Współczesne poglądy na patogenezę nadreaktywności oskrzeli w astmie dziecięcej

• Authors: Jadwiga Kroczyńska-Bednarek , Paweł Górski , Iwona Grzelewska-Rzymowska

Title variants

EN

Modern views on pathogenesis of bronchial hyperresponsiveness in childhood asthma

• Languages of publication: EN PL

Abstracts

EN

Asthma is a chronic lung disorder with the cardinal features of reversible airway obstruction, airway inflammation, and hyperresponsiveness. The last one, defines as an exaggerated bronchoconstrictor response to a nonspecific irritants, is most characteristic of asthma and is seen in all active children and most of those with no current symptoms but past diagnosis of asthma. The actual mechanism of bronchial hyperresponsiveness (BHR) in asthma remains still poorly understood, in childhood asthma also. It is widely believed that BHR is a consequence of chronic bronchial inflammation. This is supported by the observations that BHR increases with allergens exposure and is reduced by anti-inflammatory treatment. However, lack of correlation between BHR and inflammatory markers of asthma suggests the participation of other noninflammatory pathogenetic mechanisms of BHR. Both family and twin studies in asthma point to a strong genetic component of BHR. More than one genomic regions linked to asthma and associated phenotypes that include BHR had been identified in human and mouse studies. Structural remodeling of bronchial wall associated with inflammation plays an important role also. This paper reviews potential mechanisms cause of BHR which have been reported in the medical literature. It was shown that nonspecific BHR is multifactorial phenomenon with complex and still poorly known pathogenesis.

PL

Astma jest przewlekłą chorobą płuc, której głównymi cechami są odwracalna obturacja oskrzeli, zapalenie i nadreaktywność dróg oddechowych. Ostatnia z nich, określana jako nadmierna skurczowa odpowiedź oskrzeli na nieswoiste substancje drażniące, jest najbardziej charakterystyczna dla astmy i stwierdza się ją u wszystkich dzieci z czynną chorobą i większości tych aktualnie bez objawów, ale z wywiadem astmy w przeszłości. Rzeczywisty mechanizm nadreaktywności oskrzeli (NO) w astmie, także dziecięcej, pozostaje niejasny. Powszechnie sądzi się, że NO jest skutkiem przewlekłego zapalenia oskrzeli. Potwierdzają to obserwacje dotyczące wzrostu NO po ekspozycji na alergeny i jej zmniejszenia się pod wpływem leczenia przeciwzapalnego. Jednak brak korelacji między NO a wykładnikami stanu zapalnego w astmie sugeruje udział także innych, niezapalnych mechanizmów patogenetycznych NO. Zarówno badania rodzin, jak i bliźniąt z astmą wskazują na silne genetyczne uwarunkowania NO. W badaniach u ludzi i myszy zidentyfikowano więcej niż jeden obszar genowy związany z astmą i charakteryzującymi ją fenotypami, w tym NO. Istotną rolę odgrywa także związana z zapaleniem strukturalna przebudowa ściany oskrzeli. Artykuł stanowi przegląd możliwych mechanizmów wywołujących NO, które zostały omówione w literaturze medycznej. Wykazano, że nieswoista NO jest zjawiskiem wieloczynnikowym, o złożonej i wciąż niedostatecznie poznanej patogenezie.

Keywords

EN

ADAM33; airway remodeling; allergic inflammation; astma oskrzelowa; bronchial asthma; genes susceptibility for bronchial hyperresponsiveness; geny podatności do nadreaktywności oskrzeli; nieswoista nadreaktywność oskrzeli; nonspecific bronchial hyperresponsiveness; przebudowa dróg oddechowych; zapalenie alergiczne

Discipline

• MEDICINE: MEDICINE

• Publisher: Medical Communications
• Journal: Pediatria i Medycyna Rodzinna
• Year: 2010
• Volume: 6
• Issue: 2
• Pages: 77-84

Contributors

author

Jadwiga Kroczyńska-Bednarek

• Klinika Pneumonologii i Alergologii KPiA Uniwersytetu Medycznego w Łodzi. Kierownik: prof. dr hab. n. med. Paweł Górski

author

Paweł Górski

• Klinika Pneumonologii i Alergologii KPiA Uniwersytetu Medycznego w Łodzi. Kierownik: prof. dr hab. n. med. Paweł Górski

author

Iwona Grzelewska-Rzymowska

• Klinika Pneumonologii i Alergologii KPiA Uniwersytetu Medycznego w Łodzi. Kierownik: prof. dr hab. n. med. Paweł Górski

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• Document Type: article