Gil-Ramírez Yolanda, Conde-Álvarez Raquel, Palacios-Chaves Leyre, Zúñiga-Ripa Amaia, Grilló María-Jesús, Arce-Gorvel Vilma, Hanniffy Sean, Moriyón Ignacio, Iriarte Maite
Departamento de Microbiología y Parasitología e Instituto de Salud Tropical, Universidad de Navarra, 31008 Pamplona, Spain.
Instituto de Agrobiotecnología (CSIC-Universidad Pública de Navarra-Gobierno de Navarra), 31006 Pamplona, Spain.
Microb Pathog. 2014 Aug;73:53-9. doi: 10.1016/j.micpath.2014.06.002. Epub 2014 Jun 11.
Brucellosis is a worldwide extended zoonosis caused by Brucella spp. These gram-negative bacteria are not readily detected by innate immunity, a virulence-related property largely linked to their surface lipopolysaccharide (LPS). The role of the LPS lipid A and O-polysaccharide in virulence is well known. Moreover, mutation of the glycosyltransferase gene wadC of Brucella abortus, although not affecting O-polysaccharide assembly onto the lipid-A core section causes a core oligosaccharide defect that increases recognition by innate immunity. Here, we report on a second gene (wadB) encoding a LPS core glycosyltransferase not involved in the assembly of the O-polysaccharide-linked core section. As compared to wild-type B. abortus, a wadB mutant was sensitive to bactericidal peptides and non-immune serum, and was attenuated in mice and dendritic cells. These observations show that as WadC, WadB is also involved in the assembly of a branch of Brucella LPS core and support the concept that this LPS section is a virulence-related structure.
布鲁氏菌病是一种由布鲁氏菌属引起的全球广泛传播的人畜共患病。这些革兰氏阴性菌不易被固有免疫检测到,这种与毒力相关的特性很大程度上与其表面脂多糖(LPS)有关。LPS脂质A和O-多糖在毒力中的作用是众所周知的。此外,流产布鲁氏菌的糖基转移酶基因wadC发生突变,虽然不影响O-多糖组装到脂质A核心部分,但会导致核心寡糖缺陷,从而增加固有免疫的识别。在此,我们报道了第二个编码LPS核心糖基转移酶的基因(wadB),该酶不参与O-多糖连接的核心部分的组装。与野生型流产布鲁氏菌相比,wadB突变体对杀菌肽和非免疫血清敏感,并且在小鼠和树突状细胞中减毒。这些观察结果表明,与WadC一样,WadB也参与布鲁氏菌LPS核心一个分支的组装,并支持这一LPS部分是与毒力相关结构的概念。