Human mast cells produce matrix metalloproteinase 9

Kanbe, Naotomo; Tanaka, Akane; Kanbe, Michiyo; Itakura, Atsuko; Kurosawa, Motohiro

doi:10.1002/(sici)1521-4141(199908)29:08<2645::aid-immu2645>3.3.co;2-t

Cited by 23 publications

(24 citation statements)

References 6 publications

(8 reference statements)

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“…As most of these substances are found predominantly at the basement membrane, MMP‐9 is of particular interest in inflammatory skin diseases, where migration of cells across the basal layer to enter and leave the site of inflammation is required (31). For various cell types relevant in inflammatory skin diseases, the ability to produce MMP‐9 has been shown: epidermal keratinocytes (32), Langerhans cells (33), mast cells (34), T cells (35) and eosinophils (36). Here, we show that keratinocytes from patients with AD produce less MMP‐9 compared to keratinocytes from healthy controls.…”

Section: Discussionmentioning

confidence: 99%

Intrinsic alterations of pro-inflammatory mediators in unstimulated and TLR-2 stimulated keratinocytes from atopic dermatitis patients

Niebuhr

Heratizadeh

Wichmann

et al. 2011

Experimental Dermatology

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In many patients with atopic dermatitis (AD), the disease is complicated by their enhanced susceptibility to bacterial skin infections, especially with Staphylococcus aureus (S. aureus). Resistance to bacterial skin infections, e.g. S. aureus, is based on the function of intact innate immune mechanisms in the epidermis, mainly provided by keratinocytes. Toll-like receptor (TLR)-2 recognizes components of S. aureus and is known to be expressed on keratinocytes. The aim of this study was to investigate intrinsic TLR-2 expression and cytokine secretion upon TLR-2 stimulation with peptidoglycan (PGN), lipoteichoic acid (LTA) and N-palmitoyl-S-[2,3-bis(palmitoyl)-(2RS)-propyl]-(R)cysteinyl-alanyl-glycine (Pam3Cys) in keratinocytes from patients with AD compared to healthy controls. Human primary keratinocytes (HPKs) were cultivated from hair follicles of patients with AD and non-atopic healthy controls and stimulated with Pam3Cys, LTA and PGN. TLR-2, TLR-1 and TLR-6 expression were investigated at the mRNA level. IL-6, IL-8, chemokine C-C motif ligand (CCL)-20 and MMP-9 production were studied at the protein level. TLR-2, TLR-1 and TLR-6 were expressed on both HPKs from patients with AD as well as healthy controls without significant differences between these groups. HPKs from patients with AD had an intrinsically reduced capacity to produce IL-6, IL-8, CCL-20 and MMP-9 and responded less to TLR-2 stimulation compared to HPKs from healthy controls. Our findings show evidence for intrinsic alterations in HPKs from patients with AD compared to healthy controls and diminished responses upon TLR-2 stimulation that might contribute to the enhanced susceptibility to skin infections with S. aureus.

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Section: Discussionmentioning

confidence: 99%

Intrinsic alterations of pro-inflammatory mediators in unstimulated and TLR-2 stimulated keratinocytes from atopic dermatitis patients

Niebuhr

Heratizadeh

Wichmann

et al. 2011

Experimental Dermatology

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“…MMP‐2/gelatinase A and MMP‐9/gelatinase B appear to perform unique defined roles during tissue injury and repair (17). Inflammatory cells, such as mast cells (18, 19), neutrophils, macrophages, lymphocytes and eosinophils, secrete MMP‐9, while a myriad of cell types release MMP‐2. Recombinant canine SCF induces mast cell MMP‐9 expression in a dose‐dependent and selective manner (18).…”

Section: Mast Cell Phenotypesmentioning

confidence: 99%

Mast cells and angiogenesis

Norrby

2002

APMIS

319

277

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Angiogenesis is tightly regulated by pro- and anti-angiogenic factors. Secreting mast cells are able to induce and enhance angiogenesis via multiple in part interacting pathways. They include mast cell-derived (i) potent pro-angiogenic factors such as VEGF, bFGF, TGF-beta, TNF-alpha and IL-8, (ii) proteinases and heparin, that release heparin-binding pro-angiogenic factors lodged on cell surfaces and in the extracellular matrix (ECM), (iii) histamine, VEGF, and certain lipid-derived mediators that induce microvascular hyperpermeability having pro-angiogenic effects, (iv) chemotactic recruitment of monocytes/macrophages and lymphocytes that are able to contribute with angiogenesis-modulating molecules, (v) activation of platelets that release pro-angiogenic factors, (vi) activation of neighboring stationary non-mast cells, which secrete pro-angiogenic factors, ECM-degrading proteinases and stem cell factor which attracts, mitogenically stimulates and activates mast cells, (vii) auto- and paracrine stimulation of mast cells by stem cell factor, (viii) recruitment of mast cells by pro-angiogenic factors such as VEGF, bFGF and TGF-beta. As a result of ECM-degradation and changes in the microenvironment following initial mast cell secretion, the mast cell populations may change significantly in number, phenotype and function. In tumor models, mast cells have been shown to play a decisive role in inducing the angiogenic switch which precedes malignant transformation. There is, moreover, strong evidence that mast cells significantly influence angiogenesis and thus growth and progression in human cancers.

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“…Mast cells have also been shown to produce MMP-9,66 and inhalation of corticosteroids reduces submucosal expression of MMP-9 in asthmatics. As interest intensifies in the potential immunomodulatory roles of MMPs, we are likely to see advances in our understanding of allergic disorders of the anterior segment, as well as presumed immuno-inflammatory disorders of the posterior segment.…”

Section: Role In Physiological and Pathological Processesmentioning

confidence: 99%

Matrix metalloproteinase biology applied to vitreoretinal disorders

Sethi

Bailey²,

Luthert³

et al. 2000

British Journal of Ophthalmology

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Matrix metalloproteinases (MMPs) and their inhibitors are believed to have a significant role in a number of vitreoretinal diseases, from proliferative vitreoretinopathy to age related macular degeneration. The aim of this review is to summarise the current knowledge of their involvement in these diseases and to postulate potential therapeutic strategies.MMPs are a tightly regulated family of zinc dependent endopeptidases that are capable of degrading all components of the extracellular matrix (ECM) and basement membranes.1 The ECM is a complex structure that influences the behaviour of its resident cells, and those in the process of migration, by providing specific contextual information. Enzymes that modify the ECM thus have the potential to aVect basic cell biology in many physiological and pathological processes.2 Remodelling of the ECM must occur with spatial and temporal precision for normal development, morphogenesis, homeostasis, and tissue repair. As matrix degradation is a prerequisite for malignant invasion and metastasis, it is not surprising that MMP biology has attracted considerable interest, with clinical oncology trials under way in several organ systems.4-7 New proteolytic functions are also being defined for these enzymes. These include the degradation of non-matrix macromolecules such as myelin basic protein, inactivation of 1 antitrypsin, release of sequestered growth factors from ECM, and cleavage of bioactive molecules from the cell surface.

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Human mast cells produce matrix metalloproteinase 9

Cited by 23 publications

References 6 publications

Intrinsic alterations of pro-inflammatory mediators in unstimulated and TLR-2 stimulated keratinocytes from atopic dermatitis patients

Intrinsic alterations of pro-inflammatory mediators in unstimulated and TLR-2 stimulated keratinocytes from atopic dermatitis patients

Mast cells and angiogenesis

Matrix metalloproteinase biology applied to vitreoretinal disorders

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