The identification of a functional molecular moiety relating the lipopolysaccharides (LPSs) to their capacity to induce inflammation-mediated metabolic diseases needed to be performed. We previously described a proportional increase in the relative abundance of the 16 SrDNA bacterial gene from the genus Ralstonia, within the microbiota from the adipose tissue stroma vascular fraction of obese patients, suggesting a causal role of the bacteria. Therefore, we first characterized the structures of the lipids A, the inflammatory inducing moieties of LPSs, of three Ralstonia species: Ralstonia eutropha, R. mannitolilytica and R. pickettii, and then compared each, in terms of in vitro inflammatory capacities. R. pickettii lipid A displaying only 5 Fatty Acids (FA) was a weaker inducer of inflammation, compared to the two other species harboring hexa-acylated lipids A, despite the presence of 2 AraN substituents on the phosphate groups.

With regard to in vitro pro-inflammatory activities, TNF-α and IL-6 inducing capacities were compared on THP-1 cells treated with LPSs isolated from the three Ralstonia. R. pickettii, with low inflammatory capacities, and recently involved in nosocomial outcomes, could explain the low inflammatory level reported in previous studies on diabetic patients and animals. In addition, transmission electron microscopy was performed on the three Ralstonia species. It showed that the R. pickettii under-acylated LPSs, with a higher level of phosphate substitution had the capacity of producing more outer membrane vesicles (OMVs). The latter could facilitate transfer of LPSs to the blood and explain the increased low-grade inflammation observed in obese/diabetic patients.

需要进行将脂多糖（LPS）与其诱导炎症介导的代谢疾病的能力相关的功能分子部分的鉴定。我们先前描述了肥胖患者脂肪组织基质血管部分的微生物群中，来自Ralstonia属的16 SrDNA细菌基因的相对丰度成比例增加，表明该细菌具有因果关系。因此，我们首次表征脂质A，的LPS的炎症诱导部分的三个的结构青枯物种：富养产碱，R.甘露醇和R. pickettii，然后比较各自来讲体外炎症能力。与仅携带5个脂肪酸（FA）的R. pickettii脂质A相比，其他两个具有六酰化脂质A的物种，尽管在磷酸基团上存在2个AraN取代基，但它的炎症诱导作用更弱。

关于体外促炎活性，比较了用从三个罗氏菌分离的LPS处理的THP-1细胞对TNF-α和IL-6的诱导能力。R. pickettii具有较低的发炎能力，最近参与了医院治疗，这可以解释先前关于糖尿病患者和动物的研究中报道的低发炎水平。此外，对三种Ralstonia菌种进行了透射电子显微镜检查。它表明R. pickettii磷酸取代水平较高的低酰化LPS具有产生更多外膜囊泡（OMV）的能力。后者可以促进LPS向血液的转移，并可以解释在肥胖/糖尿病患者中观察到的轻度炎症增加。