P070 IL-17 and nitric oxide pathways are involved in inflammatory response during Alzheimer’s disease: A study in Algerian patients

P070 IL-17 and nitric oxide pathways are involved in inflammatory response during Alzheimer’s disease: A study in Algerian patients

Alzheimer’s disease (AD) is a neurodegenerative disorder leading to cognitive impairment (amnesia, aphasia, apraxia and agnosia), characterized by three major stages according to the evolution and the severity of the symptoms. Numerous reports have indicated that neuroinflammatory process contribute...

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Bibliographic Details
Published in:Cytokine (Philadelphia, Pa.) Vol. 59; no. 3; p. 541
Main Authors: Belkhelfa, M., Rafa, H., Medjeber, O., Behairi, N., Abada-Bendib, M., Makrelouf, M., Belarbi, S., Masmoudi, A.N., Tazir, M., Touil-Boukoffa, C.
Format: Journal Article
Language:English
Published: Elsevier Ltd 01-09-2012
Subjects:
Alzheimer's disease
Amnesia
aphasia
Cognitive ability
Evolution
Helper cells
Inflammation
Interleukin 17
Interleukin 23
Lymphocytes T
Neurodegenerative diseases
Nitric oxide
Peripheral blood mononuclear cells
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Summary:Alzheimer’s disease (AD) is a neurodegenerative disorder leading to cognitive impairment (amnesia, aphasia, apraxia and agnosia), characterized by three major stages according to the evolution and the severity of the symptoms. Numerous reports have indicated that neuroinflammatory process contributes to the pathogenesis of AD. Current theories suggest that an increase in free-radical formation such as nitric oxide (NO) may occur in AD and have a direct toxic effect. In this study we investigate the relationship among IL23/IL17 and NO production in vivo during the evolutionary stages of AD in Algerian patients (n=27) (mild Alzheimer’s, moderate Alzheimer’s and severe Alzheimer’s). We also elucidate NOSynthase2 modulation by IL-23 and IL-17A in PBMC from patients. Our results indicate a positive correlation between IL-23 and Il-17 and nitric oxide production in vivo. We noted with interest that ex vivo NO production is upregulated by both IL23 and IL-17 in PBMC from patients in severe Alzheimer Stage. Taken together our study suggests the probable involvement of Th17 subset and NO production during evolutionary inflammatory process associated with advanced Alzheimer disease (severe Alzheimer’s).
Bibliography:ObjectType-Article-2
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content type line 23
ISSN:1043-4666
1096-0023
DOI:10.1016/j.cyto.2012.06.156