Lymphocyte activation in silica-exposed workers

Rocha-Parise, Michelle; Santos, Leonilda Maria Barbosa dos; Damoiseaux, Jan; Bagatin, Ericson; Lido, Alessandro Vito; Torello, Cristiane Okuda; Tervaert, Jan Willem Cohen; Queiroz, Mary L.S.

doi:10.1016/j.ijheh.2013.11.002

Cited by 24 publications

(21 citation statements)

References 40 publications

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“…However, as this test still needs validation, it is difficult to draw conclusions on its result. Nevertheless, our LPT at least confirms that silica nanoparticles can enhance lymphocyte proliferative responses …”

Section: Discussionsupporting

confidence: 58%

Granulomatous lung disease in two workers making light bulbs

Ronsmans

Verbeken

Adams

et al. 2019

American J Industrial Med

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Section: Discussionsupporting

confidence: 58%

Granulomatous lung disease in two workers making light bulbs

Ronsmans

Verbeken

Adams

et al. 2019

American J Industrial Med

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“…The silica particles are then transported to regional lymph nodes, resulting in chronic activation of T cells and triggering autoimmune reactions in susceptible patients. [48][49][50] A higher incidence of MPO-AAV was reported after the Kobe earthquake in Japan, possibly related to increased silica exposure. 51 After closure of the last coal mine in the region of Maastricht, the Netherlands, MPO-AAV diagnoses appeared to decrease compared with the number of PR3-AAV diagnoses.…”

Section: Etiologymentioning

confidence: 99%

Proteinase 3-ANCA Vasculitis versus Myeloperoxidase-ANCA Vasculitis

Hilhorst

Paassen

Tervaert

2015

Journal of the American Society of Nephrology

177

137

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In patients with GN or vasculitis, ANCAs are directed against proteinase 3 (PR3) or myeloperoxidase (MPO). The differences between PR3-ANCA-associated vasculitis (AAV) and MPO-AAV described in the past have been supplemented during the last decade. In this review, we discuss the differences between these two small-vessel vasculitides, focusing especially on possible etiologic and pathophysiologic differences. PR3-AAV is more common in northern parts of the world, whereas MPO-AAV is more common in southern regions of Europe, Asia, and the Pacific, with the exception of New Zealand and Australia. A genetic contribution has been extensively studied, and there is a high prevalence of the HLA-DPB1*04:01 allele in patients with PR3-AAV as opposed to patients with MPO-AAV and/or healthy controls. Histologically, MPO-AAV and PR3-AAV are similar but show qualitative differences when analyzed carefully. Clinically, both serotypes are difficult to distinguish, but quantitative differences are present. More organs are affected in PR3-AAV, whereas renal limited vasculitis occurs more often in patients with MPO-AAV. For future clinical trials, we advocate classifying patients by ANCA serotype as opposed to the traditional disease type classification.

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“…Finckh and coworkers [ 6 ] found that occupational exposure to c SiO 2 , but not organic solvents, contributed to increased SLE in urban women. Other studies report SLE-like symptoms in individuals with silicosis, including lymphocyte activation and elevated antinuclear antibodies, immunoglobulins, and immune complexes [ 8 – 11 ].…”

Section: Introductionmentioning

confidence: 99%

Silica Triggers Inflammation and Ectopic Lymphoid Neogenesis in the Lungs in Parallel with Accelerated Onset of Systemic Autoimmunity and Glomerulonephritis in the Lupus-Prone NZBWF1 Mouse

et al. 2015

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Genetic predisposition and environmental factors influence the development of human autoimmune disease. Occupational exposure to crystalline silica (cSiO2) has been etiologically linked to increased incidence of autoimmunity, including systemic lupus erythematosus (SLE), but the underlying mechanisms are poorly understood. The purpose of this study was to test the hypothesis that early repeated short-term cSiO2 exposure will modulate both latency and severity of autoimmunity in the lupus-prone female NZBWF1 mouse. Weekly intranasal exposure to cSiO2 (0.25 and 1.0 mg) for 4 wk beginning at 9 wk of age both reduced latency and increased intensity of glomerulonephritis. cSiO2 elicited robust inflammatory responses in the lungs as evidenced by extensive perivascular and peribronchial lymphoplasmacytic infiltration consisting of IgG-producing plasma cells, and CD45R+ and CD3+ lymphocytes that were highly suggestive of ectopic lymphoid tissue (ELT). In addition, there were elevated concentrations of immunoglobulins and the cytokines MCP-1, TNF-α and IL-6 in bronchoalveolar lavage fluid. cSiO2-associated kidney and lung effects paralleled dose-dependent elevations of autoantibodies and proinflammatory cytokines in plasma. Taken together, cSiO2-induced pulmonary inflammation and ectopic lymphoid neogenesis in the NZBWF1 mouse corresponded closely to systemic inflammatory and autoimmune responses as well as the early initiation of pathological outcomes in the kidney. These findings suggest that following airway exposure to crystalline silica, in mice genetically prone to SLE, the lung serves as a platform for triggering systemic autoimmunity and glomerulonephritis.

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Lymphocyte activation in silica-exposed workers

Cited by 24 publications

References 40 publications

Granulomatous lung disease in two workers making light bulbs

Granulomatous lung disease in two workers making light bulbs

Proteinase 3-ANCA Vasculitis versus Myeloperoxidase-ANCA Vasculitis

Silica Triggers Inflammation and Ectopic Lymphoid Neogenesis in the Lungs in Parallel with Accelerated Onset of Systemic Autoimmunity and Glomerulonephritis in the Lupus-Prone NZBWF1 Mouse

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