Recent findings on the pathogenesis of bronchial asthma.
In the first part of this series of papers (Székely and Pataki, 102) the pathogenesis of asthma was approached as a pathological antigen-antibody complex induced vago-vagal axon reflex. In the next part (103) the contribution of individual hormonal predisposition, the environmental and the most frequent allergizing factors have been reviewed. In the first section of this last (third) part of the review the genetic factors contributing to the asthma are surveyed. In this field a great progress has been made during the last decade, a lot of genes have been pinpointed which contribute to the heredity of the disease. In the second section of this last paper on the etiology of asthma an attempt is made to summarize the previously reviewed data and some new ones. Actually a new hypothesis is proposed that beyond the multitude of genetic, environmental and hormonal factors the underlying biochemical mechanism is simple: the disequilibrium of two functionally opposing second messenger systems in the airways: the Ca i ++ liberating PLC-PKC cascade and the Ca i ++ level reducing cAMP mediated one with preponderance of the former.
Székely
J I
JI
Human Physiology Department, Medical School, Semmelweis University, Budapest, Hungary.
Pataki
A
A
D000818:Animals; D001249:Asthma / Q000201:enzymology / Q000209:etiology* / Q000235:genetics / Q000276:immunology / Q000503:physiopathology; D016084:Bronchoconstriction; D020013:Calcium Signaling; D000242:Cyclic AMP / Q000378:metabolism; D004777:Environment; D020022:Genetic Predisposition to Disease; D006801:Humans; D015544:Inositol 1,4,5-Trisphosphate / Q000378:metabolism; D010375:Pedigree; D011493:Protein Kinase C / Q000378:metabolism; D012021:Reflex, Abnormal; D012307:Risk Factors; D015290:Second Messenger Systems; D010738:Type C Phospholipases / Q000378:metabolism
D015544:Inositol 1,4,5-Trisphosphate; D000242:Cyclic AMP; D011493:Protein Kinase C; D010738:Type C Phospholipases