Recent findings on the pathogenesis of bronchial asthma. Part I. Asthma as a neurohumoral disorder, a pathological vago-vagal axon reflex.
The novel data on the pathogenesis of asthma are summarized in this three-part review. Its immunological background is well established but it is more than an immunological disorder. Multiple lines indicate that both peripheral and central neural mechanisms are also involved in the pathogenesis of asthma. In the present first part of the review asthma is described as vago-vagal axon reflex brought about by multiple positive feed-back mechanisms, receptor upregulation, wind-up, phenotypic switch and formation of a pathological conditioned reflex. In the coming second part the main dispositional (mostly hormonal) and external contributing factors are reviewed, while the third part deals with the role of inheritance, i.e., with gene alleles leading to enhanced production of mediators of asthma.
Székely
J I
JI
Department of Human Physiology, Medical School, Semmelweis University, Ulloi út 78/a, H-1085 Budapest, Hungary. maria.jozsefszekely@mail.datanet.hu
Pataki
A
A
D000818:Animals; D001249:Asthma / Q000276:immunology / Q000378:metabolism / Q000503:physiopathology*; D001369:Axons / Q000378:metabolism*; D016535:Bronchial Hyperreactivity; D006801:Humans; D008168:Lung / Q000294:innervation*; D036421:Nerve Fibers, Unmyelinated / Q000378:metabolism; D009414:Nerve Growth Factors / Q000378:metabolism; D010641:Phenotype; D017981:Receptors, Neurotransmitter / Q000378:metabolism*; D018039:Receptors, Tachykinin / Q000378:metabolism; D012018:Reflex; D011984:Sensory Receptor Cells / Q000378:metabolism; D050916:TRPV Cation Channels / Q000378:metabolism; D015320:Tachykinins / Q000378:metabolism; D014630:Vagus Nerve / Q000378:metabolism / Q000503:physiopathology*
D009414:Nerve Growth Factors; D017981:Receptors, Neurotransmitter; D018039:Receptors, Tachykinin; D050916:TRPV Cation Channels; D015320:Tachykinins