D36. Sarcoidosis: Translational Approaches 2010
DOI: 10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a5704
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Neurotrophins And Neurotrophin Receptors In Pulmonary Sarcoidosis - Granulomas As A Source Of Expression

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Cited by 5 publications
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“…There is evidence of increased expression of neurotrophins, such as nerve growth factor and their receptors, on airway lymphocytes of patients with sarcoidosis [32]. Furthermore, DAGNELL et al [33,34] have reported the presence of nerve growth factors and their receptors, such as TrkA, TrkB and TrkC, in sarcoid granulomas and alveolar macrophages. The neuronal mechanisms of cough should be explored further in patients with sarcoidosis.…”
Section: Discussionmentioning
confidence: 99%
“…There is evidence of increased expression of neurotrophins, such as nerve growth factor and their receptors, on airway lymphocytes of patients with sarcoidosis [32]. Furthermore, DAGNELL et al [33,34] have reported the presence of nerve growth factors and their receptors, such as TrkA, TrkB and TrkC, in sarcoid granulomas and alveolar macrophages. The neuronal mechanisms of cough should be explored further in patients with sarcoidosis.…”
Section: Discussionmentioning
confidence: 99%
“…Recently lymphocytes, and in particular activated T-cells, have been revealed to express BDNF and BDNF receptors in the experimental animal model of pulmonary sarcoidosis and chemical lung injury. 39,40 So, it is possible that neurotrophin up-regulation is secondary to rapid lymphocyte activation by H1N1 virus infection and that this over-expression represents an important process in the mechanisms of the inflammatory host response after viral lung infections. 23 In fact, previous studies have reported that different viral lung infections are associated with early neurotrophin biosynthesis, mainly BDNF and neurotrophin-3 (NT-3), suggesting that the changes in neurotrophin release may contribute to the development of lung inflammation and airway remodeling.…”
Section: Discussionmentioning
confidence: 99%
“…Neurotrophin plasma levels increase in several inflammatory diseases, whereas up-regulation of TrkA/TrkB receptors has been shown following different inflammatory stimuli, such as allergen provocation and asthma. Recently lymphocytes, and in particular activated T-cells, were revealed to express BDNF and BDNF receptors in the experimental animal model of pulmonary sarcoidosis and chemical lung injury [29,30]. So, it is possible that neurotrophin up-regulation is secondary to lymphocytes rapid activation by H1N1 virus infection and that this over-expression represents an important process in the mechanisms of inflammatory host response after viral lung infections [18].…”
Section: Discussionmentioning
confidence: 99%