title: Effect of cyclophosphamide on cytokines in patients with primary Sjögren's syndrome-associated interstitial lung disease in South China.
abstract: The objective of the study is to investigate the mechanisms of cyclophosphamide sequential therapy for patient with primary Sjögren's syndrome-associated interstitial lung disease (PSS-ILD). This was a retrospective review of 15 patients (2005-2008) with PSS-ILD who underwent cyclophosphamide sequential therapy. Peripheral blood and bronchoalveolar lavage (BALF) were obtained before and 3, 6, 12 and 24 months after the treatment. The TNF-α and TGF-β1 mRNA levels in peripheral blood were measured using reverse transcription polymerase chain reaction. Serum and BALF TNF-α, TGF-β1 and MMP-9 levels were measured using sandwich enzyme-linked immunosorbent assay. The average levels of serum TNF-α (0.39 ± 0.22) and TGF-β1 (0.31 ± 0.18) mRNA in patients with PSS-ILD were higher compared with that in patients with PSS without ILD. TNF-α level (0.23 ± 0.19) was significantly decreased 3 months after cyclophosphamide treatment (t = 2.533, p < 0.05), and TGF-β1 (0.31 ± 0.18) level markedly decreased after 6 months of treatment (t = 2.617, p < 0.05). The levels of serum TNF-α (11.2 ± 2.6) μg/L, TGF-β1 (72 ± 19) μg/L and MMP-9 (38 ± 9) μg/L in patients with PSS-ILD were higher than that in patients with PSS without ILD. TGF-β1 (36 ± 12) μg/L level decreased significantly after 3 months of treatment (t = 2.526, p < 0.05), and TNF-α level (7.1 ± 1.3) μg/L markedly decreased after 6 months of therapy (t = 2.578, p < 0.05). MMP-9 level (18 ± 4) μg/L decreased significantly after 12-month treatment (t = 2.329, p < 0.05). The levels of BALF TNF-α (17.1 ± 3.5) μg/L, TGF-β1 (36 ± 17) μg/L and MMP-9 (27 ± 10) μg/L in patients with PSS-ILD were higher than that in patients with PSS without ILD. TGF-β1 (21 ± 14) μg/L level decreased significantly after 3-month treatment, and TNF-α level (9.4 ± 1.7) μg/L was decreased after 6 months of cyclophosphamide treatment that may be associated with its inhabitation on production of TNF-α, TGF-β1 and MMP-9.
authors.affiliation: Department of Clinical Immunology and Rheumatology, The Affiliated Hospital of Guilin Medical College, Guilin 541001, China.
authors.forename: Lihua
authors.initials: L
authors.lastname: Zhang
authors.forename: Hanyou
authors.initials: H
authors.lastname: Mo
authors.forename: Mengya
authors.initials: M
authors.lastname: Zhu
authors.forename: Lifang
authors.initials: L
authors.lastname: Wang
mesh_terms: D000328:Adult; D000368:Aged; D003520:Cyclophosphamide / Q000627:therapeutic use*; D005260:Female; D006801:Humans; D017563:Lung Diseases, Interstitial / Q000188:drug therapy* / Q000276:immunology; D008297:Male; D020780:Matrix Metalloproteinase 9 / Q000032:analysis; D008875:Middle Aged; D012189:Retrospective Studies; D012859:Sjogren's Syndrome / Q000150:complications*; D053773:Transforming Growth Factor beta1 / Q000032:analysis / Q000235:genetics*; D014409:Tumor Necrosis Factor-alpha / Q000032:analysis / Q000235:genetics*
chemical_list: D053773:Transforming Growth Factor beta1; D014409:Tumor Necrosis Factor-alpha; D003520:Cyclophosphamide; D020780:Matrix Metalloproteinase 9