The Experts below are selected from a list of 4692 Experts worldwide ranked by ideXlab platform
Kenneth M. Tramposch - One of the best experts on this subject based on the ideXlab platform.
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inhibition of Immune Complex induced inflammation by a small molecular weight selectin antagonist
Mediators of Inflammation, 1994Co-Authors: Xina Nair, Gordon Todderud, Lynda Beth Davern, Alejandro Aruffo, Kenneth M. TramposchAbstract:The anti-inflammatory effect of a small molecular weight antagonist of P- and E-selectin-dependent cell adhesion was examined. The glycolipid sulphatide was shown to block the adherence of thrombin-activated rat platelets to HL-60 cells. This interaction is known to be dependent on P-selectin. The rat dermal reverse passive Arthus reaction was used to assess the effect of sulphatide on a neutrophil dependent inflammatory response. Sulphatide dosedependently blocked both the vascular permeability increase and cell infiltration after intraperitoneal administration. These results show that a small molecular weight compound which blocks P- and E-selectin dependent adhesion in vitro can effectively block the inflammation due to Immune Complex Deposition. A compound with this type of profile may have therapeutic potential in the treatment of Immune Complex mediated diseases.
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inhibition of Immune Complex induced inflammation by a small molecular weight selectin antagonist
Mediators of Inflammation, 1994Co-Authors: Xina Nair, Gordon Todderud, Lynda Beth Davern, Alejandro Aruffo, Kenneth M. TramposchAbstract:The anti-inflammatory effect of a small molecular weight antagonist of P- and E-selectin-dependent cell adhesion was examined. The glycolipid sulphatide was shown to block the adherence of thrombin-activated rat platelets to HL-60 cells. This interaction is known to be dependent on P-selectin. The rat dermal reverse passive Arthus reaction was used to assess the effect of sulphatide on a neutrophil dependent inflammatory response. Sulphatide dosedependently blocked both the vascular permeability increase and cell infiltration after intraperitoneal administration. These results show that a small molecular weight compound which blocks P- and E-selectin dependent adhesion in vitro can effectively block the inflammation due to Immune Complex Deposition. A compound with this type of profile may have therapeutic potential in the treatment of Immune Complex mediated diseases.
Masheka A Barrett - One of the best experts on this subject based on the ideXlab platform.
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complement receptor 1 and 2 deficiency increases coxsackievirus b3 induced myocarditis dilated cardiomyopathy and heart failure by increasing macrophages il 1β and Immune Complex Deposition in the heart
Journal of Immunology, 2006Co-Authors: De Lisa Fairweather, Sylvia Frisanchokiss, Dolores B Njoku, Jennifer F Nyland, Ziya Kaya, Susy A Yusung, Sarah E Davis, Augusto J Frisancho, Masheka A BarrettAbstract:Complement and complement receptors (CR) play a central role in Immune defense by initiating the rapid destruction of invading microorganisms, amplifying the innate and adaptive Immune responses, and mediating solubilization and clearance of Immune Complexes. Defects in the expression of C or CR have been associated with loss of tolerance to self proteins and the development of Immune Complex-mediated autoImmune diseases such as systemic lupus erythematosus. In this study, we examined the role of CR on coxsackievirus B3 (CVB3)-induced myocarditis using mice deficient in CR1/2. We found that CR1/2 deficiency significantly increased acute CVB3 myocarditis and pericardial fibrosis resulting in early progression to dilated cardiomyopathy and heart failure. The increase in inflammation was not due to increased viral replication, which was not significantly altered in the hearts of CR1/2-deficient mice, but was associated with increased numbers of macrophages, IL-1β levels, and Immune Complex Deposition in the heart. The complement regulatory protein, CR1-related gene/protein Y (Crry), was increased on cardiac macrophage populations, while immature B220 low B cells were increased in the spleen of CR1/2-deficient mice during acute CVB3-induced myocarditis. These results show that expression of CR1/2 is not necessary for effective clearance of CVB3 infection, but prevents Immune-mediated damage to the heart.
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complement receptor 1 and 2 deficiency increases coxsackievirus b3 induced myocarditis dilated cardiomyopathy and heart failure by increasing macrophages il 1β and Immune Complex Deposition in the heart
Journal of Immunology, 2006Co-Authors: De Lisa Fairweather, Sylvia Frisanchokiss, Dolores B Njoku, Jennifer F Nyland, Ziya Kaya, Susy A Yusung, Sarah E Davis, Augusto J Frisancho, Masheka A BarrettAbstract:Complement and complement receptors (CR) play a central role in Immune defense by initiating the rapid destruction of invading microorganisms, amplifying the innate and adaptive Immune responses, and mediating solubilization and clearance of Immune Complexes. Defects in the expression of C or CR have been associated with loss of tolerance to self proteins and the development of Immune Complex-mediated autoImmune diseases such as systemic lupus erythematosus. In this study, we examined the role of CR on coxsackievirus B3 (CVB3)-induced myocarditis using mice deficient in CR1/2. We found that CR1/2 deficiency significantly increased acute CVB3 myocarditis and pericardial fibrosis resulting in early progression to dilated cardiomyopathy and heart failure. The increase in inflammation was not due to increased viral replication, which was not significantly altered in the hearts of CR1/2-deficient mice, but was associated with increased numbers of macrophages, IL-1beta levels, and Immune Complex Deposition in the heart. The complement regulatory protein, CR1-related gene/protein Y (Crry), was increased on cardiac macrophage populations, while immature B220(low) B cells were increased in the spleen of CR1/2-deficient mice during acute CVB3-induced myocarditis. These results show that expression of CR1/2 is not necessary for effective clearance of CVB3 infection, but prevents Immune-mediated damage to the heart.
Ziya Kaya - One of the best experts on this subject based on the ideXlab platform.
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complement receptor 1 and 2 deficiency increases coxsackievirus b3 induced myocarditis dilated cardiomyopathy and heart failure by increasing macrophages il 1β and Immune Complex Deposition in the heart
Journal of Immunology, 2006Co-Authors: De Lisa Fairweather, Sylvia Frisanchokiss, Dolores B Njoku, Jennifer F Nyland, Ziya Kaya, Susy A Yusung, Sarah E Davis, Augusto J Frisancho, Masheka A BarrettAbstract:Complement and complement receptors (CR) play a central role in Immune defense by initiating the rapid destruction of invading microorganisms, amplifying the innate and adaptive Immune responses, and mediating solubilization and clearance of Immune Complexes. Defects in the expression of C or CR have been associated with loss of tolerance to self proteins and the development of Immune Complex-mediated autoImmune diseases such as systemic lupus erythematosus. In this study, we examined the role of CR on coxsackievirus B3 (CVB3)-induced myocarditis using mice deficient in CR1/2. We found that CR1/2 deficiency significantly increased acute CVB3 myocarditis and pericardial fibrosis resulting in early progression to dilated cardiomyopathy and heart failure. The increase in inflammation was not due to increased viral replication, which was not significantly altered in the hearts of CR1/2-deficient mice, but was associated with increased numbers of macrophages, IL-1β levels, and Immune Complex Deposition in the heart. The complement regulatory protein, CR1-related gene/protein Y (Crry), was increased on cardiac macrophage populations, while immature B220 low B cells were increased in the spleen of CR1/2-deficient mice during acute CVB3-induced myocarditis. These results show that expression of CR1/2 is not necessary for effective clearance of CVB3 infection, but prevents Immune-mediated damage to the heart.
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complement receptor 1 and 2 deficiency increases coxsackievirus b3 induced myocarditis dilated cardiomyopathy and heart failure by increasing macrophages il 1β and Immune Complex Deposition in the heart
Journal of Immunology, 2006Co-Authors: De Lisa Fairweather, Sylvia Frisanchokiss, Dolores B Njoku, Jennifer F Nyland, Ziya Kaya, Susy A Yusung, Sarah E Davis, Augusto J Frisancho, Masheka A BarrettAbstract:Complement and complement receptors (CR) play a central role in Immune defense by initiating the rapid destruction of invading microorganisms, amplifying the innate and adaptive Immune responses, and mediating solubilization and clearance of Immune Complexes. Defects in the expression of C or CR have been associated with loss of tolerance to self proteins and the development of Immune Complex-mediated autoImmune diseases such as systemic lupus erythematosus. In this study, we examined the role of CR on coxsackievirus B3 (CVB3)-induced myocarditis using mice deficient in CR1/2. We found that CR1/2 deficiency significantly increased acute CVB3 myocarditis and pericardial fibrosis resulting in early progression to dilated cardiomyopathy and heart failure. The increase in inflammation was not due to increased viral replication, which was not significantly altered in the hearts of CR1/2-deficient mice, but was associated with increased numbers of macrophages, IL-1beta levels, and Immune Complex Deposition in the heart. The complement regulatory protein, CR1-related gene/protein Y (Crry), was increased on cardiac macrophage populations, while immature B220(low) B cells were increased in the spleen of CR1/2-deficient mice during acute CVB3-induced myocarditis. These results show that expression of CR1/2 is not necessary for effective clearance of CVB3 infection, but prevents Immune-mediated damage to the heart.
Xina Nair - One of the best experts on this subject based on the ideXlab platform.
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inhibition of Immune Complex induced inflammation by a small molecular weight selectin antagonist
Mediators of Inflammation, 1994Co-Authors: Xina Nair, Gordon Todderud, Lynda Beth Davern, Alejandro Aruffo, Kenneth M. TramposchAbstract:The anti-inflammatory effect of a small molecular weight antagonist of P- and E-selectin-dependent cell adhesion was examined. The glycolipid sulphatide was shown to block the adherence of thrombin-activated rat platelets to HL-60 cells. This interaction is known to be dependent on P-selectin. The rat dermal reverse passive Arthus reaction was used to assess the effect of sulphatide on a neutrophil dependent inflammatory response. Sulphatide dosedependently blocked both the vascular permeability increase and cell infiltration after intraperitoneal administration. These results show that a small molecular weight compound which blocks P- and E-selectin dependent adhesion in vitro can effectively block the inflammation due to Immune Complex Deposition. A compound with this type of profile may have therapeutic potential in the treatment of Immune Complex mediated diseases.
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inhibition of Immune Complex induced inflammation by a small molecular weight selectin antagonist
Mediators of Inflammation, 1994Co-Authors: Xina Nair, Gordon Todderud, Lynda Beth Davern, Alejandro Aruffo, Kenneth M. TramposchAbstract:The anti-inflammatory effect of a small molecular weight antagonist of P- and E-selectin-dependent cell adhesion was examined. The glycolipid sulphatide was shown to block the adherence of thrombin-activated rat platelets to HL-60 cells. This interaction is known to be dependent on P-selectin. The rat dermal reverse passive Arthus reaction was used to assess the effect of sulphatide on a neutrophil dependent inflammatory response. Sulphatide dosedependently blocked both the vascular permeability increase and cell infiltration after intraperitoneal administration. These results show that a small molecular weight compound which blocks P- and E-selectin dependent adhesion in vitro can effectively block the inflammation due to Immune Complex Deposition. A compound with this type of profile may have therapeutic potential in the treatment of Immune Complex mediated diseases.
De Lisa Fairweather - One of the best experts on this subject based on the ideXlab platform.
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complement receptor 1 and 2 deficiency increases coxsackievirus b3 induced myocarditis dilated cardiomyopathy and heart failure by increasing macrophages il 1β and Immune Complex Deposition in the heart
Journal of Immunology, 2006Co-Authors: De Lisa Fairweather, Sylvia Frisanchokiss, Dolores B Njoku, Jennifer F Nyland, Ziya Kaya, Susy A Yusung, Sarah E Davis, Augusto J Frisancho, Masheka A BarrettAbstract:Complement and complement receptors (CR) play a central role in Immune defense by initiating the rapid destruction of invading microorganisms, amplifying the innate and adaptive Immune responses, and mediating solubilization and clearance of Immune Complexes. Defects in the expression of C or CR have been associated with loss of tolerance to self proteins and the development of Immune Complex-mediated autoImmune diseases such as systemic lupus erythematosus. In this study, we examined the role of CR on coxsackievirus B3 (CVB3)-induced myocarditis using mice deficient in CR1/2. We found that CR1/2 deficiency significantly increased acute CVB3 myocarditis and pericardial fibrosis resulting in early progression to dilated cardiomyopathy and heart failure. The increase in inflammation was not due to increased viral replication, which was not significantly altered in the hearts of CR1/2-deficient mice, but was associated with increased numbers of macrophages, IL-1β levels, and Immune Complex Deposition in the heart. The complement regulatory protein, CR1-related gene/protein Y (Crry), was increased on cardiac macrophage populations, while immature B220 low B cells were increased in the spleen of CR1/2-deficient mice during acute CVB3-induced myocarditis. These results show that expression of CR1/2 is not necessary for effective clearance of CVB3 infection, but prevents Immune-mediated damage to the heart.
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complement receptor 1 and 2 deficiency increases coxsackievirus b3 induced myocarditis dilated cardiomyopathy and heart failure by increasing macrophages il 1β and Immune Complex Deposition in the heart
Journal of Immunology, 2006Co-Authors: De Lisa Fairweather, Sylvia Frisanchokiss, Dolores B Njoku, Jennifer F Nyland, Ziya Kaya, Susy A Yusung, Sarah E Davis, Augusto J Frisancho, Masheka A BarrettAbstract:Complement and complement receptors (CR) play a central role in Immune defense by initiating the rapid destruction of invading microorganisms, amplifying the innate and adaptive Immune responses, and mediating solubilization and clearance of Immune Complexes. Defects in the expression of C or CR have been associated with loss of tolerance to self proteins and the development of Immune Complex-mediated autoImmune diseases such as systemic lupus erythematosus. In this study, we examined the role of CR on coxsackievirus B3 (CVB3)-induced myocarditis using mice deficient in CR1/2. We found that CR1/2 deficiency significantly increased acute CVB3 myocarditis and pericardial fibrosis resulting in early progression to dilated cardiomyopathy and heart failure. The increase in inflammation was not due to increased viral replication, which was not significantly altered in the hearts of CR1/2-deficient mice, but was associated with increased numbers of macrophages, IL-1beta levels, and Immune Complex Deposition in the heart. The complement regulatory protein, CR1-related gene/protein Y (Crry), was increased on cardiac macrophage populations, while immature B220(low) B cells were increased in the spleen of CR1/2-deficient mice during acute CVB3-induced myocarditis. These results show that expression of CR1/2 is not necessary for effective clearance of CVB3 infection, but prevents Immune-mediated damage to the heart.
