[Tumor necrosis factor].
Bronchial asthma is currently considered as basically an inflammatory disorder. In children there is a clear association between the allergy to aeroallergens and the development of asthma. By means of a complex interaction between environmental and genetic factors, the cellular mechanisms responsible for their pathophysiology are set off. The lymphocytes with a phenotype similar to those describe in the TH-2 mouse, are considered to be responsible for controlling this inflammatory process. By means of the production of Il-4 they would induce the hyper-production of IgE, the main alteration of the immunologic system in people who are allergic and it is eventually responsible for setting off the allergic reaction. The main effector cells involved are the eosinophils and the mastocytes, due to their capacity to segregate preformed and synthesised mediators of the inflammation again. Over the last few years the research work has been multiplied in search of the inflammatory markers of the illness, trying to co-relate them to the seriousness. In theory, the higher the level of inflammatory markers should correspond to a more serious inflammation, in this way the use of these markers would be aimed at monitoring the treatment, the response and the performance, the identification of risk patients and their application to the differential diagnosis of asthma. The TNF-alpha is a very versatile and ubiquitous cytokine that has been involved in the pathophysiology of bronchial asthma, both in the inflammatory process as well as in the bronchial hyper-reactivity. Our aim is to review the role of this inflammatory mediator in bronchial asthma in general and the specific problems of asthma in children.
Rubira García
N
N
Hospital Universitari Germans Trias i Pujol, Badalona, Barcelona, España.
D000818:Animals; D001249:Asthma / Q000503:physiopathology*; D016535:Bronchial Hyperreactivity / Q000503:physiopathology; D015815:Cell Adhesion Molecules / Q000502:physiology; D002648:Child; D016207:Cytokines / Q000502:physiology; D004804:Eosinophils / Q000502:physiology; D006801:Humans; D007249:Inflammation; D007378:Interleukins / Q000502:physiology; D016131:Lymphocyte Subsets / Q000502:physiology; D008407:Mast Cells / Q000502:physiology; D051379:Mice; D008817:Mice, Mutant Strains; D014409:Tumor Necrosis Factor-alpha / Q000502:physiology*
D015815:Cell Adhesion Molecules; D016207:Cytokines; D007378:Interleukins; D014409:Tumor Necrosis Factor-alpha
Factor de necrosis tumoral.