Rheumatoid Arthritis: Huang F

Zhu J, Huang F. · No affiliation provided · Zhonghua Nei Ke Za Zhi. · Pubmed #18953937 No free full text.

This publication has no abstract.

Gu J, Rihl M, Märker-Hermann E, Baeten D, Kuipers JG, Song YW, Maksymowych WP, Burgos-Vargas R, Veys EM, De Keyser F, Deister H, Xiong M, Huang F, Tsai WC, Yu DT. · University of California Los Angeles, 90095, USA. · J Rheumatol. · Pubmed #12375327 No free full text.

Abstract: OBJECTIVE: To use gene expression profiles of spondyloarthropathy (SpA) synovial fluid mononuclear cells (SFMC) to determine if there are transcripts that support the unfolded protein response (UPR) hypothesis, and to identify which cytokines/chemokines are being expressed and which cell fractions are involved. METHODS: Gene expression profiles were generated by microarray screening of SFMC of 5 patients with SpA, 5 patients with rheumatoid arthritis (RA), and peripheral blood mononuclear cells (PBMC) of 6 controls. Results were validated by reverse transcription polymerase chain reaction using samples from a larger panel of subjects. RESULTS: The repertoires of proinflammatory cytokines/chemokines expressed by SpA and RA SFMC were very similar: monocyte chemotractant protein 1 (MCP-1), interleukin 8 (IL-8), IL-1beta, endothelial-monocyte activating polypeptide II, interferon-gamma, and tumor necrosis factor-alpha. MCP-1 was highly expressed in SpA SFMC. There was enhanced expression of immunoglobulin heavy chain binding protein (BiP) in SpA, which is compatible with the UPR hypothesis. BiP was most highly expressed in the adherent fraction of SpA SFMC. CONCLUSION: Previous data postulating UPR in SpA are based on in vitro experiments with transfected cell lines. Our patient derived data suggest that it also occurs in vivo in the macrophages of SpA joints.

Gu J, Märker-Hermann E, Baeten D, Tsai WC, Gladman D, Xiong M, Deister H, Kuipers JG, Huang F, Song YW, Maksymowych W, Kalsi J, Bannai M, Seta N, Rihl M, Crofford LJ, Veys E, De Keyser F, Yu DT. · University of California at Los Angeles, CA 90095, USA. · Rheumatology (Oxford). · Pubmed #12096225 links to  free full text

Abstract: OBJECTIVES: To identify genes which are more highly expressed in the peripheral blood mononuclear cells (PBMC) of patients with spondyloarthropathy (SpA), rheumatoid arthritis (RA) and psoriatic arthritis (PsA), in comparison to normal subjects. METHODS: A 588-gene microarray was used as a screening tool to select a panel of such genes from PBMC of these subjects and of normal subjects. Results were then validated by reverse transcription-polymerase chain reaction (RT-PCR). RESULTS: The following genes were more highly expressed in arthritis patients than in normal subjects: macrophage differentiation marker MNDA (myeloid nuclear differentiation antigen), MRP8 and MRP14 (migratory inhibitory factor-related proteins); signalling molecules JAK3 (janus kinase 3) and MAP kinase p38 (mitogen-activated protein kinase); receptors TNFR2/p75, C-C-chemokine receptor type 1 (CCR1), C-X-C-chemokine receptor type 4 (CXCR4) and integrin beta1; and the cytokines/chemokines interleukin (IL) 1beta and IL-8. Expression of CXCR4 was unexpectedly high among all arthritis subjects. Using RT-PCR, ELISA and immunohistology, expression of stromal cell-derived factor 1 (SDF-1) was demonstrated in arthritis joints. CONCLUSIONS: The CXCR4/SDF-1 is a potential pro-inflammatory axis for RA, PsA and SpA.

Liu X, Lin H, Yuan G, Huang F. · Department of Rheumatology, General Hospital of PLA, Beijing 100853. · Zhonghua Nei Ke Za Zhi. · Pubmed #11798678 No free full text.

Abstract: OBJECTIVE: To investigate the level of interleukin-6 (IL-6) and soluble-IL-6 receptor (sIL-6R) in serum of patients with systemic lupus erythematosus (SLE) and its correlation with disease activity and to explore IL-6 signal transduction pathways in SLE patients. METHODS: By using MTT colorimetry and ELISA, the levels of IL-6 and sIL-6R in serum from 16 patients with SLE (9 active, 7 inactive), 17 with active rheumatoid arthritis (RA) and 29 controls were measured. The expressions of acute phase reaction factor (APRF) in peripheral blood mononuclear cells (PBMCs) were also detected by using electrophoresis mobility shift assays (EMSA) after the PBMCs were isolated and then stimulated by IL-6. RESULTS: Serum IL-6 and sIL-6R levels in active SLE patients were significantly higher than those in normal controls (P < 0.01), but were significantly lower than those in active RA patients (P < 0.01). Serum IL-6 rather than sIL-6R level in active SLE patients was significantly higher than that in inactive ones (P < 0.01). Serum IL-6 was correlated positively with the anti-dsDNA antibody (r = 0.658, P < 0.01), but not with CRP (r = 0.041, P > 0.05). There were no expression of APRF in PMNC from SLE patients and 8 normal controls, whereas PMNC from 11 RA patients expressed APRF activity (11/17). CONCLUSION: The level of IL-6 is a useful parameter for monitoring disease activity of SLE. In active SLE, no significant elevation of serum sIL-6R and no expression of APRF in PMBCs may be responsible for mild CRP elevation.

Gu J, Huang F, Yu D. · Department of Rheumatology, Third Affiliated Hospital of Sun Yat-sen, University of Medical Sciences, Guangzhou 510630, China. · Zhonghua Yi Xue Za Zhi. · Pubmed #11758249 No free full text.

Abstract: OBJECTIVE: To test the difference of gene expression patterns in peripheral blood mononuclear cells (PBMCs) among patients with ankylosing spondylitis (AS) or rheumatoid arthritis (RA) and healthy volunteers and to find potential discriminating genes. METHODS: The PBMC gene expression spectra of 7 patients with active AS, 6 patients with active RA, and 7 healthy volunteers were tested by microarray assay with 588 target gene filters. Semi-quantitative RT-PCR was performed to test the expression rates of thirteen inflammation related genes which had been with high expression rates in at least 4 arthritis patients by microarray assay, among 22 AS patients, 8 RA patients, and 7 healthy volunteers. RESULTS: The expression rates of inflammation related genes by cDNA microarray assay in healthy volunteer group, AS group, and RA group were 8.4%, 32.5% and 44.8% respectively (P < 0.001). The positive rate in RA patients was much higher than that in AS patients (P < 0.012). A significant increase of positive rate of these genes was also noticed in 2 active pulmonary tuberculosis patients. The expression rates of the 13 genes which were positive in at least 4 arthritis patients tested by semiquantitative RT-PCR in 22 AS patients, 8 RA patients and 7 healthy volunteers were very similar to those expression rates tested by cDNA microarray. CONCLUSION: The gene expression profiles of PBMC among AS patients are significantly abnormal and are significantly different from those among RA patients. The high expression of the 13 cytokines is not specific to AS.

Yang C, Huang F. · General Hospital of PLA, Beijing 100853, China. · Zhonghua Nei Ke Za Zhi. · Pubmed #11374178 No free full text.

Abstract: OBJECTIVE: To study the distribution and expression of type-1 plasminogen activator inhibitor (PAI-1) and type-2 plasminogen activator inhibitor (PAI-2) in synovial tissue from rheumatoid arthritis(RA) and measure the antigen levels and activity in synovial fluid and plasma of patients with RA. METHODS: Immunohistochemical analysis was used to detect PAI-1 and PAI-2 expression and distribution in synovial tissue from 24 RA patients, 18 osteoarthritis (OA) patients and 6 normal subjects. PAI-1 and PAI-2 antigen concentration and activity were determined with ELISA sandwich method. RESULTS: In RA patients, positive staining of PAI-1 and PAI-2 was seen respectively in all the 24 cases and 8 of the 24 cases; positive expression was distributed mainly in the synovial lining area. In OA patients, positive staining of PAI-1 was detected in 8 cases and its positive distribution was similar to that in RA. No PAI-2 positive staining was seen in all the OA cases. In 6 normal subjects with normal synovial tissue, the staining was negative. The concentration and activity of PAI-1 in RA synovial fluid(SF) were significantly higher than those in the plasma(P < 0.001 and P < 0.05). The concentration and activity of PAI-1 in the plasma of RA were also much higher than those in the plasma of OA(P < 0.05 and P < 0.0001) and healthy subjects(P < 0.0001 and P < 0.001). The concentration and activity of PAI-1 in SF and plasma of RA correlated positively. CONCLUSION: The up-regulated expression of PAI-1 and PAI-2 and the concentration and activity of PAI-1 in SF and plasma were significantly higher in RA than those in OA and healthy subjects, suggesting PAI especially PAI-1 may play an important role in the pathogenesis of RA.

Seta N, Granfors K, Sahly H, Kuipers JG, Song YW, Baeten D, Veys EM, Maksymowych W, Märker-Hermann E, Gu J, Huang F, Kirveskari J, Yu DT. · University of California Los Angeles, USA. · Arthritis Rheum. · Pubmed #11315932 links to  free full text

Abstract: OBJECTIVE: Reactive arthritis (ReA) is postulated to be caused by a defective host defense against gram-negative bacteria. HLA-B27 could play a role in this process, but does not account for the many HLA-B27 negative patients. The objective of this study was to test the expression of 3 macrophage scavenger receptors (SRs) that are responsible for innate immunity against gram-negative bacteria: SR class A type I (SR-AI), SR-AII, and the macrophage receptor with collagenous structure (MARCO). We postulate that defects in such receptors might also contribute to the host risk factors that increase the predisposition to ReA and perhaps other subtypes of spondylarthropathy (SpA). METHODS: Peripheral blood, synovial fluid, and synovial tissue samples were obtained from patients with recent Salmonella infection, ReA, other SpA, and rheumatoid arthritis (RA). The expression of SRs receptors was assessed by semiquantitative reverse transcriptase-polymerase chain reaction. RESULTS: Evaluation of the peripheral blood mononuclear cells (PBMC) from 4 patients who were recently infected with Salmonella, showed that PBMC from 2 patients who developed ReA expressed positive levels of MARCO, while PBMC from 2 patients who recovered from infection without sequelae did not. The synovial fluid mononuclear cells (SFMC) from some ReA patients expressed MARCO, but the levels were only moderate. The level of MARCO in the SFMC from the SpA patient group was low. In marked contrast, MARCO expression was high in almost all samples of RA SFMC. These findings also extended to synovial tissues. CONCLUSION: Expression of the host defense gene MARCO was susceptible to modulation, not only during infections, but also in the inflammatory arthritis conditions RA and SpA. MARCO is a variable to be considered as a candidate factor that might contribute to ReA.