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Attenuation of toll-like receptor 2-mediated innate immune response in patients with alcoholic chronic liver disease

Title
Attenuation of toll-like receptor 2-mediated innate immune response in patients with alcoholic chronic liver disease
Type
Article in International Scientific Journal
Year
2010
Authors
Pimentel-Nunes P
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FMUP
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Roncon-Albuquerque R Jr
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FMUP
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Gonçalves N
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FMUP
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Fernandes-Cerqueira C
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Cardoso H
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Bastos RP
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Marques M
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Marques C
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Alexandre-Sarmento J
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Costa-Santos C
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Macedo G
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Pestana M
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Dinis-Ribeiro M
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Leite-Moreira AF
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FMUP
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Journal
Title: Liver InternationalImported from Authenticus Search for Journal Publications
Vol. 30 No. 7
Pages: 1003-1011
ISSN: 1478-3223
Publisher: Wiley-Blackwell
Scientific classification
FOS: Medical and Health sciences > Other medical sciences
Other information
Authenticus ID: P-003-4GE
Abstract (EN): Background: Alcoholic chronic liver disease (ACLD) is a common form of acquired immunodeficiency. Aim: To evaluate ex vivo toll-like receptor (TLR) 2 and TLR4 innate immune response in stable ACLD. Methods: Blood was collected from 26 males with stable ACLD and from 17 controls. Serum was used for lipopolysaccharide (LPS), sCD14, LPS-binding protein (LBP), tumour necrosis factor-alpha (TNF-alpha) and interleukin 10 (IL-10) quantification. Peripheral blood monocytes (PBM) protein expression of TLR2 and TLR4 was determined by flow cytometry. Primary cultures of anti-CD11b positive selected PBM were stimulated with the TLR2/TLR6 ligand zymosan (Zym), with TLR2/TLR1 ligand lipopeptide (Lp) and with TLR4 ligand LPS. PBM TLR1, TLR2, TLR4, TLR6, MD2, CD14, TNF-alpha and IL-10 gene expression was evaluated by reverse transcription-polymerase chain reaction. Results: Stable ACLD patients showed increased circulating LPS (+22.5 +/- 4.1%), LBP (+60.6 +/- 12.2%) and sCD14 (+23.5 +/- 4.6%), with no differences in TNF-alpha and IL-10. Zym and Lp, but not LPS, induced TNF-alpha production by monocytes was blunted in ACLD (-66 +/- 20.4% Zym; -40.1 +/- 13.5% Lp; P < 0.05). Basal TNF-alpha mRNA expression was decreased in PBM from ACLD patients (-50.1 +/- 21.0%; P < 0.05), with no significant differences in the other studied genes. Results were similar in Child-Pugh A and B/C patients. Conclusions: Patients with stable ACLD show an attenuation of TLR2-mediated innate immune response in PBM, which may represent an important mechanism for acquired immunodeficiency. This was neither related with decreased TLR2 or its co-receptors expression nor with impaired TLR4 activation, being already present in the early stages of disease.
Language: English
Type (Professor's evaluation): Scientific
No. of pages: 9
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