Parasites are ubiquitous and can strongly affect their hosts through mechanisms such as behavioural changes, increased energetic costs and/or immunomodulation. When parasites are detrimental to their hosts, they should act as physiological stressors and elicit the release of glucocorticoids. Alternatively, previously elevated glucocorticoid levels could facilitate parasite infection due to neuroimmunomodulation. However, results are equivocal, with studies showing either positive, negative or no relationship between parasite infection and glucocorticoid levels. Since factors such as parasite type, infection severity or host age and sex can influence the parasite–glucocorticoid relationship, we review the main mechanisms driving this relationship. We then perform a phylogenetic meta‐analysis of 110 records from 65 studies in mammalian hosts from experimental and observational studies to quantify the general direction of this relationship and to identify ecological and methodological drivers of the observed variability. Our review produced equivocal results concerning the direction of the relationship, but there was stronger support for a positive relationship, although causality remained unclear. Mechanisms such as host manipulation for parasite survival, host response to infection, cumulative effects of multiple stressors, and neuro‐immunomodulatory effects of glucocorticoids could explain the positive relationship. Our meta‐analysis results revealed an overall positive relationship between glucocorticoids and parasitism among both experimental and observational studies. Because all experimental studies included were parasite manipulations, we conclude that parasites caused in general an increase in glucocorticoid levels. To obtain a better understanding of the directionality of this link, experimental manipulation of glucocorticoid levels is now required to assess the causal effects of high glucocorticoid levels on parasite infection. Neither parasite type, the method used to assess parasite infection nor phylogeny influenced the relationship, and there was no evidence for publication bias. Future studies should attempt to be as comprehensive as possible, including moderators potentially influencing the parasite–glucocorticoid relationship. We particularly emphasise the importance of testing hosts of a broad age range, concomitantly measuring sex hormone levels or at least reproductive status, and for observational studies, also considering food availability, host body condition and social stressors to obtain a better understanding of the parasite–glucocorticoid relationship.

中文翻译：

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哺乳动物寄生虫-糖皮质激素关系的模式和变异

寄生虫无处不在，可以通过行为改变、能量消耗增加和/或免疫调节等机制强烈影响宿主。当寄生虫对其宿主有害时，它们应该充当生理应激源并引起糖皮质激素的释放。或者，先前升高的糖皮质激素水平可能由于神经免疫调节而促进寄生虫感染。然而，结果是模棱两可的，研究表明寄生虫感染与糖皮质激素水平之间存在阳性、阴性或无关系。由于寄生虫类型、感染严重程度或宿主年龄和性别等因素会影响寄生虫与糖皮质激素的关系，我们回顾了驱动这种关系的主要机制。然后，我们对来自实验和观察研究的 65 项哺乳动物宿主研究的 110 条记录进行了系统发育荟萃分​​析，以量化这种关系的总体方向，并确定观察到的变异性的生态学和方法学驱动因素。我们的审查得出了关于关系方向的模棱两可的结果，但对积极关系有更强的支持，尽管因果关系仍不清楚。寄生虫存活的宿主操纵、宿主对感染的反应、多种应激源的累积效应以及糖皮质激素的神经免疫调节作用等机制可以解释这种正相关关系。我们的荟萃分析结果表明，在实验性和观察性研究中，糖皮质激素与寄生虫之间存在总体正相关关系。因为包括的所有实验研究都是寄生虫操作，我们得出结论，寄生虫通常会导致糖皮质激素水平升高。为了更好地了解这种联系的方向性，现在需要对糖皮质激素水平进行实验操作，以评估高糖皮质激素水平对寄生虫感染的因果影响。寄生虫类型、用于评估寄生虫感染的方法和系统发育均不影响这种关系，并且没有发表偏倚的证据。未来的研究应尽可能全面，包括可能影响寄生虫-糖皮质激素关系的调节剂。我们特别强调测试广泛年龄范围的宿主的重要性，同时测量性激素水平或至少生殖状态，