-ichi Ishibashi, Yoshiyuki Adachi, Kazufumi Tsubaki, Naohito Ohno
    Abstract:

    We recently elucidated the structure of a highly branched 1,3-beta-D-glucan with 6-monoglucopyranosyl side chains, extracted from Aureobasidium pullulans (AP-FBG). Although the biological effects of beta-D-glucans are known to depend on their structures, the effects of a highly branched 1,3-beta-D-glucan on the production of cytokines by leukocytes in mice have not yet been elucidated. In this study, we found that AP-FBG strongly induced the production of various cytokines, especially Th1 cytokines (e.g., IFN-gamma and IL-12p70) and Th17 cytokines (e.g., IL-17A), but did not induce the production of IL-4, IL-10, and TNF-alpha in DBA/2 Mouse-derived splenocytes in vitro.

  • Histopathological examination and analysis of mortality in DBA/2 Mouse vasculitis induced with CAWS, a water-soluble extracellular polysaccharide fraction obtained from Candida albicans
    Yakugaku zasshi : Journal of the Pharmaceutical Society of Japan, 2006
    Co-Authors: Naoto Hirata, Ken-ichi Ishibashi, Shin Ohta, Satoru Hata, Hiroyasu Shinohara, Mio Kitamura, Noriko Miura, Naohito Ohno
    Abstract:

    CAWS, a water-soluble extracellular polysaccharide fraction obtained from the culture supernatant of Candida albicans, is one of the fungal pathogen-associated molecular patterns (PAMPs). It has been reported to show potent activity inducing arteritis and coronaritis in mice. Especially, CAWS-induced arteritis has a 100% incidence and severe mortality in the DBA/2 Mouse strain. This artificial vasculitis was reported to provide a good murine model of Kawasaki disease and other inflammatory vascular disease. However, severe mortality was observed only in DBA/2 mice, which is a CAWS-sensitive strain. In this study, to clarify the mechanisms of CAWS-induced arteritis and mortality, we investigated microscopic histopathological changes in cardiovascular tissues in DBA/2 mice. Severe inflammatory infiltration was observed from the external elastic lamina in the aorta and proximal coronary arteries within 1 week after CAWS administration. Severe stenosis of the aorta and coronary arteries was observed more than 3 weeks after CAWS administration. Fibrinoid necrosis was observed in these vessel walls. All CAWS-treated mice died between the fifth and twelfth week after administration. Severe inflammatory change with aortic valve transformation suggested that CAWS-treated mice died of valvular endocarditis or cardiac dysfunction. Based on the simple induction method and complete incidence, these data suggest that CAWS-induced arteritis is a good model of not only Kawasaki disease but also other cardiovascular diseases such as valvular endocarditis.

  • histopathological examination and analysis of mortality in DBA 2 Mouse vasculitis induced with caws a water soluble extracellular polysaccharide fraction obtained from candida albicans
    Yakugaku Zasshi-journal of The Pharmaceutical Society of Japan, 2006
    Co-Authors: Naoto Hirata, Ken-ichi Ishibashi, Shin Ohta, Satoru Hata, Hiroyasu Shinohara, Mio Kitamura, Noriko Miura, Naohito Ohno
    Abstract:

    CAWS, a water-soluble extracellular polysaccharide fraction obtained from the culture supernatant of Candida albicans, is one of the fungal pathogen-associated molecular patterns (PAMPs). It has been reported to show potent activity inducing arteritis and coronaritis in mice. Especially, CAWS-induced arteritis has a 100% incidence and severe mortality in the DBA/2 Mouse strain. This artificial vasculitis was reported to provide a good murine model of Kawasaki disease and other inflammatory vascular disease. However, severe mortality was observed only in DBA/2 mice, which is a CAWS-sensitive strain. In this study, to clarify the mechanisms of CAWS-induced arteritis and mortality, we investigated microscopic histopathological changes in cardiovascular tissues in DBA/2 mice. Severe inflammatory infiltration was observed from the external elastic lamina in the aorta and proximal coronary arteries within 1 week after CAWS administration. Severe stenosis of the aorta and coronary arteries was observed more than 3 weeks after CAWS administration. Fibrinoid necrosis was observed in these vessel walls. All CAWS-treated mice died between the fifth and twelfth week after administration. Severe inflammatory change with aortic valve transformation suggested that CAWS-treated mice died of valvular endocarditis or cardiac dysfunction. Based on the simple induction method and complete incidence, these data suggest that CAWS-induced arteritis is a good model of not only Kawasaki disease but also other cardiovascular diseases such as valvular endocarditis.

Esther Wilk - One of the best experts on this subject based on the ideXlab platform.

  • segregation of a spontaneous klrd1 cd94 mutation in DBA 2 Mouse substrains
    G3: Genes Genomes Genetics, 2015
    Co-Authors: Dai Lun Shin, Ashutosh K. Pandey, Jesse D. Ziebarth, Megan K. Mulligan, Robert W. Williams, Robert Geffers, Bastian Hatesuer, Klaus Schughart, Esther Wilk
    Abstract:

    Current model DBA/2J (D2J) mice lack CD94 expression due to a deletion spanning the last coding exon of the Klrd1 gene that occurred in the mid- to late 1980s. In contrast, DBA/2JRj (D2Rj) mice, crosses derived from DBA/2J before 1984, and C57BL/6J (B6) mice lack the deletion and have normal CD94 expression. For example, BXD lines (BXD1–32) generated in the 1970s by crossing B6 and D2J do not segregate for the exonic deletion and have high expression, whereas BXD lines 33 and greater were generated after 1990 are segregating for the deletion and have highly variable Klrd1 expression. We performed quantitative trait locus analysis of Klrd1 expression by using BXD lines with different generation times and found that the expression difference in Klrd1 in the later BXD set is driven by a strong cis-acting expression quantitative trait locus. Although the Klrd1/CD94 locus is essential for Mousepox resistance, the genetic variation among D2 substrains and the later set of BXD strains is not associated with susceptibility to the Influenza A virus PR8 strain. Substrains with nearly identical genetic backgrounds that are segregating functional variants such as the Klrd1 deletion are useful genetic tools to investigate biological function.

  • Segregation of a Spontaneous Klrd1 (CD94) Mutation in DBA/2 Mouse Substrains
    G3 (Bethesda Md.), 2014
    Co-Authors: Dai Lun Shin, Ashutosh K. Pandey, Jesse D. Ziebarth, Megan K. Mulligan, Robert W. Williams, Robert Geffers, Bastian Hatesuer, Klaus Schughart, Esther Wilk
    Abstract:

    Current model DBA/2J (D2J) mice lack CD94 expression due to a deletion spanning the last coding exon of the Klrd1 gene that occurred in the mid- to late 1980s. In contrast, DBA/2JRj (D2Rj) mice, crosses derived from DBA/2J before 1984, and C57BL/6J (B6) mice lack the deletion and have normal CD94 expression. For example, BXD lines (BXD1–32) generated in the 1970s by crossing B6 and D2J do not segregate for the exonic deletion and have high expression, whereas BXD lines 33 and greater were generated after 1990 are segregating for the deletion and have highly variable Klrd1 expression. We performed quantitative trait locus analysis of Klrd1 expression by using BXD lines with different generation times and found that the expression difference in Klrd1 in the later BXD set is driven by a strong cis-acting expression quantitative trait locus. Although the Klrd1/CD94 locus is essential for Mousepox resistance, the genetic variation among D2 substrains and the later set of BXD strains is not associated with susceptibility to the Influenza A virus PR8 strain. Substrains with nearly identical genetic backgrounds that are segregating functional variants such as the Klrd1 deletion are useful genetic tools to investigate biological function.

Robert S. Bitner - One of the best experts on this subject based on the ideXlab platform.

Dai Lun Shin - One of the best experts on this subject based on the ideXlab platform.

  • segregation of a spontaneous klrd1 cd94 mutation in DBA 2 Mouse substrains
    G3: Genes Genomes Genetics, 2015
    Co-Authors: Dai Lun Shin, Ashutosh K. Pandey, Jesse D. Ziebarth, Megan K. Mulligan, Robert W. Williams, Robert Geffers, Bastian Hatesuer, Klaus Schughart, Esther Wilk
    Abstract:

    Current model DBA/2J (D2J) mice lack CD94 expression due to a deletion spanning the last coding exon of the Klrd1 gene that occurred in the mid- to late 1980s. In contrast, DBA/2JRj (D2Rj) mice, crosses derived from DBA/2J before 1984, and C57BL/6J (B6) mice lack the deletion and have normal CD94 expression. For example, BXD lines (BXD1–32) generated in the 1970s by crossing B6 and D2J do not segregate for the exonic deletion and have high expression, whereas BXD lines 33 and greater were generated after 1990 are segregating for the deletion and have highly variable Klrd1 expression. We performed quantitative trait locus analysis of Klrd1 expression by using BXD lines with different generation times and found that the expression difference in Klrd1 in the later BXD set is driven by a strong cis-acting expression quantitative trait locus. Although the Klrd1/CD94 locus is essential for Mousepox resistance, the genetic variation among D2 substrains and the later set of BXD strains is not associated with susceptibility to the Influenza A virus PR8 strain. Substrains with nearly identical genetic backgrounds that are segregating functional variants such as the Klrd1 deletion are useful genetic tools to investigate biological function.

  • Segregation of a Spontaneous Klrd1 (CD94) Mutation in DBA/2 Mouse Substrains
    G3 (Bethesda Md.), 2014
    Co-Authors: Dai Lun Shin, Ashutosh K. Pandey, Jesse D. Ziebarth, Megan K. Mulligan, Robert W. Williams, Robert Geffers, Bastian Hatesuer, Klaus Schughart, Esther Wilk
    Abstract:

    Current model DBA/2J (D2J) mice lack CD94 expression due to a deletion spanning the last coding exon of the Klrd1 gene that occurred in the mid- to late 1980s. In contrast, DBA/2JRj (D2Rj) mice, crosses derived from DBA/2J before 1984, and C57BL/6J (B6) mice lack the deletion and have normal CD94 expression. For example, BXD lines (BXD1–32) generated in the 1970s by crossing B6 and D2J do not segregate for the exonic deletion and have high expression, whereas BXD lines 33 and greater were generated after 1990 are segregating for the deletion and have highly variable Klrd1 expression. We performed quantitative trait locus analysis of Klrd1 expression by using BXD lines with different generation times and found that the expression difference in Klrd1 in the later BXD set is driven by a strong cis-acting expression quantitative trait locus. Although the Klrd1/CD94 locus is essential for Mousepox resistance, the genetic variation among D2 substrains and the later set of BXD strains is not associated with susceptibility to the Influenza A virus PR8 strain. Substrains with nearly identical genetic backgrounds that are segregating functional variants such as the Klrd1 deletion are useful genetic tools to investigate biological function.