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Neutrophils in multiple sclerosis are characterized by a primed phenotype


Naegele, M; Tillack, K; Reinhardt, S; Schippling, S; Martin, R; Sospedra, M (2012). Neutrophils in multiple sclerosis are characterized by a primed phenotype. Journal of Neuroimmunology, 242(1-2):60-71.

Abstract

Neutrophils are armed with proteases with indiscriminate histotoxic potential, and to minimize tissue injury, their activation involves priming with inflammatory mediators before cells are fully activated in a second step. Here, we show that neutrophils in multiple sclerosis patients are more numerous and exhibit a primed state based on reduced apoptosis, higher expression of TLR-2, fMLP receptor, IL-8 receptor and CD43, enhanced degranulation and oxidative burst as well as higher levels of neutrophil extracellular traps in serum. The chronic inflammatory environment in multiple sclerosis probably underlies this inappropriate neutrophil priming, which may result in enhanced neutrophil activation during infection.

Abstract

Neutrophils are armed with proteases with indiscriminate histotoxic potential, and to minimize tissue injury, their activation involves priming with inflammatory mediators before cells are fully activated in a second step. Here, we show that neutrophils in multiple sclerosis patients are more numerous and exhibit a primed state based on reduced apoptosis, higher expression of TLR-2, fMLP receptor, IL-8 receptor and CD43, enhanced degranulation and oxidative burst as well as higher levels of neutrophil extracellular traps in serum. The chronic inflammatory environment in multiple sclerosis probably underlies this inappropriate neutrophil priming, which may result in enhanced neutrophil activation during infection.

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Additional indexing

Item Type:Journal Article, refereed, original work
Communities & Collections:04 Faculty of Medicine > University Hospital Zurich > Clinic for Neurology
Dewey Decimal Classification:610 Medicine & health
Language:English
Date:2012
Deposited On:29 Dec 2012 14:44
Last Modified:07 Dec 2017 17:51
Publisher:Elsevier
ISSN:0165-5728
Publisher DOI:https://doi.org/10.1016/j.jneuroim.2011.11.009
PubMed ID:22169406

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