Hormones and host resistance to infection.

As biologic organization became increasingly complex during the evolutionary process, evidently survival value became attached to the development of hormonally mediated regulatory mechanisms. It would not be surprising to find that as mechanisms of resistance to infection also became more complex, these also came under hormonal influence to some degree. Thus, the study of the influence of hormones on mechanisms of resistance to infection may offer insights not only into immune processes but perhaps also into the means by which hormones regulate physiologic processes. At present no completely satisfactory mechanistic description of the action of any hormone exists. The many attempts to demonstrate specific enzymatic changes in tissues in consequence of alteration in hormonal activity have provided ample evidence that many enzymatic activities are altered after the administration of various hormones to various hosts. However, direct and specific enzymatic responses to the action of hormones have been demonstrated in but one or two instances, and the general applicability of even these is far from clear. For example, the demonstration by Villee (30) of the stimulation by estrogen of DPN-dependent uterine transhydrogenase is one of the rare examples of a hormonesensitive metabolic system operating in vitro. However, many potent estrogens do not participate in this hydrogen transfer system in a very active way and, at present, there is no way that the transhydrogenase reaction can explain, for example, the effect of estrogens on uterine growth, pituitary function, secondary sex characteristics, or thyroid binding protein of the blood. Ignorance of the mode of action of hormones both as to their general physiological effects as well as in relation to mechanisms of resistance to infection permits empirical statements only. It would not serve the purpose of the present