Matrix metalloproteinase-3 (stromelysin-1) in acute inflammatory tissue injury

Nerusu, Kamalakar C.; Warner, Roscoe L.; Bhagavathula, Narasimharao; McClintock, Shannon D.; Johnson, Kent J.; Varani, James

doi:10.1016/j.yexmp.2007.04.003

Cited by 53 publications

(52 citation statements)

References 35 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Induction of genes in H37Rv-infected iNOS -/-mice with relation to oxidative burst (phagocyte oxidase phox, myeloperoxidase (MPO), xanthine dehydrogenase (XDH) [53], lymphocyte cytosolic protein 2 LCP2 [54]) and protection against oxidative stress (superoxide dismutases, peroxireduxins, metallothioneins and glutathione reductase) or other neutrophil functions such as plastin (LCP1) [55] emphasize that neutrophils and oxidative processes are prominent in H37Rv-mediated inflammation. MMP, especially MMP3 [56], MMP8 and MMP9 [57] are involved in neutrophil-mediated inflammatory processes [56,57]. These MMP were strongly induced during H37Rv-mediated inflammation in iNOS -/-lungs as well.…”

Section: Innate Immune Responsementioning

confidence: 95%

Combination of host susceptibility and Mycobacterium tuberculosis virulence define gene expression profile in the host

Beisiegel¹,

Mollenkopf²,

Hahnke³

et al. 2009

Eur J Immunol

View full text Add to dashboard Cite

Progression and outcome of tuberculosis is governed by extensive crosstalk between pathogen and host. Analyses of global changes in gene expression during immune response to infection with Mycobacterium tuberculosis (M.tb) can help identify molecular markers of disease state and progression. Global distribution of M.tb strains with different degrees of virulence and drug resistance, especially for the immunocompromised host, make closer analyses of host responses more pressing than ever. Here, we describe global transcriptional responses of inducible nitric oxide synthase-deficient (iNOS -/-) and WT mice infected with two related M.tb strains of markedly different virulence, namely the M.tb laboratory strains H37Rv and H37Ra. Both hosts exhibited highly similar resistance to infection with H37Ra. In contrast, iNOS -/-mice rapidly succumbed to H37Rv, whereas WT mice developed chronic course of disease. By differential analyses, virulence-specific changes in global host gene expression were analyzed to identify molecular markers characteristic for chronic versus acute infection. We identified several markers unique for different stages of disease progression and not previously associated with virulencespecific host responses in tuberculosis.

show abstract

Section: Innate Immune Responsementioning

confidence: 95%

Combination of host susceptibility and Mycobacterium tuberculosis virulence define gene expression profile in the host

Beisiegel¹,

Mollenkopf²,

Hahnke³

et al. 2009

Eur J Immunol

View full text Add to dashboard Cite

show abstract

“…In mice lacking MMP-3, intratracheal administration of immunoglobulin G resulted in less lung injury and neutrophil influx [55]. In another study, investigators reported a significant difference in neutrophil recruitment between MMP-3 knockout mice and MMP-9 knockout animals with the same injury, suggesting that MMP-3 plays an essential role in migration of neutrophils from the pulmonary circulation to the alveolus [52].…”

Section: Other Inhibitorsmentioning

confidence: 96%

Matrix metalloproteinases in acute lung injury: mediators of injury and drivers of repair

Davey¹,

2011

View full text Add to dashboard Cite

Acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) comprise a spectrum of acute inflammatory pulmonary oedema resulting in refractory hypoxaemia in the absence of an underlying cardiogenic cause. There are multiple pulmonary and extrapulmonary causes and ALI/ARDS patients are a clinically heterogeneous group with associated high morbidity and mortality.Inflammatory injury to the alveolar epithelial and endothelial capillary membrane is a central event in the pathogenesis of ALI/ARDS, and involves degradation of the basement membrane. Matrix metalloproteinases (MMPs) have been implicated in a wide variety of pulmonary pathologies and are capable of degrading all components of the extracellular matrix including the basement membrane and key non-matrix mediators of lung injury such as chemokines and cell surface receptors.While many studies implicate MMPs in the injurious process, there are significant gaps in our knowledge of the role of specific proteases at different phases of injury and repair. This article examines the role of MMPs in injury and repair of the alveolar epithelial-endothelial capillary barrier and discusses the potential for MMP modulation in the prevention and treatment of ALI. The need for further mechanistic and in vivo studies to inform appropriate subsequent clinical trials of MMP modulation will be highlighted. KEYWORDS: Acute lung injury, acute respiratory distress syndrome, extracellular matrix, inflammation, matrix metalloproteinases, repair A cute lung injury (ALI) and acute respiratory distress syndrome (ARDS) are part of a disease spectrum associated with high mortality and considerable morbidity. The most recent diagnostic criteria for ALI/ARDS, developed by the 1994 American-European Consensus Conference Committee [1], are based on the gross clinico-radiological findings; acute onset, bilateral infiltrates on chest radiography, absence of left ventricular failure and the ratio of arterial oxygen tension (Pa,O 2 , expressed in mmHg) to inspired oxygen fraction (FI,O 2 ) measuring ,200 (ARDS) or ,300 (ALI) [2][3][4]. However, ALI/ARDS patients are clinically heterogeneous and this definition does not take into account the underlying aetiology or severity of illness reflected by failure of other organ systems [2]. Irrespective of aetiology, the pathogenesis of ALI/ARDS consists of an excessive and inappropriate inflammatory response to a range of pulmonary or extrapulmonary insults, resulting in damage to the alveolar epithelial-endothelial capillary barrier [3,4]. Clinically, this manifests as refractory hypoxaemia and decreased pulmonary compliance. Pathologically, three phases are recognised: an initial acute inflammatory or exudative phase characterised by

show abstract

“…Furthermore, a model of VILI [19] demonstrated that MMP-9 function is worth preserving, given that mice defi cient in this protease had increased levels of lung injury. On the other hand, MMP-3 may be detrimental, as mice lacking this MMP were protected against lung injury caused by administration of nonspecifi c IgG [20] or bleomycin [21]. Regarding MMP-8, this protease has shown diff erent eff ects depending on the experimental model.…”

Section: The Role Of Infl Ammation In Tissue Damage and Repairmentioning

confidence: 99%

Repair after Acute Lung Injury: Molecular Mechanisms and Therapeutic Opportunities

González-López¹,

Albaiceta²

2012

Annual Update in Intensive Care and Emergency Medicine 2012

View full text Add to dashboard Cite

show abstract

Matrix metalloproteinase-3 (stromelysin-1) in acute inflammatory tissue injury

Cited by 53 publications

References 35 publications

Combination of host susceptibility and Mycobacterium tuberculosis virulence define gene expression profile in the host

Combination of host susceptibility and Mycobacterium tuberculosis virulence define gene expression profile in the host

Matrix metalloproteinases in acute lung injury: mediators of injury and drivers of repair

Repair after Acute Lung Injury: Molecular Mechanisms and Therapeutic Opportunities

Contact Info

Product

Resources

About