http://www.cnr.it/ontology/cnr/individuo/prodotto/ID12346
Leptin and leptin receptor expression in asthma (Articolo in rivista)
- Type
- Label
- Leptin and leptin receptor expression in asthma (Articolo in rivista) (literal)
- Anno
- 2009-01-01T00:00:00+01:00 (literal)
- Alternative label
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- Bruno A*; Pace E*; Chanez P**; Gras D**; Vachier I***; Chiappara G*; La Guardia M****; Gerbino S*, Profita M*; Gjomarkaj M*. (literal)
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- Note
- ISI Web of Science (WOS) (literal)
- PubMe (literal)
- Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#affiliazioni
- *IBIM-CNR
**Département des Maladies Respiratoires, AP-HM, Laboratoire d'immunologie INSERM CNRS U 600, UMR6212, Université de la Méditerranée, Marseille, France
***MED BIO MED Service des maladies respiratoires CHU Montpellier, Montpellier, France
****Sezione di Fisiologia e nutrizione umana, Dipartimento (DIMPEFINU), Università di Palermo, Palermo, Italy (literal)
- Titolo
- Leptin and leptin receptor expression in asthma (literal)
- Abstract
- Background: The adipokine leptin is a potential new mediator
for bronchial epithelial homeostasis. Asthma is a chronic
inflammatory disease characterized by airway remodeling that
might affect disease chronicity and severity. TGF-b is a tissue
growth factor the dysregulation of which is associated with
airway remodeling.
Objective: We sought to determine whether a bronchial
epithelial dysfunction of the leptin/leptin receptor pathway
contributes to asthma pathogenesis and severity.
Methods: We investigated in vitro the presence of leptin/leptin
receptor on human bronchial epithelial cells. Then we studied
the effect of TGF-b and fluticasone propionate on leptin
receptor expression. Finally, the role of leptin on TGF-b release
and cell proliferation was analyzed. Ex vivo we investigated the
presence of leptin/leptin receptor in the epithelium of bronchial
biopsy specimens from subjects with asthma of various
severities and from healthy volunteers, and some features of
airway remodeling, such as reticular basement membrane
(RBM) thickness and TGF-b expression in the epithelium, were
assessed.
Results: In vitro bronchial epithelial cells express leptin/leptin
receptor. TGF-b decreased and fluticasone propionate increased
leptin receptor expression, and leptin decreased the spontaneous
release of TGF-b and increased cell proliferation. Ex vivo the
bronchial epithelium of subjects with mild, uncontrolled,
untreated asthma showed a decrease expression of leptin and its
receptor and an increased RBM thickness and TGF-b
expression when compared with values seen in healthy
volunteers. Furthermore, severe asthma was associated with a
reduced expression of leptin and its receptor and an increased
RBM thickness with unaltered TGF-b expression.
Conclusions: Decreased expression of leptin/leptin receptor
characterizes severe asthma and is associated with airway
remodeling features. (J Allergy Clin Immunol 2009;124:230-7.) (literal)
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