Proinflammatory Modulation of the Surface and Cytokine Phenotype of Monocytes in Patients With Acute Charcot Foot
Autor: | Laura Giurato, Erika Vainieri, Francesca Spasaro, Luigi Uccioli, Cristiana Almerighi, Alberto Bergamini, Anna Sinistro, Antonella Cavazza, G. Rocchi, Chiara Ciaprini, Valeria Ruotolo |
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Jazyk: | angličtina |
Rok vydání: | 2009 |
Předmět: |
Settore MED/09 - Medicina Interna
Endocrinology Diabetes and Metabolism medicine.medical_treatment Inflammation Apoptosis Diabetic angiopathy Monocytes Proinflammatory cytokine Pathogenesis Diabetic Neuropathies Antigens CD Reference Values Diabetes mellitus Internal Medicine medicine Neurologic Humans Gait Disorders Antigens Pathophysiology/Complications Gait Disorders Neurologic Original Research Advanced and Specialized Nursing business.industry Monocyte Phenotype Flow Cytometry Acute Disease Magnetic Resonance Imaging Cytokines Diabetic Angiopathies medicine.disease CD medicine.anatomical_structure Cytokine Immunology medicine.symptom business |
Zdroj: | Diabetes Care |
ISSN: | 1935-5548 0149-5992 |
Popis: | OBJECTIVEDespite increased information on the importance of an inappropriate inflammatory response in the acute Charcot process, there has been no previous attempt to define the specific pathways that mediate its pathogenesis. Here, the role played by monocytes was analyzed.RESEARCH DESIGN AND METHODSThe immune phenotype of peripheral monocytes was studied by fluorescence-activated cell sorter analysis comparing patients with acute Charcot (n = 10) in both the active and recovered phase, diabetic patients with neuropathy (with or without osteomyelitis), and normal control subjects.RESULTSWhen compared with diabetic control subjects and healthy subjects, monocytes from acute Charcot patients showed a proinflammatory immune phenotype characterized by increased production of proinflammatory cytokines, reduced secretion of anti-inflammatory cytokines, increased expression of surface costimulatory molecules, and increased resistance to serum withdrawal-induced apoptosis. In addition, the pattern of circulating cytokines confirmed activation of proinflammatory cytokines. No modulation of the monocyte phenotype was documented in diabetic control subjects and healthy subjects, thus indicating that the proinflammatory alterations of monocytes are specific and causative of acute Charcot.CONCLUSIONSTogether, these data provide evidence for the role of proinflammatory changes in the immune phenotype of monocytes in the pathogenesis of acute Charcot. These alterations may explain the abnormally intense and prolonged inflammatory response that characterizes this disorder and may represent a potential therapeutic target for specific pharmacological interventions. |
Databáze: | OpenAIRE |
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