Staphylococcal toxic-shock-syndrome-toxin-1 as a risk factor for disease relapse in Wegener's granulomatosis

Popa, Elaine R.; Stegeman, Coen A.; Abdulahad, Wayel H.; Meer, Bert van der; Arends, Jan P.; Manson, WL; Bos, Nicolaas A.; Kallenberg, Cornelis; Tervaert, Jwc

doi:10.1093/rheumatology/kem022

Cited by 107 publications

(78 citation statements)

References 24 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…A study of 57 patients with WG identified the chronic nasal presence of S. aureus as an independent risk factor for relapse (121), suggesting a role for S. aureus in the cause of ANCA-associated vasculitis. More recently, the presence of nasal S. aureus expressing the superantigen staphylococcal-toxic-shock-syndrome-toxin 1 was identified as a risk factor for relapse in WG (122). CD4 ϩ T cells from the peripheral blood of patients with WG showed reactivity to S. aureus, and a substantial number also recognized PR3, suggesting a role for staphylococci-specific CD4 ϩ T cells in triggering the immune response (123).…”

Section: Introductionmentioning

confidence: 99%

Hypotheses on the Etiology of Antineutrophil Cytoplasmic Autoantibody–Associated Vasculitis

Wijngaarden¹,

Rijn²,

Hagen³

et al. 2008

Clinical Journal of the American Society of Nephrology

View full text Add to dashboard Cite

The first description of what is now known as antineutrophil cytoplasmic autoantibody-associated necrotizing vasculitis appeared more than 140 yr ago. Since then, many aspects of the pathogenic pathway have been elucidated, indicating the involvement of antineutrophil cytoplasmic autoantibodies, but why antineutrophil cytoplasmic autoantibodies are produced in the first place remains unknown. Over the years, many hypotheses have emerged addressing the etiology of antineutrophil cytoplasmic antibody production, but no exclusive factor or set of factors can so far be held responsible. Herein is reviewed the most influential hypotheses regarding the causes of antineutrophil cytoplasmic antibody-associated vasculitis with the aim of placing in an epidemiologic background the different hypotheses that are centered on environmental and genetic influences.Clin J Am Soc Nephrol 3: 237-252, 2008237-252, . doi: 10.2215 A ntineutrophil cytoplasmic autoantibody (ANCA)-associated necrotizing vasculitis was probably first described in 1866 by Kussmaul and Maier (1) as "polyarteritis nodosa." It was not until the early 1930s when the first case of what was later named Wegener's granulomatosis (WG) was described (2). The disease was named after Friedrich Wegener, who described it as an entity in 1939 (3). In 1985, antibodies associated with the disease were detected and later became known as ANCA (4). WG is a systemic autoimmune disease that can cause damage in various organs. Later, microscopic polyangiitis (MPA) was distinguished as a separate ANCA-associated vasculitis. The disease-or its immunosuppressive treatment-can cause high levels of morbidity and death, especially in patients with renal involvement. Animal experiments have shown that ANCA directed against myeloperoxidase (MPO) can cause vasculitis that resembles human vasculitic disease (5,6); however, the cause of ANCA production remains unresolved.Theories have been developed to explain how ANCA could interact with neutrophils, along with monocytes and most probably T lymphocytes, to form the lesions that are characteristic of ANCA-associated vasculitis, such as fibrinoid necrosis and granulomas (7). A recent theory of interest has been postulated by Pendergraft et al. (8), stating that an antibody against the complementary peptide of proteinase-3 (PR3) in an idiotypic/anti-idiotypic network is essential to the development of ANCA and to the development of clinical vasculitis, but why and how these ANCA are produced in the first place remains unanswered. Nonetheless, many hypotheses have been developed about the initiating factor for ANCA production. Many factors, either directly or indirectly, have been considered important in the development of ANCA: Silica exposure (9); genetic predisposition (10); bacterial infection by Staphylococcus aureus (11); viral infection by, for instance, parvovirus B19 (12); and thyroid drugs (13) all have been correlated with and held to contribute to the incidence of ANCA-associated vasculitis. Some of these hypotheses are still th...

show abstract

Section: Introductionmentioning

confidence: 99%

Hypotheses on the Etiology of Antineutrophil Cytoplasmic Autoantibody–Associated Vasculitis

Wijngaarden¹,

Rijn²,

Hagen³

et al. 2008

Clinical Journal of the American Society of Nephrology

View full text Add to dashboard Cite

show abstract

“…In general, the presence of Staphylococcus aureus was accompanied by a higher risk for relapse, while the risk was modulated by the type of SAg, with tsst-1 being most strongly associated with disease relapse. The number of patients positive for Staphylococcus aureus tsst-1 was significantly higher with 36 % compared to the general population [7].…”

Section: The Nasal Microbiome In Granulomatosis With Polyangiitismentioning

confidence: 81%

The nasal microbiome in granulomatosis with polyangiitis

Kronbichler

2016

Wien klin Mag

View full text Add to dashboard Cite

“…Было установлено, что ре-цидивы ГПА провоцирует носительство в полости носа Staph. aureus [27], и особенно его суперантиген-токсина синдрома токсического шока 1 (toxic shock syndrome toxin 1, TSST-1) [28]. Представлены свидетельства возможной свя-зи продукции АНЦА с другими инфекциями; в частности, АНЦА с различной специфичностью обнаруживали у больных бактериальным эндокардитом (антитела к МПО и ПР3) [29,30], лепрой [31], туберкулезом (антитела к ПР3) [32], эхинококкозом (антитела к МПО и лактоферрину) [33], гепатитом С (антитела к катепсину G) [34], парвови-русом B19 (антитела к МПО и ПР3) [35].…”

Section: Discussionunclassified

Granulomatosis With Polyangiitis, Which Is Pathogenetically Associated With Antineutrophil Cytoplasmic Antibodies: Clinical Features

Бекетова¹

2012

rsp

View full text Add to dashboard Cite

Staphylococcal toxic-shock-syndrome-toxin-1 as a risk factor for disease relapse in Wegener's granulomatosis

Abstract: The risk for relapse of WG increases with the presence of tsst-1-positive S. aureus. Eradication of tsst-1-positive S. aureus in WG may show whether disease relapses can be prevented.

Cited by 107 publications

References 24 publications

Hypotheses on the Etiology of Antineutrophil Cytoplasmic Autoantibody–Associated Vasculitis

Hypotheses on the Etiology of Antineutrophil Cytoplasmic Autoantibody–Associated Vasculitis

The nasal microbiome in granulomatosis with polyangiitis

Granulomatosis With Polyangiitis, Which Is Pathogenetically Associated With Antineutrophil Cytoplasmic Antibodies: Clinical Features

Contact Info

Product

Resources

About