scholarly journals Role of Galectin-3 in the pathophysiology underlying allergic lung inflammation in a tissue inhibitor of metalloproteinases 1 knockout model of murine asthma

Immunology ◽  
2017 ◽  
Vol 153 (3) ◽  
pp. 387-396 ◽  
Author(s):  
Manoj J. Mammen ◽  
Mark F. Sands ◽  
Elaine Abou-Jaoude ◽  
Ravikumar Aalinkeel ◽  
Jessica L. Reynolds ◽  
...  
Keyword(s):  
Lung Inflammation ◽  
Tissue Inhibitor Of Metalloproteinases ◽  
Tissue Inhibitor ◽  
Allergic Lung Inflammation ◽  
Galectin 3 ◽  
Knockout Model

scholarly journals Role of tissue inhibitor of metalloproteinases-1 in the development of autoimmune lymphoproliferation

Haematologica ◽  
2010 ◽  
Vol 95 (11) ◽  
pp. 1897-1904 ◽  
Author(s):  
E. Boggio ◽  
M. Indelicato ◽  
E. Orilieri ◽  
R. Mesturini ◽  
M. C. Mazzarino ◽  
...  
Keyword(s):  
Tissue Inhibitor Of Metalloproteinases ◽  
Tissue Inhibitor

Tissue inhibitor of metalloproteinases (TIMP) regulates extracellular type I collagen degradation by chondrocytes and endothelial cells

1987 ◽  
Vol 87 (2) ◽  
pp. 357-362
Author(s):  
J. Gavrilovic ◽  
R.M. Hembry ◽  
J.J. Reynolds ◽  
G. Murphy
Keyword(s):  
Endothelial Cells ◽  
Type I Collagen ◽  
Model System ◽  
Collagen Degradation ◽  
Type I ◽  
Tissue Inhibitor Of Metalloproteinases ◽  
Regulatory Factor ◽  
Tissue Inhibitor ◽  
Cells Cultured

A specific antiserum to purified rabbit tissue inhibitor of metalloproteinases (TIMP) was raised in sheep, characterized and used to investigate the role of TIMP in a model system. Chondrocytes and endothelial cells cultured on 14C-labelled type I collagen films and stimulated to produce collagenase were unable to degrade the films unless the anti-TIMP antibody was added. The degradation induced was inhibited by a specific anti-rabbit collagenase antibody. It was concluded that TIMP is a major regulatory factor in cell-mediated collagen degradation.

scholarly journals Selective Myeloid Depletion of Galectin-3 Offers Protection Against Acute and Chronic Lung Injury

2021 ◽  
Vol 12 ◽  
Author(s):  
Duncan C. Humphries ◽  
Ross Mills ◽  
Ross Dobie ◽  
Neil C. Henderson ◽  
Tariq Sethi ◽  
...  
Keyword(s):  
Pulmonary Fibrosis ◽  
Lung Injury ◽  
Lung Inflammation ◽  
Respir Crit ◽  
Pulmonary Inflammation ◽  
Myeloid Cell ◽  
Clinical Development ◽  
Galectin 3 ◽  
Direct Targeting

Rationale: Galectin-3 (Gal-3) is an immune regulator and an important driver of fibrosis in chronic lung injury, however, its role in acute lung injury (ALI) remains unknown. Previous work has shown that global deletion of galectin-3 reduces collagen deposition in a bleomycin-induced pulmonary fibrosis model (MacKinnon et al., Am. J. Respir. Crit. Care Med., 2012, 185, 537–46). An inhaled Gal-3 inhibitor, GB0139, is undergoing Phase II clinical development for idiopathic pulmonary fibrosis (IPF). This work aims to elucidate the role of Gal-3 in the myeloid and mesenchymal compartment on the development of acute and chronic lung injury.Methods:LgalS3fl/fl mice were generated and crossed with mice expressing the myeloid (LysM) and mesenchymal (Pdgfrb) cre drivers to yield LysM-cre+/-/LgalS3fl/fl and Pdgfrb-cre+/-/LgalS3fl/fl mice. The response to acute (bleomycin or LPS) or chronic (bleomycin) lung injury was compared to globally deficient Gal-3−/− mice.Results: Myeloid depletion of Gal-3 led to a significant reduction in Gal-3 expression in alveolar macrophages and neutrophils and a reduction in neutrophil recruitment into the interstitium but not into the alveolar space. The reduction in interstitial neutrophils corelated with decreased levels of pulmonary inflammation following acute bleomycin and LPS administration. In addition, myeloid deletion decreased Gal-3 levels in bronchoalveolar lavage (BAL) and reduced lung fibrosis induced by chronic bleomycin. In contrast, no differences in BAL Gal-3 levels or fibrosis were observed in Pdgfrb-cre+/-/LgalS3fl/flmice.Conclusions: Myeloid cell derived Galectin-3 drives acute and chronic lung inflammation and supports direct targeting of galectin-3 as an attractive new therapy for lung inflammation.

scholarly journals The role of prostaglandins in allergic lung inflammation and asthma

2014 ◽  
Vol 9 (1) ◽  
pp. 55-72 ◽  
Author(s):  
Dru Claar ◽  
Tina V Hartert ◽  
Ray Stokes Peebles
Keyword(s):  
Lung Inflammation ◽  
Allergic Lung Inflammation

scholarly journals Essential role of TNF receptor superfamily 25 (TNFRSF25) in the development of allergic lung inflammation

2008 ◽  
Vol 205 (5) ◽  
pp. 1037-1048 ◽  
Author(s):  
Lei Fang ◽  
Becky Adkins ◽  
Vadim Deyev ◽  
Eckhard R. Podack
Keyword(s):  
Lung Inflammation ◽  
Tumor Necrosis Factor Receptor ◽  
Nkt Cells ◽  
Dominant Negative ◽  
Th2 Cytokine ◽  
Early Signal ◽  
Allergic Lung Inflammation ◽  
Necrosis Factor

We identify the tumor necrosis factor receptor superfamily 25 (TNFRSF25)/TNFSF15 pair as critical trigger for allergic lung inflammation, which is a cardinal feature of asthma. TNFRSF25 (TNFR25) signals are required to exert T helper cell 2 (Th2) effector function in Th2-polarized CD4 cells and co-stimulate interleukin (IL)-13 production by glycosphingolipid-activated NKT cells. In vivo, antibody blockade of TNFSF15 (TL1A), which is the ligand for TNFR25, inhibits lung inflammation and production of Th2 cytokines such as IL-13, even when administered days after airway antigen exposure. Similarly, blockade of TNFR25 by a dominant-negative (DN) transgene, DN TNFR25, confers resistance to lung inflammation in mice. Allergic lung inflammation–resistant, NKT-deficient mice become susceptible upon adoptive transfer of wild-type NKT cells, but not after transfer of DN TNFR25 transgenic NKT cells. The TNFR25/TL1A pair appears to provide an early signal for Th2 cytokine production in the lung, and therefore may be a drug target in attempts to attenuate lung inflammation in asthmatics.

Stability analysis of latent and active 72-kDa type IV collagenase: The role of tissue inhibitor of metalloproteinases-2 (TIMP-2)

Biochemistry ◽  
1993 ◽  
Vol 32 (6) ◽  
pp. 1583-1592 ◽  
Author(s):  
David E. Kleiner ◽  
Ari Tuuttila ◽  
Karl Tryggvason ◽  
William G. Stetler-Stevenson
Keyword(s):  
Stability Analysis ◽  
Tissue Inhibitor Of Metalloproteinases ◽  
Tissue Inhibitor ◽  
Type Iv Collagenase ◽  
Type Iv

Cellular recruitment and cytokine generation in a rat model of allergic lung inflammation are differentially modulated by progesterone and estradiol

2007 ◽  
Vol 293 (3) ◽  
pp. C1120-C1128 ◽  
Author(s):  
Ana Paula Ligeiro de Oliveira ◽  
Helori Vanni Domingos ◽  
Gabriela Cavriani ◽  
Amilcar Sabino Damazo ◽  
Adriana Lino dos Santos Franco ◽  
...  
Keyword(s):  
Lung Inflammation ◽  
Estradiol Treatment ◽  
Cell Recruitment ◽  
Ovx Rats ◽  
Allergic Lung Inflammation ◽  
Tnf Α ◽  
Cellular Recruitment ◽  
Additional Reduction

We evaluated the role of estradiol and progesterone in allergic lung inflammation. Rats were ovariectomized (Ovx) and, 7 days later, were sensitized with ovalbumin (OA) and challenged after 2 wk with inhaled OA; experiments were performed 1 day thereafter. Ovx-allergic rats showed reduced cell recruitment into the bronchoalveolar lavage (BAL) fluid relative to sham-Ovx allergic rats, as was observed in intact allergic rats treated with ICI-182,780. Estradiol increased the number of cells in the BAL of Ovx-allergic rats, whereas progesterone induced an additional reduction. Cells of BAL and bone marrow (BM) of Ovx-allergic rats released elevated amounts of IL-10 and reduced IL-1β and TNF-α. BM cells of Ovx-allergic rats released increased amounts of IL-10 and lower amounts of IL-4. Estradiol treatment of Ovx-allergic rats decreased the release of IL-10 but increased that of IL-4 by BM cells. Estradiol also caused an increased release of IL-1β and TNF-α by BAL cells. Progesterone significantly increased the release of IL-10, IL-1β, and TNF-α by BAL cells and augmented that of IL-4 by BM cells. Degranulation of bronchial mast cells from Ovx rats was reduced after in vitro challenge, an effect reverted by estradiol but not by progesterone. We suggest that the serum estradiol-to-progesterone ratio might drive cellular recruitment, modulating the pulmonary allergy and profile of release of anti-inflammatory or inflammatory cytokines. The existence of such dual hormonal effects suggests that the hormone therapy of asthmatic postmenopausal women and of those suffering of premenstrual asthma should take into account the possibility of worsening the pulmonary conditions.

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