Polski merkuriusz lekarski : organ Polskiego Towarzystwa Lekarskiego · 2007
[The role of interleukin 17A in inducing neutrophilic inflammation in the pulmonary tract].
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Semik-Orzech Aleksandra, Barczyk Adam, Pierzchała Władysław
Аннотация
UNLABELLED: Interleukine 17A is a proinflammatory cytokine produced by activated memory T-cells, which indirectly connects these cells with the enhanced accumulation of the polymorphonuclear cells in the site of inflammation.
AIM OF THE STUDY: The aim of this paper is to present the current knowledge on the role of interleukin 17A in the pathogenesis of inflammatory diseases of the pulmonary tract. IL-17A-induced accumulation of neutrophils in pulmonary tissues proceeds mainly through its influence on stomal cells which produce larger amounts of neutrophilic chemotactic factors (CXC chemokines) as well as granulocyte and granulocyte-macrophage colony-stimulating factors (G-CSF, GM-CSF), leading to the enhanced maturing of CD34+ progenitor cells and their further differentiation into neutrophils in bone marrow.
CONCLUSIONS: Although neutrophilic inflammation, which is a consequence of IL-17A activity, is an important element of pulmonary host defence, the prolonged action of this cytokine directed on the proliferation, maturing and chemotaxis of neutrophils to the pulmonary tract may contribute to chronic tissue destruction. Scientific research supplies proves, that this cytokine is co-responsible for the development of many functional abnormalities (e.g. bronchial hyperresponsiveness, enhanced mucus secretion, airway remodeling) in course of diseases such as: chronic bronchitis, chronic obstructive pulmonary disease and bronchial asthma.
AIM OF THE STUDY: The aim of this paper is to present the current knowledge on the role of interleukin 17A in the pathogenesis of inflammatory diseases of the pulmonary tract. IL-17A-induced accumulation of neutrophils in pulmonary tissues proceeds mainly through its influence on stomal cells which produce larger amounts of neutrophilic chemotactic factors (CXC chemokines) as well as granulocyte and granulocyte-macrophage colony-stimulating factors (G-CSF, GM-CSF), leading to the enhanced maturing of CD34+ progenitor cells and their further differentiation into neutrophils in bone marrow.
CONCLUSIONS: Although neutrophilic inflammation, which is a consequence of IL-17A activity, is an important element of pulmonary host defence, the prolonged action of this cytokine directed on the proliferation, maturing and chemotaxis of neutrophils to the pulmonary tract may contribute to chronic tissue destruction. Scientific research supplies proves, that this cytokine is co-responsible for the development of many functional abnormalities (e.g. bronchial hyperresponsiveness, enhanced mucus secretion, airway remodeling) in course of diseases such as: chronic bronchitis, chronic obstructive pulmonary disease and bronchial asthma.