Oligosaccharyltransferase (OST) complex catalyzes the N-glycosylation of nascent polypeptides in the endoplasmic reticulum. Glycoproteins are critical for normal cell–cell interactions, especially during an immune response. Abnormal glycosylation is an insignia of several inflammatory diseases. However, the mechanisms that regulate the differential N-glycosylation are not fully understood. The OST complex can be assembled with one out of two catalytic subunits, STT3A or STT3B, which have different enzymatic properties. In this work, we investigated the expression of STT3A and STT3B in several mouse models such as a crossbreeding of normal and abortion-prone mice and an intestinal inflammation model. These animals were either exposed or not to acoustic stress (acute or chronic). The expression of the isoforms was analysed by immunohistochemistry and protein immunoblot. Finally, we investigated the gene regulatory elements employing public databases.

Results demonstrated that inflammation alters the balance between the expression of both isoforms in the affected tissues. In homoeostatic conditions, STT3A expression predominates over STT3B, especially in epithelial cells. This relation is reversed as a consequence of inflammation. An increase in STT3B activity was associated to the generation of mannose-rich N-glycans. Accordingly, this type of N-glycans were found to decorate diverse inflamed tissues. The STT3A and STT3B genes are differentially regulated, which could account for the differences in the expression levels observed here. Our results support the idea that these isoforms could play different roles in cellular physiology. This study opens the possibility of studying the STT3A/STT3B expression ratio as a biomarker in acute inflammation or chronic diseases.

寡糖基转移酶（OST）复合物催化内质网中新生多肽的N-糖基化。糖蛋白对于正常的细胞间相互作用至关重要，特别是在免疫反应过程中。糖基化异常是几种炎症性疾病的标志。但是，调节差异N-糖基化的机制尚未完全了解。OST复合物可以与两个催化亚基之一STT3A或STT3B组装在一起，它们具有不同的酶促性质。在这项工作中，我们研究了STT3A和STT3B在几种小鼠模型中的表达，例如正常和易流产小鼠的杂交以及肠道炎症模型。这些动物或者暴露于或不遭受声压（急性或慢性）。通过免疫组织化学和蛋白质免疫印迹分析同工型的表达。最后，我们使用公共数据库研究了基因调控元件。

结果表明，炎症改变了受影响组织中两种同工型表达之间的平衡。在均质条件下，STT3A的表达高于STT3B，尤其是在上皮细胞中。这种关系由于炎症而逆转。STT3B活性的增加与富含甘露糖的N-聚糖的产生有关。因此，发现这种类型的N-聚糖可装饰各种发炎的组织。STT3A和STT3B基因受到差异调节，这可以解释此处观察到的表达水平差异。我们的结果支持了这些同工型可能在细胞生理学中发挥不同作用的想法。这项研究为研究STT3A / STT3B表达比率作为急性炎症或慢性疾病中的生物标志物提供了可能性。