The role of mast cells in demyelination. 1. Myelin proteins are degraded by mast cell proteases and myelin basic protein and P2 can stimulate mast cell degranulation

Johnson, David; Seeldrayers, Pierrette; Weiner, Howard L.

doi:10.1016/0006-8993(88)90929-8

Cited by 104 publications

(48 citation statements)

References 15 publications

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“…The P2 receptor-mediated degranulation and release of cytokines from mast cells (IL-4, IL-13, IFNγ, and TNFα) increases the permeabilization of vascular endothelium, influences immune cells trafficking to the inflamed sites, and guides differentiation of CD4 + T cells to Th1 or Th2 subsets. Mast cell proteases degrade myelin, and myelin could, in turn, stimulate degranulation of mast cells [116,117]. As was noted above, ATP mediates release of IL-33 from glial cells.…”

Section: Mast Cellmentioning

confidence: 89%

P2 receptor-mediated signaling in mast cell biology

Bulanova

Bulfone–Paus∥

2009

Purinergic Signalling

101

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Mast cells are widely recognized as effector cells of allergic inflammatory reactions. They contribute to the pathogenesis of different chronic inflammatory diseases, wound healing, fibrosis, thrombosis/fibrinolysis, and antitumor immune responses. In this paper, we summarized the role of P2X and P2Y receptors in mast cell activation and effector functions. Mast cells are an abundant source of ATP which is stored in their granules and secreted upon activation. We discuss the contribution of mast cells to the extracellular ATP release and to the maintenance of extracellular nucleotides pool. Recent publications highlight the importance of purinergic signaling for the pathogenesis of chronic airway inflammation. Therefore, the role of ATP and P2 receptors in allergic inflammation with focus on mast cells was analyzed. Finally, ATP functions as mast cell autocrine/paracrine factor and as messenger in intercellular communication between mast cells, nerves, and glia in the central nervous system.

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Section: Mast Cellmentioning

confidence: 89%

P2 receptor-mediated signaling in mast cell biology

Bulanova

Bulfone–Paus∥

2009

Purinergic Signalling

101

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“…Probably dietary factors produced in the CNS itself, alone or in combination with hormone(s) which triggers the mast cells to the release of potent mediators such as histamineinducing oedemas-and neutral proteases-dissolving myelin [29]. Neurotensine, substance P, ATP and catestatin may stimulate mast cells in experimental animal in vitro systems [30][31][32][33].…”

Section: Discussionmentioning

confidence: 99%

Mast cells and multiple sclerosis in females and males

Krüger¹,

Mörk²

2012

WJNS

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Mast cells were observed in autopsies from 11 females and 8 males. We confirm earlier observations that mast cells are more frequent in close vicinity to MSplaques. In these plaque-border zone areas, defined as the area within 1 mm distance of the actual plaques, the average number of mast cells was 2.34/mm 2 in males and 4.77/mm 2 in females, which in average is appr. 10 times more than earlier observed in MS. The difference in number of mast cells between females and males is significant (p < 0.005) and is of interest since females are more inclined to developing MS than males. Mast cells were rare in areas without visible plaques. The mast cells were preferably located close to capillaries and venules. A mechanism for the probable role of mast cells, based on diet-factors and mast cell mediators in the pathogenesis of MS is discussed.

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“…Estos cambios se han demostrado en pacientes con otitis media crónica, aun sin presentar paráli-sis facial 19 . Los mastocitos, elevados en algunas neuropatías periféricas 20 , podrían actuar mediante sus proteasas para producir los focos de desmielinización 21 .…”

Section: Inflamaciónunclassified

Parálisis facial en otitis media: Revisión bibliográfica

Rivas³

2007

Rev. Otorrinolaringol. Cir. Cabeza Cuello

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RESUMENLa parálisis facial secundaria a una otitis media es una conocida complicación de infecciones agudas y crónicas. Su fisiopatología es desconocida pero la presión elevada en el oído medio, la osteítis, la invasión bacteriana y la neurotoxicidad, podrían estar involucradas. Los exámenes de laboratorio no entregan mayor información para determinar la etiología de la parálisis facial y la tomografía computada de oídos sería el estudio radiológico de elección ya que permite identificar el compromiso óseo, la extensión de la enfermedad y posibles alteraciones anatómicas existentes, además de ser utilizado para el diagnóstico de eventuales complicaciones intracraneales. El tratamiento de la parálisis en el curso de una otitis media aguda es médico, con antibióticos y esteroides, con buen pronóstico de recuperación; mientras en una otitis media crónica el tratamiento es quirúrgico y el pronóstico global peor.Palabras clave: Parálisis facial, otitis media, colesteatoma. ABSTRACTFacial paralysis secondary to otitis media is a well known complication of acute and chronic infection. The physiopathology of facial nerve paralysis secondary to otitis media of not known, but high middle ear pressure, osteitis, direct bacterial invasion and neurotoxicity could be involved. Laboratory studies have failed to provide clues as to determining the etiology of facial nerve palsy. Ear CT is the radiologic study of choice, as it allows the identification of bone destruction, disease extension and possible anatomic alterations, and may also be used as a screening for intracranial complications. Acute otitis media treatment is medical with antibiotics and steroids, with good prognosis, whereas in chronic otitis media the treatment is surgical, with worst global prognosis.

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The role of mast cells in demyelination. 1. Myelin proteins are degraded by mast cell proteases and myelin basic protein and P2 can stimulate mast cell degranulation

Cited by 104 publications

References 15 publications

P2 receptor-mediated signaling in mast cell biology

P2 receptor-mediated signaling in mast cell biology

Mast cells and multiple sclerosis in females and males

Parálisis facial en otitis media: Revisión bibliográfica

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