Extracellular matrix components remodeling and lung function parameters in experimental emphysema and allergic asthma: Differences among the mouse strains

Oliveira, Milena V.; Silva, Pedro L.; Rocco, Patrícia Rieken Macêdo

doi:10.1016/j.ddmod.2019.04.001

Cited by 2 publications

(2 citation statements)

References 107 publications

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“…In summary, in airway epithelial remodeling, an imbalance occurs between profibrotic and proteolytic factors in response to stress from successive allergen exposures, as an attempt to restore homeostasis, and such excessive changes, in turn, culminate in pronounced bronchoconstriction ( Banno et al, 2020 ; Hough et al, 2020 ). Extracellular matrix (ECM) changes encompass the connective tissue composed of collagen and elastin fibers, mechanically connected via microfibrils/proteoglycans, and responsible for alleviating the primary stress of respiration, promoting structural integrity and elasticity ( Oliveira et al, 2019 ; Mariano et al, 2023 ).…”

Section: Discussionmentioning

confidence: 99%

Copaiba oil minimizes inflammation and promotes parenchyma re-epithelization in acute allergic asthma model induced by ovalbumin in BALB/c mice

Caputo,

Alves,

Laranjeira

et al. 2024

Front. Pharmacol.

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Introduction: Asthma is a condition of airflow limitation, common throughout the world, with high mortality rates, especially as it still faces some obstacles in its management. As it constitutes a public health challenge, this study aimed to investigate the effect of copaiba oil (e.g., Copaifera langsdorffii), as a treatment resource, at doses of 50 and 100 mg/kg on certain mediators of acute lung inflammation (IL-33, GATA3, FOXP3, STAT3, and TBET) and early mechanisms of lung remodeling (degradation of elastic fiber tissues, collagen deposition, and goblet cell hyperplasia).Methods: Using an ovalbumin-induced acute allergic asthma model in BALB/c mice, we analyzed the inflammatory mediators through immunohistochemistry and the mechanisms of lung remodeling through histopathology, employing orcein, Masson’s trichrome, and periodic acid-Schiff staining.Results: Copaiba oil treatment (CO) reduced IL-33 and increased FOXP3 by stimulating the FOXP3/GATA3 and FOXP3/STAT3 pathways. Additionally, it upregulated TBET, suggesting an additional role in controlling GATA3 activity. In the respiratory epithelium, CO decreased the fragmentation of elastic fibers while increasing the deposition of collagen fibers, favoring epithelial restructuring. Simultaneously, CO reduced goblet cell hyperplasia.Discussion: Although additional research is warranted, the demonstrated anti-inflammatory and re-epithelializing action makes CO a viable option in exploring new treatments for acute allergic asthma.

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Section: Discussionmentioning

confidence: 99%

Copaiba oil minimizes inflammation and promotes parenchyma re-epithelization in acute allergic asthma model induced by ovalbumin in BALB/c mice

Caputo,

Alves,

Laranjeira

et al. 2024

Front. Pharmacol.

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“…Similarly, the DLCO%pre and FEV 1 %pre levels decreased with the increase of collagen fibers. A reason for this may be that the proportion of collagen fibers increased and the proportion of elastic fibers decreased, resulting in the decrease of pulmonary compliance and pulmonary elastic retraction [ 33 , 34 ]. The alteration of collagen fibers and elastic fibers raises the possibility of a remodeling process occurring in the connective matrix in alveolar walls, and connective tissue changes are part of the pathological events in emphysema [ 35 ].…”

Section: Discussionmentioning

confidence: 99%

Expression of Matrix Metalloproteinase-2, Matrix Metalloproteinase-9, Tissue Inhibitor of Metalloproteinase-1, and Changes in Alveolar Septa in Patients with Chronic Obstructive Pulmonary Disease

Zhang

et al. 2020

Med Sci Monit

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Background This study investigated the relationship between the pathological alteration of alveolar septa and (1) pulmonary function and (2) matrix metalloproteinase (MMP)-2, MMP-9, and tissue inhibitor matrix metalloproteinase 1 (TIMP-1) expression in chronic obstructive pulmonary disease (COPD). Material/Methods Sixty patients with pulmonary disease were divided into control (n=20) and COPD (n=40) groups. Postoperative lung tissue specimens were examined. Hematoxylin and eosin and elastin van Gieson staining detected pathological alterations of pulmonary alveolar septa. Septa thickness was measured. MMP-2, MMP-9, and TIMP-1 expression levels were detected by immunohistochemical staining. Correlations were determined by Pearson analysis. Results Forced expiratory volume in 1 s (FEV 1 ), forced vital capacity, FEV 1 percent predicted (FEV 1 %pre), and diffusion capacity of carbon monoxide percent predicted (DLCO%pre) in COPD patients were significantly lower than in those of the control group ( P <0.05). MMP-2, MMP-9, and TIMP-1 expression levels were significantly higher in the COPD group than in control, especially the severe group ( P <0.05). Septa thickness was negatively correlated with FEV 1 %pre ( r =−0.335; P <0.05) and positively correlated with MMP-2 and TIMP-1 expression ( P <0.05). Proportion of collagenous fiber was negatively correlated with FEV 1 %pre and DLCO%pre ( P <0.01), and positively correlated with MMP-2, MMP-9, and TIMP-1 expression ( P <0.01). Proportion of elastic fibers was negatively correlated with collagenous fiber. Conclusions The pathological alteration of alveolar septa was correlated with pulmonary function and expression levels of MMP-2, MMP-9, and TIMP-1, which can play vital roles in COPD progression.

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Extracellular matrix components remodeling and lung function parameters in experimental emphysema and allergic asthma: Differences among the mouse strains

Cited by 2 publications

References 107 publications

Copaiba oil minimizes inflammation and promotes parenchyma re-epithelization in acute allergic asthma model induced by ovalbumin in BALB/c mice

Copaiba oil minimizes inflammation and promotes parenchyma re-epithelization in acute allergic asthma model induced by ovalbumin in BALB/c mice

Expression of Matrix Metalloproteinase-2, Matrix Metalloproteinase-9, Tissue Inhibitor of Metalloproteinase-1, and Changes in Alveolar Septa in Patients with Chronic Obstructive Pulmonary Disease

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