Transforming Growth Factor- β Expression in Mucosal Biopsies in Asthma and Chronic Bronchitis

Vignola, Antonio M.; Chanez, Pascal; Chiappara, Giuseppina; Merendino, Anna Maria; Pace, Elisabetta; Rizzo, Aroldo; Rocca, Alberto; Bellia, Vincenzo; Bonsignore, G; Bousquet, Jean

doi:10.1164/ajrccm.156.2.9609066

Cited by 536 publications

(465 citation statements)

References 31 publications

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“…2,6,7,33 Smad proteins, c-Jun NH2-terminal kinase, and mitogen-activated protein kinase are reported to be involved in TGF-b signaling. 33,34 These factors are targets for PPAR-c regulation.…”

Section: Discussionmentioning

confidence: 99%

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Peroxisome proliferator–activated receptor γ is expressed in airways and inhibits features of airway remodeling in a mouse asthma model☆

Honda

Marquillies

Capron

et al. 2004

Journal of Allergy and Clinical Immunology

132

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Section: Discussionmentioning

confidence: 99%

“…5 In most studies TGF-b expression correlates with basement membrane thickness, fibroblast numbers, and disease severity. 2,6,7 Nuclear receptors are ligand-activated transcription factors. 8 The glucocorticoid receptor a (GR-a) mediates the anti-inflammatory effects of corticosteroids.…”

mentioning

confidence: 99%

Peroxisome proliferator–activated receptor γ is expressed in airways and inhibits features of airway remodeling in a mouse asthma model☆

Honda

Marquillies

Capron

et al. 2004

Journal of Allergy and Clinical Immunology

132

View full text Add to dashboard Cite

“…This cytokine has been implicated in the profibrotic changes occurring in airway remodeling (37). Investigators have further linked expression of TGF-␤ 1 with eosinophils (38,39) and have found significantly increased levels in BAL fluid after allergen challenge (40) in humans. Our finding of unaffected TGF-␤ 1 concentrations in murine BAL samples was an unexpected result in light of the suppressed eosinophil numbers.…”

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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“…Indeed, in addition to their conventional effector functions, which are based on the release of lipid mediators and cationic granule proteins, eosinophils may functionally interact with immune cells or interstitial cells by presenting Ags (17) and producing cytokines (e.g., IL-4) and growth factors (e.g., TGF-␤) (18). In particular, the association between human eosinophils and TGF-␤1, a factor involved in immunoregulation and wound healing, has been studied extensively in patients with asthma (19,20) and atopic dermatitis (21).…”

Section: Marked Airway Eosinophilia Prevents Development Of Airwaymentioning

confidence: 99%

Marked Airway Eosinophilia Prevents Development of Airway Hyper-responsiveness During an Allergic Response in IL-5 Transgenic Mice

Kobayashi

Izutsu

Kita

2003

The Journal of Immunology

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Tissue eosinophilia probably plays important roles in the pathophysiology of bronchial asthma and allergic disorders; however, this concept was challenged recently by controversial results in mouse models of bronchial asthma treated with anti-IL-5 Ab and the failure of anti-IL-5 therapy in humans. We have now used a unique model, IL-5 transgenic (TG) mice, to address a fundamental question: is airway eosinophilia beneficial or detrimental in the allergic response? After sensitization and challenge with OVA, IL-5 TG mice showed a marked airway eosinophilia. Surprisingly, these IL-5 TG mice showed lower airway reactivity to methacholine. Immunohistochemical analysis of the lungs revealed a marked peribronchial infiltration of eosinophils, but no eosinophil degranulation. In vitro, mouse eosinophils from peritoneal lavage fluids did not produce superoxide anion, but did produce an anti-inflammatory and fibrotic cytokine, TGF-β1. Indeed, the TGF-β1 levels in bronchoalveolar lavage fluid specimens from IL-5 TG mice directly correlated with airway eosinophilia (r = 0.755). Furthermore, anti-IL-5 treatment of IL-5 TG mice decreased both airway eosinophilia and TGF-β1 levels in bronchoalveolar lavage fluids and increased airway reactivity. Thus, in mice, marked eosinophilia prevents the development of airway hyper-reactivity during an allergic response. Overall, the roles of eosinophils in asthma and in animal models need to be addressed carefully for their potentially detrimental and beneficial effects.

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Transforming Growth Factor- β Expression in Mucosal Biopsies in Asthma and Chronic Bronchitis

Cited by 536 publications

References 31 publications

Peroxisome proliferator–activated receptor γ is expressed in airways and inhibits features of airway remodeling in a mouse asthma model☆

Peroxisome proliferator–activated receptor γ is expressed in airways and inhibits features of airway remodeling in a mouse asthma model☆

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

Marked Airway Eosinophilia Prevents Development of Airway Hyper-responsiveness During an Allergic Response in IL-5 Transgenic Mice

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