Lipopolysaccharides (LPSs) induce a wide spectrum of functional activities after interaction with blood cells. Effect of structure of toxic LPS from S- and Re-chemotypes of E. coli and/or non-toxic LPS of Rhodobacter capsulatus PG (R. caps.) on activation of neutrophils and monocytes of human whole blood were studied, particularly, expression of TLR4, CD14 and CD11b receptors, phagocytosis of BioParticles Alexa Fluor 488, synthesis of cytokines and chemokines. A leading role of CD11b receptor in phagocytic activity of neutrophils primed by LPS from various E. coli chemotypes was shown. The non-toxic LPS of R. caps. does not affect the efficiency of phagocytosis activity of the neutrophils. The LPS of R. caps. was shown to induce production of TRIF-dependent cytokine IFN-β in human whole blood leukocytes selectively, without activating MyD88-dependent pathway of pro-inflammatory cytokine synthesis, displaying properties of patrial agonist of TLR4. Structure and biological activity of LPS R. caps. allows considering it as a promising immunity stimulating pharmacological agent.

脂多糖 (LPS) 在与血细胞相互作用后可诱导广泛的功能活动。研究了来自大肠杆菌S-和Re-化学型的毒性LPS和/或R. capsulatus PG（R. caps. ）无毒LPS的结构对人全血中性粒细胞和单核细胞活化的影响，特别是表达TLR4、CD14 和 CD11b 受体、BioParticles Alexa Fluor 488 的吞噬作用、细胞因子和趋化因子的合成。显示了 CD11b 受体在由来自各种大肠杆菌化学型的 LPS 引发的嗜中性粒细胞的吞噬活性中的主导作用。R. caps的无毒 LPS 。不影响中性粒细胞吞噬活性的效率。LPS 的R. 盖帽。显示选择性诱导人全血白细胞中 TRIF 依赖性细胞因子 IFN-β 的产生，而不激活促炎细胞因子合成的 MyD88 依赖性途径，显示 TLR4 父激动剂的特性。LPS R. caps的结构和生物活性。允许将其视为一种有前途的免疫刺激药物。