A mechanism for masking receptors with particular application to asthma

This study ensconces the concept currently popular in neurophysiology that nerve terminals can be sensitized by 'unmasking' more receptors, but goes on to propose that the unknown substance masking the remainder is surface-active phospholipid. These molecules are considered to bind reversibly by adsorption to receptor surfaces just as they are known to do at a variety of tissue surfaces at which they impart 'barrier' properties very similar to those much exploited in the physical sciences. This model of nonspecific adsorption is further extended to a wide variety of receptors in lung airways including those on smooth muscle, to explain the normal control of sensitivity of reflex bronchoconstriction indicated by many physiological features. In the corollary hypothesis, asthma is attributed to a basic deficiency in surfactant causing undue unmasking of receptors exposed to the next noxious stimulus to enter the lungs. This model is shown to be compatible with the actions of a very wide variety of sensitizing agents which are physical, chemical and biological in nature; while the inflammation arising from the more biological routes can be correlated according to whether they release surfactant or disrupt it. Special attention is focused upon the diverse actions of nonsteroidal anti-inflammatory drugs versus steroids widely prescribed for asthma which promote the secretion of surfactant, as do the popular beta-agonists.