Інформація призначена тільки для фахівців сфери охорони здоров'я, осіб,
які мають вищу або середню спеціальну медичну освіту.

Підтвердіть, що Ви є фахівцем у сфері охорони здоров'я.

"Child`s Health" 7 (58) 2014

Back to issue

Markers of the airway remodeling in bronchopulmonary diseases

Authors: Chernyshova O. Ye.

Categories: Pediatrics/Neonatology

Sections: Specialist manual

print version

The article presents information about markers of airway remodeling in bronchopulmonary diseases. In the last decade there is a significant increase in the number of allergic diseases, especially asthma, which is seen as a problem of world-class and is the focus of clinicians of different specialties.

Inflammation developing bronchial asthma under the influence of specific and non-specific factors cause morphological and functional changes in the structures of the bronchi, i.e. airway remodeling. Remodeling is a heterogeneous process, which leads to changes in the structure of the respiratory tract, resulting in under the influence of mediators and biologically active substances to "break" the biophysical components that determine the contraction of smooth muscle elements. Subepithelial fibrosis occurs due to the accumulation of reticular plate fragments of the extracellular matrix related to various types of collagen under the action of mediators of fibrinogen, in particular, peptides (endothelin-1 and endothelin-3), cytokines, growth factors, histamine, thrombin, tryptase.

Significant role in airway remodeling play matrix metalloproteinases (MMPs). MMP-9 is involved in the breakdown of extracellular matrix proteins. Secretion of MMP-9 contribute to the cellular elements involved in the pathogenesis of asthma. Inhibition of MMP-9 may be nonspecific, α2-macroglobulin is carried out, and a specific, under the influence of tissue inhibitor of metalloproteinases (TIMP-1). Production of TIMP-1 is carried out by different cell populations, activation - cytokines and growth factors. Tissue inhibitor-1 reduces the activity of MMP-9, breaks cell growth due to the acceleration of apoptosis and stimulation of cell proliferation.

TGF-β can inhibit or enhance the proliferation of mesenchymal cells. Furthermore, it increases the synthesis of proteins of the extracellular matrix, particularly fibronectin, collagen I, III type and synthesis of proteoglycans and reduces proteinases. Under the action of the connective tissue growth factor TGF-β promotes transformation of fibroblasts into myofibroblasts.

Endothelin-1 causes bronchoconstriction, bronchial tubes enhances responses to inhaled antigens, increases the migration of neutrophils in the area of ​​inflammation, cytokine production, is involved in the formation of edema, and in the process of airway remodeling. When inflammation generation of endothelin-1 is increased, this contributes to chronic inflammation and degree of airway obstruction.

Prolonged inflammation can  lead to irreversible morphological changes in the bronchi as a sharp thickening of the basement membrane with impaired microcirculation and the development of multiple sclerosis bronchial wall. Among the markers, determining the degree of structural changes in the airways are matrix metalloproteinase tissue inhibitor of matrix metalloproteinase, transforming growth factor autoantibody to collagen type III, endothelin-1.

Describes the influence of matrix metalloproteinase, tissue inhibitor of matrix metalloproteinase, transforming growth factor, collagen autoantibody III type, endothelin-1 on morphological reconstruction processes as airway smooth muscle hypertrophy, enhanced revascularization, epithelial cell hyperplasia, collagen deposition, compaction of the basal membrane, observed in bronchial asthma.



Back to issue