Shandong Provincial Key Laboratory of Animal Cells and Developmental Biology, School of Life Sciences, Shandong University, Qingdao 266237, Shandong, China.
Shandong Provincial Key Laboratory of Animal Cells and Developmental Biology, School of Life Sciences, Shandong University, Qingdao 266237, Shandong, China;
J Immunol. 2021 Mar 15;206(6):1140-1150. doi: 10.4049/jimmunol.2000116. Epub 2021 Feb 1.
Intestinal microbiota are closely related to host physiology. Over the long course of evolution and interaction, both commensal bacteria and their host have evolved multiple strategies to adapt to each other. However, in invertebrates, the regulatory mechanism of intestinal microbiota homeostasis is largely unknown. In the current study, a digestive tract-specific C-type lectin, designated as CTL33, was identified because of its abundance and response to bacteria in the intestine of kuruma shrimp (). Silencing of expression led directly to intestinal dysbiosis, tissue damage, and shrimp death. CTL33 could facilitate biofilm formation by the intestinal bacteria. This function originated from its unique architecture, with a lectin domain responsible for bacteria recognition and a coiled coil region that mediated CTL33 dimerization and cross-linked the bacteria into a biofilm-like complex. By mediating the formation of a biofilm, CTL33 promoted the establishment of intestinal bacteria in intestine and maintained the homeostasis of the microbiota. Thus, to our knowledge, we demonstrated a new mechanism of C-type lectin-mediated biofilm formation by intestinal bacteria, providing new insights into intestinal homeostasis regulation in invertebrates.
肠道微生物群与宿主生理学密切相关。在漫长的进化和相互作用过程中，共生菌及其宿主都进化出了多种策略来相互适应。然而，在无脊椎动物中，肠道微生物群稳态的调节机制在很大程度上是未知的。在本研究中，由于其在虾肠道中的丰度和对细菌的反应，鉴定了一种称为 CTL33 的肠道特异性 C 型凝集素。的表达沉默直接导致肠道菌群失调、组织损伤和虾死亡。CTL33 可以促进肠道细菌的生物膜形成。这种功能源于其独特的结构，其中凝集素结构域负责细菌识别，而卷曲螺旋区介导 CTL33 二聚化，并将细菌交联成类似生物膜的复合物。通过介导生物膜的形成，CTL33 促进了肠道细菌在肠道中的定植，并维持了微生物群的稳态。因此，据我们所知，我们证明了一种肠道细菌介导的 C 型凝集素生物膜形成的新机制，为无脊椎动物肠道稳态调节提供了新的见解。
