Paradoxically decreased intracellular collagenase activity in macrophages from bronchoalveolar lavage fluid in current smokers and patients with obstructive ventilatory disorder

Hakoda, Yusuke; Ohkubo, Hirotsugu; Tago, H; Yoshida, Tsuyoshi; Minemura, Kazushige; Utsumi, Kenta; Aoshima, Masahiro; Ohyashiki, Kazuma

doi:10.3892/ijmm.13.6.859

Cited by 1 publication

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“…Increased release from alveolar macrophages cultures of elastolytic enzymes including cysteine, serine, and matrix metalloproteinases (MMP) as MMP-2 and MMP-9 [124][125] and decreased macrophage release of TGF-beta 1 (transforming growth factor) and tissue inhibitors of MMP (TIMP) has been reported in COPD subjects [125][126]. However, a more recent study reported decreased intracellular activity of MMPs [127] and decreased macrophage release of inflammatory mediators, TGF-beta1 (transforming growth factor) and TIMP-1 (tissue inhibitor of metalloproteinase) in BALF of COPD patients [128].…”

Section: Apoptosis In Copd Urinementioning

confidence: 98%

“…Urine sample analysis is an easy method to measure elastin breakdown and collagen degradation products ( Table 4). One study reported no difference in urinary markers of elastin or collagen degradation between COPD patients and smokers, however, ↑ neutrophils [112][113][114][115][142][143][144] ↑ CD8 lymphocytes [30,42,115,[129][130][131][142][143][144] ↑ eosinophils [42,115] ↑ apoptosis mediators [90,92,94,[107][108] ↓ Toll-like recognition receptors, TLR2, TLR4 and CD14 [109] ↓ Histone deacetylases (HDACs) [110] ↑ IL-6, IL-8, MPO (myeloperoxidase), GRO-a, GSH (glutathione), [132,[111][112][113][114][115][116][117][118][119][120][121] ↑ Collagenase 1 and 2 (MMP-1, MMP-8) and gelatinases A and B (MMP-2 , MMP-9) [122][123][124][125][126][127][128] ↓ TGF-beta 1 (transforming grow...…”

Section: Apoptosis In Copd Urinementioning

confidence: 99%

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Biomarkers in COPD

Tzortzaki¹,

Lambiri²,

Vlachaki³

et al. 2007

CMC

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Chronic Obstructive Pulmonary Disease is characterized by an abnormal inflammatory response of the lungs to noxious particles and gases, caused primarily by cigarette smoking. Although COPD affects the lung, it also produces significant systemic consequences. Inflammation, proteases-antiproteases imbalance, oxidative stress, tissue damage and tissue repair, apoptosis and several genes seem to be involved in the pathogenesis of the disease. The cellular and molecular events underlying COPD pathogenesis are driven by multifunctional molecules including enzymes, cytokines, chemokines, growth factors, lipid mediators and their respective receptors. A large number of biomarkers evaluated in COPD, showed a high degree of redundancy. Nevertheless, current understanding of the pathobiology of COPD suggests a number of biomarkers as potential candidates. The development of relevant markers of lung damage, pulmonary inflammation, and systemic disease will be essential to our further understanding of the natural history of COPD and the discovery of new, effective treatments for its progression. This review summarizes recent findings, on potential pulmonary biomarkers in the induced sputum, the exhaled air condensate, the peripheral blood, the urine, the bronchoalveolar lavage fluid, and in selective cases, in bronchial biopsies.

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Section: Apoptosis In Copd Urinementioning

confidence: 98%