Matrix metalloproteinases and TIMP‐1 production by peripheral blood granulocytes from COPD patients and asthmatics

Cataldo, Didier; Munaut, Carine; Noël, Agnès; Frankenne, Françis; Bartsch, Pierre; Foidart, Jean-Michel; Louis, Renaud

doi:10.1034/j.1398-9995.2001.056002145.x

Cited by 54 publications

(44 citation statements)

References 30 publications

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“…Increased levels of MMP-9 were indeed detected in bronchoalveolar lavage fluid (Mautino et al, 1997), sputum induced by the inhalation of hypertonic saline (Cataldo et al, 2000;Vignola et al, 1998b) and in serum of asthmatic patients (Bosse et al, 1999). The increased MMP-9 activity observed in the airways of asthmatic patients seems related to an increased number of granulocytes and more precisely neutrophils in the airways rather than to an enhancement of MMP-9 secretion by those cells (Cataldo et al, 2001;Prause et al, 2004). Other authors have suggested that eosinophils, key cells in asthma-related airway inflammation, could also be a major source for MMP-9 in this disease (Ohno et al, 1997).…”

mentioning

confidence: 83%

“…Besides MMP-9 production, neutrophils also produce MMP-8 that is stored in their secondary granules and released upon stimulation. An increase of MMP-8 expression has been reported in bronchial biopsies and in bronchoalveolar lavage from asthmatic patients suggesting that this enzyme could play an important role in this disease (Cataldo et al, 2001;Prikk et al, 2002). To verify this hypothesis, we recently applied a mouse model of asthma to MMP-8 deficient mice (MMP-8 KO) and we found surprisingly that mice lacking MMP-8 displayed a severe granulocytic inflammation in airways after allergen exposure .…”

Section: Implication Of Mmps In the Pathogenesis Of Asthmamentioning

confidence: 99%

“…Smooth muscle cells are also a source of MT1 -MMP, TIMP-1 and TIMP-2 and produce MMP-3 and MMP-7 mRNA in moderate levels (Elshaw et al, 2004). Among inflammatory cells, neutrophils produce MMP-9, MMP-8 and TIMP-1 which are synthesized and released from their secondary granules upon activation (Cataldo et al, 2001). Alveolar macrophages produce MMP-1, MMP-9, MMP-12 and TIMP-1.…”

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confidence: 99%

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Matrix metalloproteinases (MMPs) and tissue inhibitors of MMPs in the respiratory tract: Potential implications in asthma and other lung diseases

Guéders

Foidart

Noël

et al. 2006

European Journal of Pharmacology

279

224

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In healthy lung, Matrix Metalloproteinases (MMPs) and their physiological inhibitors, tissue inhibitors of matrix metalloproteinases (TIMPs), are produced in the respiratory tract by a panel of different structural cells. These activities are mandatory for many physiological processes including development, wound healing and cell trafficking. Deregulation of proteolytic-antiproteolytic network and inappropriate secretion of various MMPs by stimulated structural or inflammatory cells is thought to take part to pathophysiology of numerous lung diseases including asthma, chronic obstructive pulmonary disease (COPD), lung fibrosis and lung cancer. Cytokines and growth factors are involved in these inflammatory processes and some of those mediators interact directly with MMPs and TIMPs leading either to a regulation of their expression or changes in their biological activities by proteolytic cleavage. In turn, cytokines and growth factors modulate secretion of MMPs establishing a complex network of reciprocal interactions. Every MMP seem to play a rather specific role and some variations of their expression are observed in different lung diseases. The precise role of these enzymes and their inhibitors is now studied in depth as they could represent relevant therapeutic targets for many diseases. Indeed, MMP inhibition can lead either to a decrease of the intensity of a pathological process or, in the contrary for some of them, to an increase of disease severity. In this review, we focus on the role played by MMPs and TIMPs in asthma and we provide an overview of their potential roles in COPD, lung fibrosis and lung cancer, with a special emphasis on loops including MMPs and cytokines and growth factors relevant in these diseases.Keywords: Matrix metalloproteinase; Tissue inhibitor of MMP; Asthma; Cytokine; Growth factors Matrix metalloproteinases (MMPs) and tissue inhibitors of metalloproteinases (TIMPs)Matrix metalloproteinases (MMPs), or matrixins, belong to the metzincin superfamily of metalloproteinases, also including astacins, ADAMs (a protein with a disintegrin and metallopro-tease domain) and ADAM-TS proteases (ADAM with a thrombospondin-like motif) (Sternlicht and Werb, 2001;Folgueras et al., 2004;Handsley and Edwards, 2005;Noel et al., 2004). MMPs are proteolytic enzymes believed to be implicated in many physiological and pathological processes including embryonic development, morphogenesis, reproductive processes, bone remodeling, wound healing, cancer, arthritis, atherosclerosis, MMPs are zinc and calciumdependent enzymes being able to degrade virtually all extracellular matrix components. This can modulate cell behaviour by creating influential cellular environment (Shapiro, 1998). The extracellular matrix is a complex network of molecules including collagens, fibronectin, laminin, entactin/ nidogen and heparan sulfate proteoglycans (Mott and Werb, 2004). The extracellular matrix is a mechanical support for cells but also acts as a reservoir for cytokines and growth factors (vascular endothelial ...

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confidence: 83%

Section: Implication Of Mmps In the Pathogenesis Of Asthmamentioning

confidence: 99%

mentioning

confidence: 99%

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Matrix metalloproteinases (MMPs) and tissue inhibitors of MMPs in the respiratory tract: Potential implications in asthma and other lung diseases

Guéders

Foidart

Noël

et al. 2006

European Journal of Pharmacology

279

224

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“…Neutrophils are an important source of MMP-9 and TIMP-1 [23,24]. CATALDO et al [24] reported that the spontaneous release of TIMP-1 and MMP-9 secretion by circulating granulocytes was similar in COPD patients, asthmatic subjects and control subjects.…”

Section: Discussionmentioning

confidence: 99%

Increased serum concentrations of tissue inhibitor of metalloproteinase-1 in COPD patients

Higashimoto

Yamagata²,

Iwata³

et al. 2005

Eur Respir J

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Matrix metalloproteinase (MMP)-9 and tissue inhibitors of metalloproteinase (TIMP)-1 concentrations are increased in the sputum of asthma and chronic bronchitis patients, and are thought to be related to airflow obstruction. However, serum concentrations of these enzymes have not been clearly evaluated in patients with chronic obstructive pulmonary disease (COPD). The aim of this study was to examine the serum concentrations of these enzymes in COPD and asthmatic patients in order to determine their relationship with airway obstruction.Serum samples were obtained from 72 patients with COPD: 66 control subjects and 26 patients with asthma. Smoking histories of control subjects were matched with those of COPD patients. Serum concentrations of TIMP-1 and MMP-9 were determined by ELISA.The circulating TIMP-1 concentration was significantly higher in stable COPD patients than in control and asthmatic subjects, and was significantly negatively correlated with forced expiratory volume in one second/forced vital capacity in COPD patients. The molar ratio between MMP-9 and TIMP-1 was significantly lower in COPD patients than in control subjects. In patients with COPD, the serum TIMP-1 concentration was significantly increased during disease exacerbation.In conclusion, the current findings suggest that serum tissue inhibitors of metalloproteinase-1 concentration can be used as a serum marker of airway obstruction and exacerbation in chronic obstructive pulmonary disease patients.KEYWORDS: Bronchial asthma, chronic obstructive pulmonary disease, exacerbation, metalloproteinases, serum markers, tissue inhibitors of matrix metalloproteinases P ulmonary emphysema, the major contributor to morbidity and mortality in patients with chronic obstructive pulmonary disease (COPD), is characterised by progressive destruction of the extracellular matrix (ECM) of the lung [1-4]. The most widely accepted theory of the pathogenesis of pulmonary emphysema is a proteinase-antiproteinase imbalance. Although a number of studies have demonstrated the important role of increased elastolytic activity derived from neutrophils in emphysema [4,5], recent studies have shown that matrix metalloproteinases (MMPs) play key roles in tissue remodelling of the airways in COPD and asthma patients [2,[6][7][8]. MMPs are a family of structurally related enzymes that are capable of degrading all components of the ECM [9]. Members of the MMP family are selectively inhibited by tissue inhibitors of metalloproteinases (TIMPs). TIMP-1 has been shown to bind to both the active and precursor form of MMP-9, in a 1:1 proportion, and to inhibit its enzymatic activity. Sputum concentrations of MMP-9 and TIMP-1 are increased in patients with COPD and asthma [2,10]. RUSSELL et al. [11] showed that alveolar macrophages from patients with COPD release larger amounts of MMP-9 with greater enzymatic activity than those from healthy smokers. Two recent studies found that the MMP-9/TIMP-1 ratio was correlated with the degree of airway obstruction. BOSSE et al. [12]...

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“…31 We elucidate the subcellular distribution of the p65 NF-kB subunit in granulocytes treated with TNF-a (50 ng/ml) for 4 h in vitro. 3T3 cell lysates were used as reference controls.…”

Section: Resultsmentioning

confidence: 99%

SOCS3 dictates the transition of divergent time-phased events in granulocyte TNF-α signaling

2013

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Tumor-necrosis factor-a (TNF-a)-driven nuclear factor-kB (NF-kB) activation and apoptosis are opposing pathways; the growing recognition of these conflicting roles of TNF-a is perplexing. Here, we show that inflammation and apoptosis are time-phased events following TNF-a signaling and that emergence of suppressor of cytokine signaling 3 (SOCS3) expression limits the ongoing NF-kB activation and promotes apoptosis; further, we suggest an altered view of how inflammatory diseases are initiated and sustained. In vitro, TNF-a (50 ng/ml) induced granulocyte SOCS3 protein, inhibited nuclear accumulation of the p65NF-kB subunit and enhanced apoptosis, as shown by DNA laddering, annexin V positivity, and overexpression of caspase-3 and Bax in the late phase, whereas the early phase was marked by NF-kB activation. Conversely, SOCS3 knockdown by small interfering RNA (siRNA) inhibited granulocyte apoptosis and enhanced nuclear accumulation of p65 and 59 lipooxygenase expression in the late phase of TNF-a signaling. As apoptosis is associated with SOCS3 abundance, we suggest that these divergent TNF-a-driven events are time-phased, interconnected, opposing control mechanisms and one of the central features through which the immune system resolves pulmonary inflammation. Dysregulation may initiate mucosal inflammation, thus changing the landscape of asthma therapy.

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Matrix metalloproteinases and TIMP‐1 production by peripheral blood granulocytes from COPD patients and asthmatics

Cited by 54 publications

References 30 publications

Matrix metalloproteinases (MMPs) and tissue inhibitors of MMPs in the respiratory tract: Potential implications in asthma and other lung diseases

Matrix metalloproteinases (MMPs) and tissue inhibitors of MMPs in the respiratory tract: Potential implications in asthma and other lung diseases

Increased serum concentrations of tissue inhibitor of metalloproteinase-1 in COPD patients

SOCS3 dictates the transition of divergent time-phased events in granulocyte TNF-α signaling

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