Monocyte chemoattractant protein 1, interleukin 8, and chronic airways inflammation in COPD

Boer, Willem I. de; Sont, Jacob K.; Schadewijk, Annemarie van; Stolk, Jan; Krieken, J. Han van; Hiemstra, Pieter S.

doi:10.1002/(sici)1096-9896(200004)190:5<619::aid-path555>3.0.co;2-6

Cited by 271 publications

(176 citation statements)

References 32 publications

(55 reference statements)

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“…Staining intensities for EMMPRIN, MMP-2, MMP-7 and MMP-9 expression were then scored for each cell type at the same magnification using a visual scoring method with grades ranging from 0 to 3 (0 = no staining; 1 = moderate staining; 2 = intense staining; 3 = very intense staining), as previously described (20). We evaluated co-localization of EMMPRIN with MMPs on serial sections from the same tissue block.…”

Section: Semi-quantification Of Immunohistochemistrymentioning

confidence: 57%

Extracellular matrix metalloproteinase inducer in interstitial pneumonias

et al. 2006

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Extracellular matrix metalloproteinase inducer (EMMPRIN), a glycosylated transmembrane protein that induces matrix metalloproteinases (MMPs), is minimally expressed in the normal adult lung. We previously reported that it is upregulated in murine bleomycin-induced lung injury. In this study, we determined the expression of EMMPRIN and its association with MMPs-2, -7, and -9 in interstitial pneumonias (IPs). We performed immunohistochemistry for EMMPRIN and MMPs on lung tissue from 22 subjects with various IPs. We did bronchoalveolar lavage (BAL) on 9 of these subjects and 13 others with Thank you for the review of our manuscript, "Extracellular Matrix Metalloproteinase Inducer in Interstitial Pneumonias". We appreciate the constructive comments from you and the reviewers. We are pleased to enclose a revised manuscript, marked version of the manuscript and point-by-point responses to the comments of the reviewers.In the revised manuscript, we added a new table (labeled Table 2) according to the suggestion of reviewer 2. That table demonstrates that we have analyzed the three histological patterns of IPs, UIP, NSIP, and OP, separately. While the present findings do not point to mechanisms for EMMPRIN induction in IPs or a role of EMMPRIN in the development of IPs, we speculate that EMMPRIN affects reepithelialization in IPs via its capacity to induce the expression of MMPs, particularly in hyperplastic type II cells. We feel that the manuscript has been improved as a result of the review process and look forward to a favorable response to this revision.Thank you for your attention. Response to ReviewersThe problem with this study is that the authors lump usual interstitia l pneumonia, nonspecific interstitia l pneumonia, and organizing pneumonia together as IPs. Although it is true that each of the three histological patterns can be classified as an IP, they are a very diverse group and their pathogeneses are most likely different. Therefore, for scientific purposes they should be analyzed separately. The data presented in the manuscript do not suggest a functional role of EMMPRIN in IPs. It merely indicates that reactive epithelial cells of all kinds may overexpress EMMPRIN.Otherwise, the scientific methods appear to be valid, the manuscript is well written, and the figures are of acceptable quality.We appreciate the reviewer's comments. According to the reviewer's suggestions, we have added new data demonstrating the individual scores for each type of abnormal epithelial cells and analyzed them in UIP, NSIP and OP, separately (new Table 2 in the revised manuscript). To reflect this change we have revised the manuscript as follows:"Neither squamous metaplasia nor bronchiolization was observed in OP. Only hyperplastic type II cells were present, and these cells expressed EMMPRIN to various degrees. Accordingly, we evaluated EMMPRIN only in UIP and NSIP. There were no statistical differences in the score of EMMPRIN in each type of epithelial cells between UIP and NSIP. Therefore, we compared the immunore...

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Section: Semi-quantification Of Immunohistochemistrymentioning

confidence: 57%

Extracellular matrix metalloproteinase inducer in interstitial pneumonias

et al. 2006

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“…IL-8 and MCP-1, which are chemotactic factors for monocytes and neutrophils, respectively, produced mainly by vascular endothelial cells of the lungs, 18,19 are thought to be involved in the development of acute lung injury and inflammation. [20][21][22][23] The levels of IL-8 and MCP-1 in bronchoalveolar lavage fluid have been reported to correlate with clinical severity and mortality in patients with acute lung injury. 23 Regarding the pathogenesis of RPE, the pulmonary microvascular endothelium is mechanically destroyed immediately after the collapsed lung has been expanded, and ischemia-reperfusion injury subsequently occurs in the injured pulmonary microvessels.…”

Section: Discussionmentioning

confidence: 93%

Severe Re-expansion Pulmonary Edema Induced by One-Lung Ventilation

Sugiyama

Shimizu

et al. 2015

Respir Care

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We present 2 cases of severe re-expansion pulmonary edema (RPE) after one-lung ventilation (OLV) for thoracic surgery. A 32-y-old woman with multiple lung metastases developed severe RPE after OLV during lung resection surgery. A 37-y-old man with infective endocarditis also developed severe RPE after OLV for mitral valve plasty with minimally invasive cardiac surgery. In both cases, results of a preoperative pulmonary function test and oxygenation were almost normal, and pleural effusion or pulmonary congestion was not detected in preoperative computed tomography; however, there was a possibility that subclinical lung injury existed before surgery. The levels of interleukin-8 and monocyte chemotactic protein-1, which are thought to play important roles in the development of lung injury, in bronchial secretions were extremely high after the onset of RPE. These results suggest that the pathogenesis of RPE shares, at least in part, a common pathophysiology of acute lung injury. Key words: pulmonary edema; one-lung ventilation; interleukin-8; monocyte chemotactic protein-1. [Respir Care 2015;60(8):e134 -e140.

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“…However, monocytes/macrophages are the major source of CCL2 (27). In line with this cellular pattern of CCL2 expression, De Boer et al reported a strong signal for CCL2 in macrophages and a weak signal in alveolar epithelial cells (13).…”

Section: Discussionmentioning

confidence: 99%

“…CCL2 (MCP-1; monocyte chemoattractant protein-1) is produced by many cell types, including fibroblasts, endothelial, epithelial, smooth muscle, mesangial, astrocytic, monocytic and microglial cells. It has been shown to be elevated in tissue sections in ex-smokers with, as compared to exsmokers without, COPD (13). CCL7, previously called MCP-3 (monocyte chemoattractant protein-3), has an expression pattern that is more restricted compared with CCL2.…”

Section: Chemokine Expression By Small Sputum Macrophages In Copdmentioning

confidence: 99%

Chemokine Expression by Small Sputum Macrophages in COPD

Frankenberger

Eder

Hofer

et al. 2011

Mol Med

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Small sputum macrophages represent highly active cells that increase in the airways of patients with inflammatory diseases such as chronic obstructive pulmonary disease (COPD). It has been reported often that levels of cytokines, chemokines and proteases are increased in sputum supernatants of these patients. In COPD, the small sputum macrophages may contribute to these supernatant proteins and recruit additional cells via specific chemokine expression patterns. We therefore investigated the expression profile of chemokines in sputum macrophages obtained from COPD patients in comparison to cells from healthy donors and cells isolated after inhalation of lipopolysaccharide (LPS). We used the minimally invasive procedure of sputum induction and have purified macrophages with the RosetteSep technology. Using macrophage purification and flow cytometry we show that in COPD small sputum macrophages account for 85.9% ± 8.3% compared with 12.9% ± 7.1% of total macrophages in control donors. When looking at chemokine expression we found, for the small macrophages in COPD, increased transcript and protein levels for CCL2, CCL7, CCL13 and CCL22 with a more than 100-fold increase for CCL13 mRNA (P < 0.001). Looking at active smokers without COPD, there is a substantial increase of small macrophages to 60% ± 15% and, here, chemokine expression is increased as well. In a model of airway inflammation healthy volunteers inhaled 20 μg of lipopolysaccharide (LPS), which resulted in an increase of small sputum macrophages from 18% ± 19% to 64% ± 25%. The pattern of chemokine expression was, however, different with an upregulation for CCL2 and CCL7, while CCL13 was downregulated three-fold in the LPS-induced small macrophages. These data demonstrate that sputum macrophages in COPD show induction of a specific set of CCL chemokines, which is distinct from what can be induced by LPS.

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Monocyte chemoattractant protein 1, interleukin 8, and chronic airways inflammation in COPD

Cited by 271 publications

References 32 publications

Extracellular matrix metalloproteinase inducer in interstitial pneumonias

Extracellular matrix metalloproteinase inducer in interstitial pneumonias

Severe Re-expansion Pulmonary Edema Induced by One-Lung Ventilation

Chemokine Expression by Small Sputum Macrophages in COPD

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