Systemic TNF blockade does not modulate synovial expression of the pro-inflammatory mediator HMGB1 in rheumatoid arthritis patients: a prospective clinical study

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Fältnamn	Indikatorer	Metadata
000		04818naa a2200613 4500
001		oai:DiVA.org:kth-34276
003		SwePub
008		110531s2008 \| \|\|\|\|\|\|\|\|\|\|\|000 \|\|eng\|
009		oai:prod.swepub.kib.ki.se:117199606
024	7	a https://urn.kb.se/resolve?urn=urn:nbn:se:kth:diva-342762 URI
024	7	a https://doi.org/10.1186/ar23872 DOI
024	7	a http://kipublications.ki.se/Default.aspx?queryparsed=id:1171996062 URI
040		a (SwePub)kthd (SwePub)ki
041		a engb eng
042		9 SwePub
072	7	a ref2 swepub-contenttype
072	7	a art2 swepub-publicationtype
100	1	a Sundberg, Eriku Karolinska Institutet4 aut
245	1 0	a Systemic TNF blockade does not modulate synovial expression of the pro-inflammatory mediator HMGB1 in rheumatoid arthritis patients :b a prospective clinical study
264	1	b Springer Science and Business Media LLC,c 2008
338		a print2 rdacarrier
500		a QC 20110531
520		a Introduction High-mobility group box chromosomal protein 1 (HMGB1) has recently been identified as an endogenous mediator of arthritis. TNF and IL-1 beta, pivotal cytokines in arthritis pathogenesis, both have the ability to induce the release of HMGB1 from myeloid and dendritic cells. It was, therefore, decided to investigate whether treatment based on TNF blockade in rheumatoid arthritis (RA) affects the expression of synovial HMGB1. Methods Repeated arthroscopy-guided sampling of synovial tissue was performed in nine patients with RA before and nine weeks after initiation of anti-TNF mAb (infliximab) therapy. Synovial biopsy specimens were analysed for HMGB1 protein by immunohistochemical staining and for HMGB1 mRNA expression by real-time reverse transcriptase PCR (RT-PCR). Statistical evaluations were based on Wilcoxon's signed rank tests or Spearman rank sum tests. Results Aberrant, extranuclear HMGB1 and constitutive nuclear HMGB1 expression, with histological signs of inflammation, were evident in all biopsies obtained before infliximab therapy. Signs of inflammation were still evident in the second biopsies obtained nine weeks after initiation of infliximab therapy. The cytoplasmic and extracellular expression of HMGB1 decreased in five patients, remained unchanged in one patient and increased in three patients, making the overall change in HMGB1 protein expression not significant. No correlation between the clinical response, as measured by disease activity score calculated for 28 joints (DAS28) or the American College of Rheumatology response criteria (ACR 20, 50, and 70), and the direction of change of HMGB1 expression in individual patients could be discerned. In addition, infliximab therapy did not alter HMGB1 mRNA synthesis. Conclusion Pro-inflammatory HMGB1 expression during rheumatoid synovitis was not consistently influenced by TNF-blocking therapy with infliximab. This suggests that TNF is not the main inducer of extranuclear HMGB1 during synovitis and that HMGB1 may represent a TNF-independent molecule that could be considered as a possible target for future therapeutic intervention in RA.
650	7	a MEDICIN OCH HÄLSOVETENSKAPx Klinisk medicinx Reumatologi och inflammation0 (SwePub)302102 hsv//swe
650	7	a MEDICAL AND HEALTH SCIENCESx Clinical Medicinex Rheumatology and Autoimmunity0 (SwePub)302102 hsv//eng
650	7	a TEKNIK OCH TEKNOLOGIERx Industriell bioteknik0 (SwePub)2092 hsv//swe
650	7	a ENGINEERING AND TECHNOLOGYx Industrial Biotechnology0 (SwePub)2092 hsv//eng
653		a MOBILITY GROUP BOX-1
653		a COLLAGEN-INDUCED ARTHRITIS
653		a CHROMATIN PROTEIN HMGB1
653		a DENDRITIC CELLS
653		a NECROTIC CELLS
653		a ACTIVATION
653		a RELEASE
653		a CHROMOSOMAL-PROTEIN-1
653		a METHOTREXATE
653		a MATURATION
653		a Rheumatology
653		a Reumatologi
653		a Bioengineering
653		a Bioteknik
700	1	a Grundtman, Ceciliau Karolinska Institutet4 aut
700	1	a Klint, Erik A. F.4 aut
700	1	a Lindberg, Johanu KTH,Genteknologi4 aut0 (Swepub:kth)u120i6c2
700	1	a Ernestam, Sofia4 aut
700	1	a Ulfgren, Ann-Kristin4 aut
700	1	a Erlandsson Harris, Helenau Karolinska Institutet4 aut
700	1	a Andersson, Ulfu Karolinska Institutet4 aut
710	2	a Karolinska Institutetb Genteknologi4 org
773	0	t Arthritis Research & Therapyd : Springer Science and Business Media LLCg 10:2, s. R33-q 10:2<R33-x 1478-6362x 1478-6354
856	4	u https://arthritis-research.biomedcentral.com/track/pdf/10.1186/ar2387
856	4 8	u https://urn.kb.se/resolve?urn=urn:nbn:se:kth:diva-34276
856	4 8	u https://doi.org/10.1186/ar2387
856	4 8	u http://kipublications.ki.se/Default.aspx?queryparsed=id:117199606

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