Data from: The coral immune response facilitates protection against microbes during tissue regeneration

Increasing physical damage on coral reefs from predation, storms and
anthropogenic disturbances highlights the need to understand the impact of
injury on the coral immune system. In this study, we examined the
regulation of the coral immune response over 10 days following physical
trauma artificially inflicted on in situ colonies of the coral Acropora
aspera, simultaneously with bacterial colonization of the lesions. Corals
responded to injury by increasing the expression of immune system-related
genes involved in the Toll-like and NOD-like receptor signalling pathways
and the lectin–complement system in three phases (<2, 4 and 10 days
post-injury). Phenoloxidase activity was also significantly upregulated in
two phases (<3 and 10 days post-injury), as were levels of
non-fluorescent chromoprotein. In addition, green fluorescent protein
expression was upregulated in response to injury from 4 days post-injury,
while cyan fluorescent protein expression was reduced. No shifts in the
composition of coral-associated bacterial communities were evident
following injury based on 16S rRNA gene amplicon pyrosequencing.
Bacteria-specific fluorescence in situ hybridization also showed no
evidence of bacterial colonization of the wound or regenerating tissues.
Coral tissues showed near-complete regeneration of lesions within 10 days.
This study demonstrates that corals exhibit immune responses that support
rapid recovery following physical injury, maintain coral microbial
homeostasis and prevent bacterial infestation that may compromise coral
fitness.

捕食、风暴及人为扰动造成的珊瑚礁物理损伤日益加剧，这凸显了阐明损伤对珊瑚免疫系统影响的必要性。本研究针对人工施加物理创伤后的野外原位鹿角杯形珊瑚（Acropora aspera）群落，持续10天观测其免疫应答的调控过程，同时追踪病灶处的细菌定植情况。珊瑚对损伤的应答表现为分三个阶段（损伤后<2天、4天及10天）上调与免疫系统相关的基因表达，这些基因参与Toll样受体（Toll-like receptor）与NOD样受体（NOD-like receptor）信号通路及凝集素-补体系统（lectin–complement system）的调控。酚氧化酶（phenoloxidase）活性同样在两个阶段（损伤后<3天及10天）显著上调，无色铬蛋白（non-fluorescent chromoprotein）的含量变化亦呈现相同趋势。此外，绿色荧光蛋白（green fluorescent protein）的表达自损伤后4天起显著上调，而青色荧光蛋白（cyan fluorescent protein）的表达则出现下调。基于16S rRNA基因扩增子焦磷酸测序（16S rRNA gene amplicon pyrosequencing）的分析结果显示，损伤后珊瑚共生细菌群落的组成未发生明显变化。细菌特异性荧光原位杂交（fluorescence in situ hybridization）实验同样未发现伤口或再生组织存在细菌定植的迹象。珊瑚组织可在10天内实现病灶的近乎完全再生。本研究表明，珊瑚可通过免疫应答实现物理损伤后的快速修复，维持珊瑚微生物群落稳态，并抵御可能降低珊瑚生存适合度的细菌侵染。