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Haugen, Torbjørn; Nakstad, Britt; Lyberg, Torstein

doi:10.1023/a:1020283316002

Cited by 6 publications

(1 citation statement)

References 24 publications

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“…Research on both human and animal AMs challenged the homogeneity of this population [ 31 , 32 ]. Instead, density-gradient centrifugation splits them into distinct subpopulations with differences in the expression of surface markers and intracellular enzymes as well as tumour lysis, migration, cytotoxicity, phagocytosis, lymphoproliferative response augmentation, soluble mediator release, and procoagulant activity [ 33 – 42 ].…”

Section: Lung Macrophage Populations In Mice and Humansmentioning

confidence: 99%

Dysregulated Functions of Lung Macrophage Populations in COPD

Kapellos

Baßler

Aschenbrenner

et al. 2018

Journal of Immunology Research

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Chronic obstructive pulmonary disease (COPD) is a diverse respiratory disease characterised by bronchiolitis, small airway obstruction, and emphysema. Innate immune cells play a pivotal role in the disease's progression, and in particular, lung macrophages exploit their prevalence and strategic localisation to orchestrate immune responses. To date, alveolar and interstitial resident macrophages as well as blood monocytes have been described in the lungs of patients with COPD contributing to disease pathology by changes in their functional repertoire. In this review, we summarise recent evidence from human studies and work with animal models of COPD with regard to altered functions of each of these myeloid cell populations. We primarily focus on the dysregulated capacity of alveolar macrophages to secrete proinflammatory mediators and proteases, induce oxidative stress, engulf microbes and apoptotic cells, and express surface and intracellular markers in patients with COPD. In addition, we discuss the differences in the responses between alveolar macrophages and interstitial macrophages/monocytes in the disease and propose how the field should advance to better understand the implications of lung macrophage functions in COPD.

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Section: Lung Macrophage Populations In Mice and Humansmentioning

confidence: 99%

Dysregulated Functions of Lung Macrophage Populations in COPD

Kapellos

Baßler

Aschenbrenner

et al. 2018

Journal of Immunology Research

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Alveolar Macrophages as Orchestrators of COPD

Barnes

2004

COPD: Journal of Chronic Obstructive Pulmonary Disease

311

208

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Alveolar macrophages play a critical role in the pathophysiology of COPD and are a major target for future anti-inflammatory therapy. Macrophage numbers are markedly increased in the lung and alveolar space of patients with COPD and are localized to sites of alveolar destruction. The increased numbers of macrophages may result from increased recruitment of blood monocytes, prolonged survival in the lung and to a lesser extent to increased proliferation in the lung. Alveolar macrophages from COPD patients have an increased baseline and stimulated secretion of inflammatory proteins, including certain cytokines, chemokines, reactive oxygen species and elastolytic enzymes, which together could account for all of the pathophysiological features of COPD. Alveolar macrophages form COPD appear to be resistant to the anti-inflammatory effects of corticosteriods and this is linked to reduced activity and expression of histone deacetylase 2, a nuclear enzyme that switches off inflammatory genes activated through the transcription factor nuclear factor-KB. Alternative anti-inflammatory therapies that inhibit macrophages are therefore needed in the future to deal with the chronic inflammation of COPD. These drugs may include resveratrol, theophylline derivatives, MAP kinase inhibitors and phosphodiesterase-4 inhibitors.

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Heterogeneity in lipopolysaccharide responsiveness of endothelial cells identified by gene expression profiling: role of transcription factors

Beck

Rafat

Brinkkoetter³

et al. 2006

Clinical and Experimental Immunology

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SummaryInterindividual differences of endothelial cells in response to endotoxins might contribute to the diversity in clinical outcome among septic patients. The present study was conducted to test the hypothesis that endothelial cells (EC) with high and low proinflammatory potential exist and to dissect the molecular basis underlying this phenomenon. Thirty human umbilical vein endothelial cell (HUVEC) lines were stimulated for 24 h with lipopolysaccharide (LPS) and screened for interleukin (IL)-8 production. Based on IL-8 production five low and five high producers, tentatively called types I and II responders, respectively, were selected for genome-wide gene expression profiling. From the 74 genes that were modulated by LPS in all type II responders, 33 genes were not influenced in type I responders. Among the 41 genes that were increased in both responders, 17 were expressed significantly stronger in type II responders. Apart from IL-8, significant differences in the expression of proinflammatory related genes between types I and II responders were found for adhesion molecules [intercellular adhesion molecule (ICAM-1), Eselectin)], chemokines [monocyte chemoattractant protein (MCP-1), granulocyte chemotactic protein (GCP-2)], cytokines (IL-6) and the transcription factor CCAAT/enhancer binding protein-delta (C/EBP-δ δ δ δ ). Type I responders also displayed a low response towards tumour necrosis factor (TNF)-α α α α . In general, maximal activation of nuclear factor (NF)-κ κ κ κ B was achieved in type I responders at higher concentrations of LPS compared to type II responders. In the present study we demonstrate that LPS-mediated gene expression differs quantitatively and qualitatively in types I and II responders. Our results suggest a pivotal role for common transcription factors as a low inflammatory response was also observed after TNF-α α α α stimulation. Further studies are required to elucidate the relevance of these findings in terms of clinical outcome in septic patients.

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Untitled

Cited by 6 publications

References 24 publications

Dysregulated Functions of Lung Macrophage Populations in COPD

Dysregulated Functions of Lung Macrophage Populations in COPD

Alveolar Macrophages as Orchestrators of COPD

Heterogeneity in lipopolysaccharide responsiveness of endothelial cells identified by gene expression profiling: role of transcription factors

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