Instituto de Inmunología, Genética y Metabolismo (INIGEM), Facultad de Farmacia y Bioquímica, Universidad de Buenos Aires (UBA), Consejo Nacional de Investigaciones Científicas y Técnicas (CONICET), Buenos Aires, Argentina.
Instituto de Investigaciones Biomédicas en Retrovirus y Sida (INBIRS), Facultad de Medicina, Universidad de Buenos Aires (UBA), Consejo Nacional de Investigaciones Científicas y Técnicas (CONICET), Buenos Aires, Argentina.
Front Endocrinol (Lausanne). 2020 Sep 18;11:585923. doi: 10.3389/fendo.2020.585923. eCollection 2020.
Brucellosis is a prevalent global zoonotic infection but has far more impact in developing countries. The adipocytes are the most abundant cell type of adipose tissue and their secreted factors play an important role in several aspects of the innate and adaptive immune response. Here, we demonstrated the ability of to infect and replicate in both adipocytes and its precursor cells (pre-adipocytes) derived from 3T3-L1 cell line. Additionally, infection of pre-adipocytes also inhibited adipogenesis in a mechanism independent of bacterial viability and dependent on lipidated outer membrane protein (L-Omp19). infection was able to modulate the secretion of IL-6 and the matrix metalloproteases (MMPs) -2 and-9 in pre-adipocytes and adipocytes, and also modulated de transcription of adiponectin, leptin, and resistin in differentiated adipocytes. -infected macrophages also modulate adipocyte differentiation involving a TNF-α dependent mechanism, thus suggesting a plausible interplay between , adipocytes, and macrophages. In conclusion, is able to alter adipogenesis process in adipocytes and its precursors directly after their infection, or merely their exposure to the lipoproteins, and indirectly through soluble factors released by -infected macrophages.
布鲁氏菌病是一种流行的全球人畜共患病，但在发展中国家的影响更大。脂肪细胞是脂肪组织中最丰富的细胞类型，其分泌的因子在先天和适应性免疫反应的几个方面发挥着重要作用。在这里，我们证明了能够感染和复制 3T3-L1 细胞系来源的脂肪细胞及其前体细胞（前脂肪细胞）。此外，感染前脂肪细胞也能以不依赖于细菌活力且依赖于脂化外膜蛋白（L-Omp19）的机制抑制脂肪生成。感染能够调节前脂肪细胞和脂肪细胞中 IL-6 和基质金属蛋白酶（MMPs）-2 和-9 的分泌，并调节分化脂肪细胞中脂联素、瘦素和抵抗素的转录。感染的巨噬细胞也能调节脂肪细胞分化，涉及 TNF-α 依赖的机制，因此表明 、脂肪细胞和巨噬细胞之间可能存在相互作用。总之，能够直接在感染后或仅仅在暴露于 脂蛋白后改变脂肪细胞及其前体细胞的脂肪生成过程，并通过感染的巨噬细胞释放的可溶性因子间接改变。
