Release of transforming growth factor-beta (TGF-β) and fibronectin by alveolar macrophages in airway diseases

Vignola, A. M.; Chanez, Pascal; Chiappara, Giuseppina; Merendino, Anna Maria; Zinnanti, E; Bousquet, Jean; Bellia, Vincenzo; Bonsignore, G

doi:10.1046/j.1365-2249.1996.d01-811.x

Cited by 98 publications

(64 citation statements)

References 29 publications

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“…Our finding of unaffected TGF-␤ 1 concentrations in murine BAL samples was an unexpected result in light of the suppressed eosinophil numbers. Although a complete account of the relative role that airway macrophages may play in TGF-␤ 1 levels, and thus remodeling, remains to determined, it is known that these cells can produce this cytokine (41), and activated macrophages may have been an important source in our experiment. In any event, the TGF-␤ 1 finding in this study does encourage a more thorough examination of the effects mycobacteria may have on airway remodeling.…”

Section: Discussionmentioning

confidence: 99%

Airway Hyperresponsiveness, Late Allergic Response, and Eosinophilia Are Reversed with Mycobacterial Antigens in Ovalbumin-Presensitized Mice

Hopfenspirger

Agrawal

2002

The Journal of Immunology

121

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Pretreatment with mycobacterial Ags has been shown to be effective in preventing allergic airway inflammation from occurring in a mouse model. Because most asthmatics are treated after the development of asthma, it is crucial to determine whether mycobacterial Ags can reverse established allergic airway inflammation in the presensitized state. Our hypothesis, based upon our previous findings, is that mycobacteria treatment in presensitized mice will suppress the allergic airway inflammation with associated clinical correlates of established asthma, with the noted exception of factors associated with the early allergic response (EAR). BALB/c mice sensitized and challenged with OVA were evaluated for pulmonary functions during both the EAR and late allergic response, and airway hyperresponsiveness to methacholine. Following this, sensitized mice were randomized and treated with placebo or a single dose (1 × 105 CFUs) of bacillus Calmette-Guérin (BCG) or Mycobacterium vaccae via nasal or peritoneal injection. One week later, the mice were rechallenged with OVA and methacholine, followed by bronchoalveolar lavage (BAL) and tissue collection. Mice treated with intranasal BCG were most significantly protected from the late allergic response (p < 0.02), airway hypersensitivity (p < 0.001) and hyperreactivity (p < 0.05) to methacholine, BAL (p < 0.05) and peribronchial (p < 0.01) eosinophilia, and BAL fluid IL-5 levels (p < 0.01) as compared with vehicle-treated, sensitized controls. Intranasal M. vaccae treatment was less effective, suppressing airway hypersensitivity (p < 0.01) and BAL eosinophilia (p < 0.05). No changes were observed in the EAR, BAL fluid IL-4 levels, or serum total and Ag-specific IgE. These data suggest that mycobacterial Ags (BCG≫M. vaccae) are effective in attenuating allergic airway inflammation and associated changes in pulmonary functions in an allergen-presensitized state.

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Section: Discussionmentioning

confidence: 99%

Airway Hyperresponsiveness, Late Allergic Response, and Eosinophilia Are Reversed with Mycobacterial Antigens in Ovalbumin-Presensitized Mice

Hopfenspirger

Agrawal

2002

The Journal of Immunology

121

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“…Although it is unclear which structural cell produces the majority of TGF-b1 in the airway, epithelial-derived TGF-b1 is suggested to be an important contributor to asthma pathogenesis (36). However, much of the elevation of TGF-b1 in the airway of subjects with asthma may result from the secretion of TGF-b1 by invading inflammatory cells in asthma (37)(38)(39), with eosinophils accounting for the largest source of TGF-b1 in the airway (37).…”

Section: Tgf-b1 and Airway Diseasementioning

confidence: 99%

Transforming Growth Factor β1 Function in Airway Remodeling and Hyperresponsiveness. The Missing Link?

Ojiaku

Yoo

Panettieri

2017

Am J Respir Cell Mol Biol

106

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The pathogenesis of asthma includes a complex interplay among airway inflammation, hyperresponsiveness, and remodeling. Current evidence suggests that airway structural cells, including bronchial smooth muscle cells, myofibroblasts, fibroblasts, and epithelial cells, mediate all three aspects of asthma pathogenesis. Although studies show a connection between airway remodeling and changes in bronchomotor tone, the relationship between the two remains unclear. Transforming growth factor b1 (TGF-b1), a growth factor elevated in the airway of patients with asthma, plays a role in airway remodeling and in the shortening of various airway structural cells. However, the role of TGF-b1 in mediating airway hyperresponsiveness remains unclear. In this review, we summarize the literature addressing the role of TGF-b1 in airway remodeling and shortening. Through our review, we aim to further elucidate the role of TGF-b1 in asthma pathogenesis and the link between airway remodeling and airway hyperresponsiveness in asthma and to define TGF-b1 as a potential therapeutic target for reducing asthma morbidity and mortality.

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“…These may be released from inflammatory cells in the airways, such as macrophages and eosinophils, but also by structural cells such as airway epithelium, endothelial cells and 54s [55]. In addition, increased release of TGF-b and fibronectin from alveolar macrophages from patients with chronic bronchitis has been observed [56]. Growth factors may also stimulate the proliferation and growth of airway smooth muscle cells.…”

Section: Airway Wall Remodelling Cytokinesmentioning

confidence: 99%

Cytokines in chronic obstructive pulmonary disease

Kf¹

2001

Eur Respir J

528

346

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Chronic obstructive pulmonary disease (COPD) is characterized by chronic obstruction of expiratory flow affecting peripheral airways, associated with chronic bronchitis (mucus hypersecretion with goblet cell and submucosal gland hyperplasia) and emphysema (destruction of airway parenchyma), together with fibrosis and tissue damage, and inflammation of the small airways. Cytokines are extracellular signalling proteins. Increased levels of interleukin (IL)‐6, IL‐1β, tumour necrosis factor‐α (TNF‐α) and IL‐8 have been measured in sputum, with further increases during exacerbations, and the bronchiolar epithelium over-expresses monocyte chemotactic protein (MCP)‐1 and IL‐8. IL‐8 can account for some chemotactic activity of sputum, and sputum IL‐8 levels correlate with airway bacterial load and blood myeloperoxidase levels. The expression of chemokines such as regulated on activation, normal T‐cell expressed and secreted (RANTES) may underlie the airway eosinophilia observed in some COPD patients. Cytokines may be involved in tissue remodelling. TNF‐α and IL‐1β stimulate macrophages to produced matrix metalloproteinase‐9 (MMP‐9), and bronchial epithelial cells to produce extracellular matrix glycoproteins such as tenascin. Increased expression of transforming growth factor‐β (TGFβ) and of epidermal growth factor (EGF) occurs in the epithelium and submucosal cells of patients with chronic bronchitis. TGFβ and EGF activate proliferation of fibroblasts, while activation of the EGF receptor leads to mucin gene expression.The cytokine profile seen in chronic obstructive pulmonary disease is different from that observed in asthma. The role of these cytokines needs to be defined and there is a potential for anticytokine therapy in chronic obstructive pulmonary disease.

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Release of transforming growth factor-beta (TGF-β) and fibronectin by alveolar macrophages in airway diseases

Cited by 98 publications

References 29 publications

Airway Hyperresponsiveness, Late Allergic Response, and Eosinophilia Are Reversed with Mycobacterial Antigens in Ovalbumin-Presensitized Mice

Airway Hyperresponsiveness, Late Allergic Response, and Eosinophilia Are Reversed with Mycobacterial Antigens in Ovalbumin-Presensitized Mice

Transforming Growth Factor β1 Function in Airway Remodeling and Hyperresponsiveness. The Missing Link?

Cytokines in chronic obstructive pulmonary disease

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