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ABSTRACT: Abdominal aortic aneurysm (AAA) is sometimes detected in patients with atherosclerosis. One of the histological characteristics of AAA walls is infiltration of inflammatory cells, in which autoimmunity may be involved. Thereby, we here surveyed autoantigens in AAA walls by proteomics. Specifically, we separated proteins extracted from AAA wall samples by 2-dimentional electrophoresis and detected candidate autoantigens by western blotting. One of the detected candidates was carbonic anhydrase 1 (CA1). ELISA confirmed that the autoantibodies to CA1 were detected more frequently in AAA patients (n=13) than in healthy donors (n=25) (p=0.03). Interestingly, some serum samples from the AAA patients reacted to CA1 of the AAA walls stronger than to CA1 of peripheral blood mononuclear cells from healthy donors. Our data indicate that CA1 in the AAA walls would be modified to express neo-epitope(s) and that the autoimmunity to CA1 may be involved in the pathogenesis of AAA.
Human immunology 04/2013; · 2.55 Impact Factor
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ABSTRACT: Analysis of autoantibodies/antigens has very important impact for investigation of the pathogenesis of autoimmune diseases, including systemic lupus erythematosus (SLE). Recent progress has enabled us to detect and analyze the autoantibodies/antigens easily by using a proteomics approach. By proteomics, we can directly detect proteins as gene products as well as their alterations by post-translational modification and internal abscission which are characteristically observed in proteins. For example, we pick up autoantigens of interest as spots through combination of two-dimensional electrophoresis and western blot, and identify them by analysis using mass spectrometry. These methods allow us to use clinical specimens, including various tissues as a source of autoantigens. In this review, we introduce application of proteomics approach to autoimmune diseases, referring to our study of the autoantigens detected by anti-neuronal antibodies in SLE patients with central nervous system involvement.
Japanese Journal of Clinical Immunology 03/2009; 32(1):43-7.
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ABSTRACT: Henoch-Schönlein purpura is a systemic vasculitis of small vessels characterized by purpura, arthralgias, glomerulonephritis and gastrointestinal involvements which can cause intestinal perforation. A 75-year-old man with renal dysfunction and palpable purpura (petechiae) of which dermal specimen showed leukocytoclastic vasculitis was diagnosed as Henoch-Schönlein purpura. Corticosteroid and cyclosporine were effective, but subsequently he developed pneumocystis pneumonia. After he improved by treatment with trimethoprim-sulfamethoxazole, he presented sudden abdominal pain, caused by perforation of the gallbladder. Histological analysis revealed infiltration of inflammatory cells with bleeding in the gallbladder wall at the site of perforation. It is suggested that inflammatory disruption of capillary walls might lead to the perforation of the gallbladder.
Rheumatology International 11/2008; 29(4):441-3. · 1.88 Impact Factor
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Miho Kimura,
Kaori Aramaki,
Tatsuhiko Wada,
Kazuo Nishi,
Reiko Matsushita, Nobuko Iizuka,
Atsushi Hashimoto,
Sumiaki Tanaka,
Akira Ishikawa,
Hirahito Endo,
Shunsei Hirohata
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ABSTRACT: We report two cases presenting focal neurological deficits with high intensity lesions in fluid attenuated inversion recovery (FLAIR) images on brain magnetic resonance imaging (MRI), which almost completely improved by corticosteroid therapy. Marked elevation of cerebrospinal fluid IL-6 was also noted when these patients showed neurological deficits. As far as we explored, there have been thirteen published case reports of systemic lupus erythematosus patients with reversible focal neurological deficits. The neurological symptoms varied from case to case, but could be attributed to the lesions on MRI scans. The completely reversible feature of neurological manifestations as well as MRI findings on corticosteroid therapy is distinct from any other disorder, including cerebrovascular disease and demyelinating syndrome, in the 1999 American College of Rheumatology nomenclature. Therefore, we propose that reversible focal neurological deficits should be added to the 1999 nomenclature and classification and case definitions.
Journal of the Neurological Sciences 07/2008; 272(1-2):71-6. · 2.35 Impact Factor
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Atsushi Hashimoto,
Izumi Hayashi,
Yousuke Murakami,
Yoshinori Sato,
Hidero Kitasato,
Reiko Matsushita, Nobuko Iizuka,
Ken Urabe,
Moritoshi Itoman,
Shunsei Hirohata,
Hirahito Endo
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ABSTRACT: To evaluate the role of an antiinflammatory lipid mediator, lipoxin A4 (LXA4), in inflammatory arthritis, we measured the level of LXA4 in synovial fluid and lipoxin A4 receptor (ALX) expression in synovial tissues obtained from patients with rheumatoid arthritis (RA) and osteoarthritis (OA).
Levels of LXA4 and its analog (15-epi-LXA4) in synovial fluid from 30 patients with RA and 15 patients with OA were measured by a specific ELISA. Reverse transcription-polymerase chain reaction (RT-PCR), real-time quantitative PCR, and in situ hybridization were performed to detect mRNA for ALX and 15-LOX, and LXA4 synthetase, in synovial tissues from 20 patients with RA and 10 patients with OA. RESULTS Both LXA4 and 15-epi-LXA4 showed significantly higher levels in RA synovial fluid (10.34 +/- 14.12 ng/ml for LXA4) than OA synovial fluid (0.66 +/- 0.77 ng/ml for LXA4). Logarithmic concentration of LXA4 was significantly correlated with that of leukotriene B4 and prostaglandin E2 in RA and OA synovial fluids. Expressions of ALX and 15-LOX mRNA were stronger in RA synovium than OA synovium. Expression of mRNA for interleukin 13 (IL-13), which induces 15-LOX, was significantly stronger in RA synovium than OA synovium.
ALX is an important target of LXA4 in synovial tissues of patients with RA. 15-LOX induced by IL-13 might regulate the production of LXA4 to have an antiinflammatory effect against proinflammatory lipid mediators in inflamed joints. These findings could lead to the development of new therapy for inflammatory arthritis such as RA.
The Journal of Rheumatology 12/2007; 34(11):2144-53. · 3.69 Impact Factor
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Yasuhiko Tanaka,
Manabu Nakamura,
Toshihiro Matsui, Nobuko Iizuka,
Hirobumi Kondo,
Shigeto Tohma,
Kayo Masuko,
Kazuo Yudoh,
Hiroshi Nakamura,
Kusuki Nishioka,
Izumi Koizuka,
Tomohiro Kato
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ABSTRACT: Relapsing polychondritis (RP) is a systemic inflammatory disease, in which autoimmunity to cartilage-related components is thought to be involved in its pathogenesis. However, the autoimmune profile in RP has not been studied fully. We therefore investigated autoantibodies/autoantigens in RP comprehensively, by 2-dimensional electrophoresis (2DE), subsequent western blotting (WB) and mass spectrometry, using cell-extracted proteins as the antigen source. As a result, we detected 15 autoantigens on 2DE-WB, and further identified five of them. On average, one RP serum recognized approximately 8 out of the 15 autoantigens. Frequencies of the autoantibodies to the 5 identified antigens of tubulin alpha ubiquitous/6, vimentin, alpha enolase, calreticulin, and colligin-1/-2 were 91%, 46%, 36%, 82%, and 36%, respectively. ELISA using recombinant proteins for them revealed that frequencies of the autoantibodies to tubulin alpha ubiquitous, vimentin, alpha enolase, calreticulin, and colligin-1 were 36%, 64%, 46%, 27%, and 18%, respectively. Our data demonstrated that the autoimmune reaction was not restricted to cartilagerelated components, rather a variety of autoimmune responses occurred in patients with RP, which may be involved in the pathophysiology of RP. In addition, the proteomic approach using cell-extracted proteins would be a powerful way to investigate autoantigens.
Microbiology and Immunology 02/2006; 50(2):117-26. · 1.30 Impact Factor
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Nippon rinsho. Japanese journal of clinical medicine 06/2005; 63 Suppl 5:708-12.
