scholarly journals Allergen-Induced Airway Remodeling Is Impaired in Galectin-3–Deficient Mice

2010 ◽  
Vol 185 (2) ◽  
pp. 1205-1214 ◽  
Author(s):  
Xiao Na Ge ◽  
Nooshin S. Bahaie ◽  
Bit Na Kang ◽  
M. Reza Hosseinkhani ◽  
Sung Gil Ha ◽  
...  
Keyword(s):  
Airway Remodeling ◽  
Galectin 3 ◽  
Deficient Mice

scholarly journals Galectin‐3 mediates chronic airway allergic inflammation and airway remodeling

2010 ◽  
Vol 24 (S1) ◽  
Author(s):  
Xiao Na Ge ◽  
Nooshin S Bahaie ◽  
Bit Na Kang ◽  
Reza M Hosseinkhani ◽  
Sung Gil Ha ◽  
...  
Keyword(s):  
Airway Remodeling ◽  
Allergic Inflammation ◽  
Galectin 3 ◽  
Chronic Airway

Divergent immune responses to house dust mite lead to distinct structural-functional phenotypes

2007 ◽  
Vol 293 (3) ◽  
pp. L730-L739 ◽  
Author(s):  
Jill R. Johnson ◽  
Filip K. Swirski ◽  
Beata U. Gajewska ◽  
Ryan E. Wiley ◽  
Ramzi Fattouh ◽  
...  
Keyword(s):  
Airway Inflammation ◽  
Inflammatory Responses ◽  
Airway Remodeling ◽  
Bronchial Hyperresponsiveness ◽  
Airway Disease ◽  
Allergic Airway Disease ◽  
Th Cell ◽  
And Function ◽  
Deficient Mice ◽  
Chronic Airway

Asthma is a chronic airway inflammatory disease that encompasses three cardinal processes: T helper (Th) cell type 2 (Th2)-polarized inflammation, bronchial hyperreactivity, and airway wall remodeling. However, the link between the immune-inflammatory phenotype and the structural-functional phenotype remains to be fully defined. The objective of these studies was to evaluate the relationship between the immunologic nature of chronic airway inflammation and the development of abnormal airway structure and function in a mouse model of chronic asthma. Using IL-4-competent and IL-4-deficient mice, we created divergent immune-inflammatory responses to chronic aeroallergen challenge. Immune-inflammatory, structural, and physiological parameters of chronic allergic airway disease were evaluated in both strains of mice. Although both strains developed airway inflammation, the profiles of the immune-inflammatory responses were markedly different: IL-4-competent mice elicited a Th2-polarized response and IL-4-deficient mice developed a Th1-polarized response. Importantly, this chronic Th1-polarized immune response was not associated with airway remodeling or bronchial hyperresponsiveness. Transient reconstitution of IL-4 in IL-4-deficient mice via an airway gene transfer approach led to partial Th2 repolarization and increased bronchial hyperresponsiveness, along with full reconstitution of airway remodeling. These data show that distinct structural-functional phenotypes associated with chronic airway inflammation are strictly dependent on the nature of the immune-inflammatory response.

scholarly journals Chanzyme TRPM7 protects against cardiovascular inflammation and fibrosis

2019 ◽  
Vol 116 (3) ◽  
pp. 721-735 ◽  
Author(s):  
Francisco J Rios ◽  
Zhi-Guo Zou ◽  
Adam P Harvey ◽  
Katie Y Harvey ◽  
Ryszard Nosalski ◽  
...  
Keyword(s):  
Cardiovascular System ◽  
Molecular Mechanisms ◽  
Transient Receptor Potential ◽  
Inflammatory Responses ◽  
Cardiac Fibroblasts ◽  
Nuclear Antigen ◽  
Culture Systems ◽  
Transient Receptor Potential Melastatin ◽  
Galectin 3 ◽  
Deficient Mice

Abstract Aims Transient Receptor Potential Melastatin 7 (TRPM7) cation channel is a chanzyme (channel + kinase) that influences cellular Mg2+ homeostasis and vascular signalling. However, the pathophysiological significance of TRPM7 in the cardiovascular system is unclear. The aim of this study was to investigate the role of this chanzyme in the cardiovascular system focusing on inflammation and fibrosis. Methods and results TRPM7-deficient mice with deletion of the kinase domain (TRPM7+/Δkinase) were studied and molecular mechanisms investigated in TRPM7+/Δkinase bone marrow-derived macrophages (BMDM) and co-culture systems with cardiac fibroblasts. TRPM7-deficient mice had significant cardiac hypertrophy, fibrosis, and inflammation. Cardiac collagen and fibronectin content, expression of pro-inflammatory mediators (SMAD3, TGFβ) and cytokines [interleukin (IL)-6, IL-10, IL-12, tumour necrosis factor-α] and phosphorylation of the pro-inflammatory signalling molecule Stat1, were increased in TRPM7+/Δkinase mice. These processes were associated with infiltration of inflammatory cells (F4/80+CD206+ cardiac macrophages) and increased galectin-3 expression. Cardiac [Mg2+]i, but not [Ca2+]i, was reduced in TRPM7+/Δkinase mice. Calpain, a downstream TRPM7 target, was upregulated (increased expression and activation) in TRPM7+/Δkinase hearts. Vascular functional and inflammatory responses, assessed in vivo by intra-vital microscopy, demonstrated impaired neutrophil rolling, increased neutrophil: endothelial attachment and transmigration of leucocytes in TRPM7+/Δkinase mice. TRPM7+/Δkinase BMDMs had increased levels of galectin-3, IL-10, and IL-6. In co-culture systems, TRPM7+/Δkinase macrophages increased expression of fibronectin, proliferating cell nuclear antigen, and TGFβ in cardiac fibroblasts from wild-type mice, effects ameliorated by MgCl2 treatment. Conclusions We identify a novel anti-inflammatory and anti-fibrotic role for TRPM7 and suggest that its protective effects are mediated, in part, through Mg2+-sensitive processes.

Reduced peribronchial fibrosis in allergen-challenged MMP-9-deficient mice

2006 ◽  
Vol 291 (2) ◽  
pp. L265-L271 ◽  
Author(s):  
Dae Hyun Lim ◽  
Jae Youn Cho ◽  
Marina Miller ◽  
Kirsti McElwain ◽  
Shauna McElwain ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Airway Remodeling ◽  
Muscle Thickness ◽  
Muscle Layer ◽  
Airway Responsiveness ◽  
Wild Type ◽  
Extracellular Proteases ◽  
Significant Difference ◽  
Deficient Mice ◽  
Modest Reduction

Matrix metalloproteinases (MMPs) are a family of extracellular proteases that are responsible for the degradation of the extracellular matrix during tissue remodeling. We have used a mouse model of allergen-induced airway remodeling to determine whether MMP-9 plays a role in airway remodeling. MMP-9-deficient and wild-type (WT) mice were repetitively challenged intranasally with ovalbumin (OVA) antigen to develop features of airway remodeling including peribronchial fibrosis and increased thickness of the peribronchial smooth muscle layer. OVA-challenged MMP-9-deficient mice had less peribronchial fibrosis and total lung collagen compared with OVA-challenged WT mice. There was no reduction in mucus expression, smooth muscle thickness, or airway responsiveness in OVA-challenged MMP-9-deficient compared with OVA-challenged WT mice. OVA-challenged MMP-9-deficient mice had reduced levels of bronchoalveolar lavage (BAL) regulated on activation, normal T cell expressed, and secreted (RANTES), as well as reduced numbers of BAL and peribronchial eosinophils compared with OVA-challenged WT mice. There were no significant difference in levels of BAL eotaxin, thymus- and activation-regulated chemokine (TARC), or macrophage-derived chemokine (MDC) in OVA-challenged WT compared with MMP-9-deficient mice. Overall, this study demonstrates that MMP-9 may play a role in mediating selected aspects of allergen-induced airway remodeling (i.e., modest reduction in levels of peribronchial fibrosis) but does not play a significant role in mucus expression, smooth muscle thickness, or airway responsiveness.

scholarly journals Galectin-3: an early predictive biomarker of modulation of airway remodeling in patients with severe asthma treated with omalizumab for 36 months

2017 ◽  
Vol 7 (1) ◽  
Author(s):  
Anna Maria Riccio ◽  
Pierluigi Mauri ◽  
Laura De Ferrari ◽  
Rossana Rossi ◽  
Dario Di Silvestre ◽  
...  
Keyword(s):  
Severe Asthma ◽  
Airway Remodeling ◽  
Predictive Biomarker ◽  
Galectin 3

scholarly journals Differential development of oil granulomas induced by pristane injection in galectin-3 deficient mice

2015 ◽  
Vol 16 (1) ◽  
Author(s):  
Camila Brand ◽  
Thayse Pinheiro da Costa ◽  
Emerson Soares Bernardes ◽  
Camila Maria Longo Machado ◽  
Leonardo Rodrigues Andrade ◽  
...  
Keyword(s):  
Differential Development ◽  
Galectin 3 ◽  
Deficient Mice
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