Bronchoalveoloar lavage fluid cytokines and chemokines as markers and predictors for the outcome of interstitial lung disease in systemic sclerosis patients

Schmidt, Karl‐Hermann; Martínez-Gamboa, Lorena; Meier, Susan; Witt, Christian; Meisel, Christian; Hanitsch, Leif G.; Becker, Mike; Huscher, Dörte; Burmester, Gerd R.; Riemekasten, Gabriela

doi:10.1186/ar2766

Cited by 110 publications

(84 citation statements)

References 39 publications

(40 reference statements)

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“…Currently, several biological markers, such as neutrophilic alveolitis surfactant A and D [14], or cytokines, such as tumour necrosis factor-a [15], and chemokines, such as interleukin-8 [16] and CCL2 [16][17][18], and alveolar concentration of nitric oxide [19,20], have been shown to be associated with the severity of ILD in SSc. Nevertheless, for each biomarker, long-term follow-up studies showing relevant prognostic value for progression are lacking.…”

Section: Discussionmentioning

confidence: 99%

Serum CC chemokine ligand-18 predicts lung disease worsening in systemic sclerosis

Tiev¹,

Hua-Huy²,

Kettaneh³

et al. 2011

Eur Respir J

100

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Elevated serum CC chemokine ligand (CCL)18 reflects lung fibrosis activity in systemic sclerosis (SSc) and could be an early marker of lung function worsening. Therefore, we sought to evaluate whether serum CCL18 levels at baseline could predict worsening of lung disease in SSc.In this prospective study, 83 SSc patients were analysed longitudinally over a 4-yr observation period for the risk of occurrence of combined deleterious events, defined as a 10% decrease from baseline of total lung capacity or forced vital capacity % predicted, or death, according to serum CCL18 at inclusion. Receiver operating characteristic (ROC) curve analysis was performed for prediction of events during the first year after inclusion. The best cut-off level of serum CCL18 for prediction of a combined event within the follow-up period was 187 ng?mL -1 , with 53% sensitivity and 96% specificity (area under the ROC curve 0.86; p,0.001). After a mean¡SD follow-up of 33.7¡10.8 months, a higher rate of disease progression occurred in the group with serum CCL18 levels .187 ng?mL -1 . The adjusted hazard ratio was 5.36 (95% CI 2.44-11.75; p,0.001). In summary, serum CCL18 is an accurate predictive biomarker for the identification of patients with a higher risk of subsequent scleroderma lung disease worsening.

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Section: Discussionmentioning

confidence: 99%

Serum CC chemokine ligand-18 predicts lung disease worsening in systemic sclerosis

Tiev¹,

Hua-Huy²,

Kettaneh³

et al. 2011

Eur Respir J

100

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“…Biomarkers of various kinds have an important theoretical role in this regard, both in initial evaluation and in monitoring. However, candidate serum, bronchoalveolar lavage and imaging biomarkers in CTD-ILD have mostly been studied only at a single point in time [34], including surfactant protein A and B (SP-A, SP-B) [35,36,37], Krebs von den Lungen (KL)-6 [35,38,39,40,41], other lung epithelium-derived proteins, as well as chemokines, cytokines, matrix metalloproteinases and interleukins [34,42,43,44,45,46,47,48]. Serial biomarker trends have the potential to refine prognostic evaluation with exciting possibilities with the introduction of a therapy, and short-term biomarker changes might provide invaluable information on longer-term efficacy.…”

Section: Pulmonary ‘Disease Activity' In Monitoringmentioning

confidence: 99%

Monitoring of Lung Involvement in Rheumatologic Disease

Paschalaki

Jacob²,

Wells

2016

Respiration

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The monitoring of lung involvement in patients with connective tissue diseases is central to optimal long-term management and is directed towards: (a) the detection of supervening lung involvement not present at presentation and (b) the identification of disease progression in established lung disease. For both goals, accurate surveillance requires multi-disciplinary evaluation with the integration of symptomatic change, serial pulmonary function trends and imaging data. Evaluated in isolation, each of these monitoring domains has significant limitations. Symptomatic change may be confounded by a wide variety of systemic factors. Pulmonary function tests provide the most reliable data, but are limited by measurement variability, the heterogeneity of functional patterns and the confounding effects of non-pulmonary factors. Chest radiography is insensitive to change but may provide rapid confirmation of major disease progression or alert the clinician to respiratory co-morbidities. Although high-resolution computed tomography has a central role in assessing disease severity, it should be used very selectively as a monitoring tool due to the associated radiation burden. Ancillary tests include echocardiography and exercise testing to proactively identify cases of pulmonary hypertension and worsening of oxygenation. In summary, a multi-disciplinary approach is essential for the identification of disease progression and prompt treatment of comorbidities that severely impact on the morbidity and mortality of disease.

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“…8). MCP-1 is commonly upregulated in the lungs of patients with inflammatory conditions such as ARDS, PF, and systemic sclerosis (1,13,15,29). It also correlates with the level of lung injury in the later stages of ARDS (15).…”

Section: Discussionmentioning

confidence: 99%

Sequential expression of IGF-IB followed by active TGF-β1 induces synergistic pulmonary fibroproliferation in vivo

Andonegui

Léger

et al. 2012

American Journal of Physiology-Lung Cellular and Molecular Phys

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Pulmonary fibrosis, the end stage of a variety of fibroproliferative lung diseases, is usually induced after repetitive or chronic lung injury or inflammation. The mechanisms of fibroproliferation are poorly understood. Insulin-like growth factor-I (IGF-I) is significantly elevated in patients with pulmonary fibrosis and fibroproliferative acute respiratory distress syndrome. However, we showed that IGF-I overexpression alone in wild-type mouse lungs does not cause fibroproliferation. We therefore questioned whether IGF-I, acting together with active TGF-β1, a known profibrotic cytokine, enhances pulmonary fibroproliferation caused by active TGF-β1. A unique sequential adenoviral transgene mouse model was used expressing AdEmpty/AdTGF-β1 or AdhIGF-IB/AdTGF-β1 transgenes. IGF-IB plus active TGF-β1 transgene expression synergistically increased collagen deposition in the lung parenchyma compared with active TGF-β1 expression alone. The enhanced fibrosis was accompanied by an increased recruitment of macrophages and lymphocytes into the bronchoalveolar lavage fluid (BALF) and inflammatory cells in the lungs. α-Smooth muscle actin expression, a marker of myofibroblast proliferation and differentiation, was also increased. Finally, fibroblasts exposed ex vivo to BALF isolated from AdhIGF-IB/AdTGF-β1-transduced mice showed synergistic collagen induction compared with BALF from AdEmpty/AdTGF-β1-transduced mice. This study provides the first direct evidence that IGF-I is able to synergistically enhance pulmonary fibroproliferation in cooperation with TGF-β1.

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Bronchoalveoloar lavage fluid cytokines and chemokines as markers and predictors for the outcome of interstitial lung disease in systemic sclerosis patients

Cited by 110 publications

References 39 publications

Serum CC chemokine ligand-18 predicts lung disease worsening in systemic sclerosis

Serum CC chemokine ligand-18 predicts lung disease worsening in systemic sclerosis

Monitoring of Lung Involvement in Rheumatologic Disease

Sequential expression of IGF-IB followed by active TGF-β1 induces synergistic pulmonary fibroproliferation in vivo

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