Global change is shifting both temperature patterns and the geographic distribution of pathogens, and infection has already been shown to substantially reduce host thermal performance, potentially placing populations at greater risk that previously thought. But what about individuals that are able to successfully clear an infection? Whilst the direct damage a pathogen causes will likely lead to reductions in host's thermal tolerance, the response to infection often shares many underlying pathways with the general stress response, potentially acting as a buffer against subsequent thermal stress. Here, by exposing Drosophila melanogaster to heat‐killed bacterial pathogens, we investigate how activation of a host's immune system can modify any response to both heat and cold temperature stress. In a single focal population, we find that immune activation can improve a host's knockdown times during heat shock, potentially offsetting some of the damage that would subsequently arise as an infection progresses. Conversely, immune activation had a detrimental effect on CTmax and did not influence lower thermal tolerance as measured by chill‐coma recovery time. However, we also find that the influence of immune activation on heat knockdown times is not generalizable across an entire cline of locally adapted populations. Instead, immune activation led to signals of local adaptation to temperature being lost, erasing the previous advantage that populations in warmer regions had when challenged with heat stress. Our results suggest that activation of the immune system may help buffer individuals against the detrimental impact of infection on thermal tolerance; however, any response will be population specific and potentially not easily predicted across larger geographic scales, and dependent on the form of thermal stress faced by a host.

中文翻译：

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免疫激活对沿纬度梯度热耐受性的影响

全球变化正在改变温度模式和病原体的地理分布，并且已经证明感染会大大降低宿主的热性能，可能使人群面临比以前认为的更大的风险。但是那些能够成功清除感染的人呢？虽然病原体造成的直接损害可能会导致宿主的热耐受性降低，但对感染的反应通常与一般应激反应共享许多潜在途径，可能充当对随后热应激的缓冲。在这里，通过将黑腹果蝇暴露于热杀死的细菌病原体，我们研究了宿主免疫系统的激活如何改变对热和冷温度应激的任何反应。在单一的焦点人群中，我们发现免疫激活可以改善热休克期间宿主的击倒时间，可能会抵消随着感染进展而随后出现的一些损害。相反，免疫激活对 CTmax 有不利影响，并且不影响通过冷昏迷恢复时间衡量的较低的热耐受性。然而，我们还发现免疫激活对热击倒时间的影响在整个局部适应人群的整个基因组中是不可推广的。取而代之的是，免疫激活导致局部适应温度的信号消失，消除了温暖地区人口在受到热应激挑战时的先前优势。我们的结果表明，免疫系统的激活可能有助于缓冲个体免受感染对热耐受性的不利影响；然而，