Bailenger J, Cabannes A
Ann Parasitol Hum Comp. 1976 Sep-Oct;51(5):563-76.
In lactating females of many animal species infested by Nematoda, the self-cure is, if not suppressed, at least very distinctly delayed. It does not appear that an immunological deficiency is the cause of this. We show that this phenomenon also exists in lactating female rats with Strongyloides ratti parasites. In fact, for Strongyloides ratti, the maintenance of the worms is not the only notable modification determined by lactation; much more important is the decrease in the intensity of the parasitism. This aspect is not mentioned by writers who have only studied the different parasitic states in their final phase. Parallel to these alterations in the parasitism, the evolution of the corticosteronemy differs, from two points of view, from that described in infested virgin rats: --Suppression of the hypercorticosteronemy which normally appears 48 hours after infestation; --Attenuation of the hypocorticosteronemy which usually sets in from the tenth day of infestation. This opposition of lactation to the variations in the corticosteronemy induced by the worms is explained by the effect of lactation on the secretion of gluco-cortico-steroids, described under the term of "buffer effect of lactation". The decrease in the intensity of the parasitism may be explained by the fact that lactation, by preventing the hypercorticosteronemy normally caused by larval migration, permits the intervention of aspecific defences. As for the prolongation of the parasitism, it would seem to result on one hand, from a reduced solicitation of the means of defence owing to a smaller number of worms and, on another hand, from the slowing down of the hypocorticosteronemy through the buffer effect of lactation with all the consequences flowing from this at the level of the specific and aspecific defence reactions.
在许多受线虫感染的哺乳类动物中，哺乳期雌性动物即便不会抑制自愈，至少自愈也会明显延迟。这一现象的原因似乎并非免疫缺陷。我们发现，感染鼠类圆线虫的哺乳期雌性大鼠也存在这种现象。事实上，对于鼠类圆线虫而言，哺乳期不仅决定了寄生虫数量的维持，更重要的是寄生虫感染强度的降低。仅研究寄生虫不同终末阶段状态的作者并未提及这一方面。与寄生虫感染的这些变化同时发生的是，皮质酮水平的变化在两个方面与感染未生育大鼠的情况有所不同：——感染后48小时通常出现的高皮质酮血症受到抑制；——通常在感染后第十天开始出现的低皮质酮血症有所减轻。哺乳期对蠕虫诱导的皮质酮水平变化的这种对抗作用，是由哺乳期对糖皮质激素分泌的影响来解释的，这种影响被称为“哺乳期缓冲效应”。寄生虫感染强度的降低可能是因为哺乳期阻止了幼虫移行通常引起的高皮质酮血症，从而使非特异性防御机制得以发挥作用。至于寄生虫感染期的延长，一方面似乎是由于蠕虫数量减少导致防御机制受到的刺激减弱，另一方面是由于哺乳期的缓冲效应减缓了低皮质酮血症，这在特异性和非特异性防御反应层面都产生了相应的后果。
