ArticleLung1993
Increased interleukin 6 production by bronchoalveolar lavage cells in patients with active sarcoidosis.
Article in Lung, 1993. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
9 citing papers in PubMed, 43 citations in OpenAlex.
- The Convergence of Fibrosis and Granulomatous Inflammation: A Case Series on the Diagnostic and Therapeutic Challenges of Systemic Sclerosis and Sarcoidosis Overlap Syndrome.Diagnostics (Basel, Switzerland) · 2026Article
- Biochemical and genomic identification of novel biomarkers in progressive sarcoidosis: HBEGF, eNAMPT, and ANG-2.Frontiers in medicine · 2022Article
- Models Contribution to the Understanding of Sarcoidosis Pathogenesis: "Are There Good Models of Sarcoidosis?"Journal of clinical medicine · 2020Review
- Adaptive Immunity in Pulmonary Sarcoidosis and Chronic Beryllium Disease.Frontiers in immunology · 2020Review
- Disordered Toll-like receptor 2 responses in the pathogenesis of pulmonary sarcoidosis.Clinical and experimental immunology · 2013Article
- Article
- Evaluation of inflammatory cytokine secretion by human alveolar macrophages.Mediators of inflammation · 1999Article
- Article
- Imbalance of pro- and anti-inflammatory cytokines in pulmonary sarcoidosis.Mediators of inflammation · 1996Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Alveolitis of sarcoidosis is characterized by activated alveolar macrophages (AMs) and T cells. The mediators interleukin-1 (IL-1) and interleukin 6 (IL-6) released by AMs represent essential factors for the progression of the T cells in the cell cycle. The role of IL-1 in pulmonary sarcoidosis has previously been studied; however, the relevance of other mediators (i.e. IL-6) has not yet been evaluated. We measured the spontaneous and lipopolysaccharide (LPS)-induced release of IL-6 and tumor necrosis factor alpha (TNF alpha) by bronchoalveolar lavage cells (BAL) and peripheral blood mononuclear cells (PBMNC) in 6 control subjects (group A) and in 15 patients with sarcoidosis, 10 with active (group B), 5 with inactive disease (group C). IL-6 as well as TNF alpha were spontaneously released by BAL cells of the active group in significantly greater amounts compared to both other groups; IL-6: A, 165.5 pg/ml/24 hr/10(6) cells (range, 0-604), B, 946 (0-2467), C, 16.6 (0-83); TNF alpha: A, 162 pg/ml/24 hr/10(6) cells (0-523), B, 803 (100-17352), C, 100 (0-379). In all groups autologous PBMNC proved to be quiescent, releasing only baseline levels of the cytokines tested. After stimulation with LPS all these cells released great quantities of IL-6 and TNF alpha. In active disease a positive correlation between IL-6 and TNF alpha release was observed (r = 0.77, p < 0.02). The present study documents that in active sarcoidosis the spontaneous release of IL-6 by BAL cells parallels the spontaneous release of TNF alpha. IL-6 is capable of initiating the proliferation and activation of T cells in the lung.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.