The Experts below are selected from a list of 111 Experts worldwide ranked by ideXlab platform
Orlando Paciello - One of the best experts on this subject based on the ideXlab platform.
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Role of serotonergic system in the pathogenesis of fibrosis in canine idiopathic inflammatory myopathies
Neuromuscular disorders : NMD, 2012Co-Authors: Luigi Michele Pavone, S Papparella, Silvana Rea, Francesca Trapani, Valeria De Pasquale, Simona Tafuri, Orlando PacielloAbstract:Idiopathic inflammatory myopathies are Muscle diseases characterized by inflammation, necrosis, and fibrosis. The neurotransmitter serotonin (5-HT) has been shown to promote fibrosis in many tissues and organs by activating TGFβ-1 signaling. In this study, we evaluated the potential role of 5-HT in the pathogenesis of fibrosis in canine idiopathic inflammatory myopathies. Muscle biopsies from dogs affected by Masticatory Muscle Myositis or polyMyositis and from healthy dogs were processed for immunohistochemistry and Western blotting. The immunohistochemical analysis showed a strong expression of 5-HT in Muscle tissues of affected dogs, whereas the amine was absent in the Muscles of healthy dogs. Biochemical analysis showed increased expression levels of the selective 5-HT2A receptor in the Muscle specimens of the most severely affected dogs versus controls. Further, increased phosphorylation levels of the TGFβ-1 signaling mediators SMAD2/3 and ERK1/2 were detected in tissue samples from affected dogs as compared to tissues from healthy dogs. Although further studies are needed, our findings highlight for the first time a potential role of 5-HT in the development of fibrosis in canine idiopathic inflammatory myopathies, thus supporting other evidence that 5-HT pro-fibrotic activity occurs via activation of TGFβ-1 signaling pathway.
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Role of serotonergic system in the pathogenesis of fibrosis in canine idiopathic inflammatory myopathies
'Elsevier BV', 2012Co-Authors: Luigi Michele Pavone, S Papparella, Silvana Rea, Francesca Trapani, Valeria De Pasquale, Simona Tafuri, Orlando PacielloAbstract:Idiopathic inflammatory myopathies are Muscle diseases characterized by inflammation, necrosis, and fibrosis. The neurotransmitter serotonin (5-HT) has been shown to promote fibrosis in many tissues and organs by activating TGF beta-1 signaling. In this study, we evaluated the potential role of 5-HT in the pathogenesis of fibrosis in canine idiopathic inflammatory myopathies. Muscle biopsies from dogs affected by Masticatory Muscle Myositis or polyMyositis and from healthy dogs were processed for immunohistochemistry and Western blotting. The immunohistochemical analysis showed a strong expression of 5-HT in Muscle tissues of affected dogs, whereas the amine was absent in the Muscles of healthy dogs. Biochemical analysis showed increased expression levels of the selective 5-HT2A receptor in the Muscle specimens of the most severely affected dogs versus controls. Further, increased phosphorylation levels of the TGF beta-1 signaling mediators SMAD2/3 and ERK1/2 were detected in tissue samples from affected dogs as compared to tissues from healthy clogs. Although further studies are needed, our findings highlight for the first time a potential role of 5-HT in the development of fibrosis in canine idiopathic inflammatory myopathies, thus supporting other evidence that 5-HT pro-fibrotic activity occurs via activation of TGF beta-1 signaling pathway. (C) 2012 Elsevier B.V. All rights reserved
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expression of major histocompatibility complex class i and class ii antigens in canine Masticatory Muscle Myositis
Neuromuscular Disorders, 2007Co-Authors: Orlando Paciello, Diane G Shelton, S PapparellaAbstract:Studies in human immune-mediated inflammatory myopathies have documented expression of major histocompatibility complex class I (MHC class I) and class II (MHC class II) antigens on Muscle fiber membranes in the presence or absence of cellular infiltration. Here we evaluate the presence and distribution of these antigens in canine Masticatory Muscle Myositis, an immune-mediated inflammatory myopathy. Twelve samples of temporalis and masseter Muscles from dogs with a clinical diagnosis of canine Masticatory Muscle Myositis were examined by immunohistochemistry and double-immunofluorescence confocal microscopy. MHC class I and class II antigens were expressed in Muscle fibers independent of inflammatory cell infiltration. Furthermore MHC class I and class II antigens were expressed on the sarcolemma and co-localized with dystrophin. Our results suggest that MHC class I and class II expression in canine Masticatory Muscle Myositis may play a role in the initiation and maintenance of the pathological condition, rather than just a consequence of a preceding local inflammation.
T. Bilzer - One of the best experts on this subject based on the ideXlab platform.
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evidence for mhc i restricted cd8 t cell mediated immunopathology in canine Masticatory Muscle Myositis and polyMyositis
Muscle & Nerve, 2006Co-Authors: J. Neumann, T. BilzerAbstract:Masticatory Muscle Myositis (MMM) is the most common inflammatory myopathy (IM) in dogs, associated with antibodies against myosin. To further elucidate the immunopathogenesis, we investigated Muscles of 53 dogs with MMM, 32 dogs with polyMyositis (PM), and 4 dogs suffering from both, with regard to the presence and location of CD4 + and CD8 + T cells, B cells, macrophages, major histocompatibility complex (MHC) class I and class II antigens, and autoantibodies. CD8 + T cells were found in MMM (91%) and PM (75%), mostly paralleled (68% and 61%) by enhanced expression of MHC class I antigen on Muscle fibers. CD8 + T cells invading intact and neighboring necrotic Muscle fibers were present in MMM (39%) and PM (42%). Dogs with MMM lacking intramuscular (26%) and circulating (36%) autoantibodies also had CD8 + T-cell infiltrations and Muscle-fiber lesions. Since MHC class I antigen and CD8 + T cells were detected in the presence of CD4 + T cells, regardless of antimuscular antibodies, we consider MMM and PM in the dog as a CD8 + T-cell-mediated immuno-pathological disease that initiates Muscle-fiber destruction and leads to production of myosin autoantibodies.
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Evidence for MHC I–restricted CD8+ T-cell–mediated immunopathology in canine Masticatory Muscle Myositis and polyMyositis
Muscle & nerve, 2006Co-Authors: J. Neumann, T. BilzerAbstract:Masticatory Muscle Myositis (MMM) is the most common inflammatory myopathy (IM) in dogs, associated with antibodies against myosin. To further elucidate the immunopathogenesis, we investigated Muscles of 53 dogs with MMM, 32 dogs with polyMyositis (PM), and 4 dogs suffering from both, with regard to the presence and location of CD4 + and CD8 + T cells, B cells, macrophages, major histocompatibility complex (MHC) class I and class II antigens, and autoantibodies. CD8 + T cells were found in MMM (91%) and PM (75%), mostly paralleled (68% and 61%) by enhanced expression of MHC class I antigen on Muscle fibers. CD8 + T cells invading intact and neighboring necrotic Muscle fibers were present in MMM (39%) and PM (42%). Dogs with MMM lacking intramuscular (26%) and circulating (36%) autoantibodies also had CD8 + T-cell infiltrations and Muscle-fiber lesions. Since MHC class I antigen and CD8 + T cells were detected in the presence of CD4 + T cells, regardless of antimuscular antibodies, we consider MMM and PM in the dog as a CD8 + T-cell-mediated immuno-pathological disease that initiates Muscle-fiber destruction and leads to production of myosin autoantibodies.
Diane G Shelton - One of the best experts on this subject based on the ideXlab platform.
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life threatening complication associated with anesthesia in a dog with Masticatory Muscle Myositis
Veterinary Surgery, 2009Co-Authors: Beatrix Nanai, Lesley Phillips, Jeffrey S Christiansen, Diane G SheltonAbstract:Objective— To report a serious complication in a dog with Masticatory Muscle Myositis (MMM) that occurred during general anesthesia for diagnostic testing. Study Design— Case report. Animals— A 2-year-old male Pug. Methods— MMM was diagnosed in a Pug with a 2-week history of trismus by electrodiagnostics, histopathology, and 2M antibody test. During anesthesia tongue protrusion occurred and because of trismus, an inability to reposition the tongue resulted in venous congestion and severe swelling. Forceful physical attempts and subsequent removal of the rostral digastricus and masseter Muscle attachments from the mandible did not increase jaw mobility. Mandibular symphysiotomy was necessary to resolve lingual venous congestion and to reposition the tongue into the oral cavity. Results— Tongue swelling rapidly subsided after symphysiotomy allowing the tongue to be repositioned into the oral cavity. After treatment of MMM with corticosteroids, jaw range of motion improved and at 6 months was ∼70% normal. Conclusions— Trismus could not be overcome by detachment of the masseter and digastricus Muscle insertions from the mandible, and symphysiotomy was required to reposition the tongue in the oral cavity. Clinical Relevance— In dogs with MMM, tongue position should be monitored during anesthesia to avoid inadvertent protrusion and swelling from venous congestion. Use of anesthetic monitoring equipment on the tongue, such as a pulse oximeter probe, should be avoided in these patients.
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autoantibodies in canine Masticatory Muscle Myositis recognize a novel myosin binding protein c family member
Journal of Immunology, 2007Co-Authors: Randolph Brooks, Elizabeth A Komives, Justin W Torpey, Eva Engvall, Steven L Gonias, Diane G SheltonAbstract:Inflammatory myopathies are a group of autoimmune diseases that affect Muscles. In humans, the most common inflammatory myopathies are polyMyositis, dermatoMyositis, and inclusion body Myositis. Autoantibodies may be found in humans with inflammatory myopathies, and these play an important role in diagnosis and disease classification. However, these Abs are typically not Muscle specific. Spontaneously occurring canine inflammatory myopathies may be good parallel disorders and provide insights into human Myositis. In dogs with inflammatory myopathy, Muscle-specific autoantibodies have been found, especially in Masticatory Muscle Myositis. We have identified the major Ag recognized by the autoantibodies in canine Masticatory Muscle Myositis. This Ag is a novel member of the myosin binding protein-C family, which we call Masticatory myosin binding protein-C (mMyBP-C). mMyBP-C is localized not only within the Masticatory Muscle fibers, but also at or near their cell surface, perhaps making it accessible as an immunogen. The gene for mMyBP-C also exists in humans, and mMyBP-C could potentially play a role in certain human inflammatory myopathies. Understanding the role of mMyBP-C in this canine inflammatory myopathy may advance our knowledge of mechanisms of autoimmune inflammatory Muscle diseases, not only in dogs, but also in humans.
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expression of major histocompatibility complex class i and class ii antigens in canine Masticatory Muscle Myositis
Neuromuscular Disorders, 2007Co-Authors: Orlando Paciello, Diane G Shelton, S PapparellaAbstract:Studies in human immune-mediated inflammatory myopathies have documented expression of major histocompatibility complex class I (MHC class I) and class II (MHC class II) antigens on Muscle fiber membranes in the presence or absence of cellular infiltration. Here we evaluate the presence and distribution of these antigens in canine Masticatory Muscle Myositis, an immune-mediated inflammatory myopathy. Twelve samples of temporalis and masseter Muscles from dogs with a clinical diagnosis of canine Masticatory Muscle Myositis were examined by immunohistochemistry and double-immunofluorescence confocal microscopy. MHC class I and class II antigens were expressed in Muscle fibers independent of inflammatory cell infiltration. Furthermore MHC class I and class II antigens were expressed on the sarcolemma and co-localized with dystrophin. Our results suggest that MHC class I and class II expression in canine Masticatory Muscle Myositis may play a role in the initiation and maintenance of the pathological condition, rather than just a consequence of a preceding local inflammation.
S Papparella - One of the best experts on this subject based on the ideXlab platform.
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Role of serotonergic system in the pathogenesis of fibrosis in canine idiopathic inflammatory myopathies
Neuromuscular disorders : NMD, 2012Co-Authors: Luigi Michele Pavone, S Papparella, Silvana Rea, Francesca Trapani, Valeria De Pasquale, Simona Tafuri, Orlando PacielloAbstract:Idiopathic inflammatory myopathies are Muscle diseases characterized by inflammation, necrosis, and fibrosis. The neurotransmitter serotonin (5-HT) has been shown to promote fibrosis in many tissues and organs by activating TGFβ-1 signaling. In this study, we evaluated the potential role of 5-HT in the pathogenesis of fibrosis in canine idiopathic inflammatory myopathies. Muscle biopsies from dogs affected by Masticatory Muscle Myositis or polyMyositis and from healthy dogs were processed for immunohistochemistry and Western blotting. The immunohistochemical analysis showed a strong expression of 5-HT in Muscle tissues of affected dogs, whereas the amine was absent in the Muscles of healthy dogs. Biochemical analysis showed increased expression levels of the selective 5-HT2A receptor in the Muscle specimens of the most severely affected dogs versus controls. Further, increased phosphorylation levels of the TGFβ-1 signaling mediators SMAD2/3 and ERK1/2 were detected in tissue samples from affected dogs as compared to tissues from healthy dogs. Although further studies are needed, our findings highlight for the first time a potential role of 5-HT in the development of fibrosis in canine idiopathic inflammatory myopathies, thus supporting other evidence that 5-HT pro-fibrotic activity occurs via activation of TGFβ-1 signaling pathway.
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Role of serotonergic system in the pathogenesis of fibrosis in canine idiopathic inflammatory myopathies
'Elsevier BV', 2012Co-Authors: Luigi Michele Pavone, S Papparella, Silvana Rea, Francesca Trapani, Valeria De Pasquale, Simona Tafuri, Orlando PacielloAbstract:Idiopathic inflammatory myopathies are Muscle diseases characterized by inflammation, necrosis, and fibrosis. The neurotransmitter serotonin (5-HT) has been shown to promote fibrosis in many tissues and organs by activating TGF beta-1 signaling. In this study, we evaluated the potential role of 5-HT in the pathogenesis of fibrosis in canine idiopathic inflammatory myopathies. Muscle biopsies from dogs affected by Masticatory Muscle Myositis or polyMyositis and from healthy dogs were processed for immunohistochemistry and Western blotting. The immunohistochemical analysis showed a strong expression of 5-HT in Muscle tissues of affected dogs, whereas the amine was absent in the Muscles of healthy dogs. Biochemical analysis showed increased expression levels of the selective 5-HT2A receptor in the Muscle specimens of the most severely affected dogs versus controls. Further, increased phosphorylation levels of the TGF beta-1 signaling mediators SMAD2/3 and ERK1/2 were detected in tissue samples from affected dogs as compared to tissues from healthy clogs. Although further studies are needed, our findings highlight for the first time a potential role of 5-HT in the development of fibrosis in canine idiopathic inflammatory myopathies, thus supporting other evidence that 5-HT pro-fibrotic activity occurs via activation of TGF beta-1 signaling pathway. (C) 2012 Elsevier B.V. All rights reserved
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expression of major histocompatibility complex class i and class ii antigens in canine Masticatory Muscle Myositis
Neuromuscular Disorders, 2007Co-Authors: Orlando Paciello, Diane G Shelton, S PapparellaAbstract:Studies in human immune-mediated inflammatory myopathies have documented expression of major histocompatibility complex class I (MHC class I) and class II (MHC class II) antigens on Muscle fiber membranes in the presence or absence of cellular infiltration. Here we evaluate the presence and distribution of these antigens in canine Masticatory Muscle Myositis, an immune-mediated inflammatory myopathy. Twelve samples of temporalis and masseter Muscles from dogs with a clinical diagnosis of canine Masticatory Muscle Myositis were examined by immunohistochemistry and double-immunofluorescence confocal microscopy. MHC class I and class II antigens were expressed in Muscle fibers independent of inflammatory cell infiltration. Furthermore MHC class I and class II antigens were expressed on the sarcolemma and co-localized with dystrophin. Our results suggest that MHC class I and class II expression in canine Masticatory Muscle Myositis may play a role in the initiation and maintenance of the pathological condition, rather than just a consequence of a preceding local inflammation.
J. Neumann - One of the best experts on this subject based on the ideXlab platform.
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evidence for mhc i restricted cd8 t cell mediated immunopathology in canine Masticatory Muscle Myositis and polyMyositis
Muscle & Nerve, 2006Co-Authors: J. Neumann, T. BilzerAbstract:Masticatory Muscle Myositis (MMM) is the most common inflammatory myopathy (IM) in dogs, associated with antibodies against myosin. To further elucidate the immunopathogenesis, we investigated Muscles of 53 dogs with MMM, 32 dogs with polyMyositis (PM), and 4 dogs suffering from both, with regard to the presence and location of CD4 + and CD8 + T cells, B cells, macrophages, major histocompatibility complex (MHC) class I and class II antigens, and autoantibodies. CD8 + T cells were found in MMM (91%) and PM (75%), mostly paralleled (68% and 61%) by enhanced expression of MHC class I antigen on Muscle fibers. CD8 + T cells invading intact and neighboring necrotic Muscle fibers were present in MMM (39%) and PM (42%). Dogs with MMM lacking intramuscular (26%) and circulating (36%) autoantibodies also had CD8 + T-cell infiltrations and Muscle-fiber lesions. Since MHC class I antigen and CD8 + T cells were detected in the presence of CD4 + T cells, regardless of antimuscular antibodies, we consider MMM and PM in the dog as a CD8 + T-cell-mediated immuno-pathological disease that initiates Muscle-fiber destruction and leads to production of myosin autoantibodies.
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Evidence for MHC I–restricted CD8+ T-cell–mediated immunopathology in canine Masticatory Muscle Myositis and polyMyositis
Muscle & nerve, 2006Co-Authors: J. Neumann, T. BilzerAbstract:Masticatory Muscle Myositis (MMM) is the most common inflammatory myopathy (IM) in dogs, associated with antibodies against myosin. To further elucidate the immunopathogenesis, we investigated Muscles of 53 dogs with MMM, 32 dogs with polyMyositis (PM), and 4 dogs suffering from both, with regard to the presence and location of CD4 + and CD8 + T cells, B cells, macrophages, major histocompatibility complex (MHC) class I and class II antigens, and autoantibodies. CD8 + T cells were found in MMM (91%) and PM (75%), mostly paralleled (68% and 61%) by enhanced expression of MHC class I antigen on Muscle fibers. CD8 + T cells invading intact and neighboring necrotic Muscle fibers were present in MMM (39%) and PM (42%). Dogs with MMM lacking intramuscular (26%) and circulating (36%) autoantibodies also had CD8 + T-cell infiltrations and Muscle-fiber lesions. Since MHC class I antigen and CD8 + T cells were detected in the presence of CD4 + T cells, regardless of antimuscular antibodies, we consider MMM and PM in the dog as a CD8 + T-cell-mediated immuno-pathological disease that initiates Muscle-fiber destruction and leads to production of myosin autoantibodies.