Pectins have anti-inflammatory effects via Toll-like receptor (TLR) inhibition in a degree of methyl-esterification-(DM)-dependent manner. However, pectins also vary in distribution of methyl-esters over the galacturonic-acid (GalA) backbone (Degree of Blockiness - DB) and impact of this on anti-inflammatory capacity is unknown. Pectins mainly inhibit TLR2-1 but magnitude depends on both DM and DB. Low DM pectins (DM18/19) with both low (DB86) and high DB (DB94) strongly inhibit TLR2-1. However, pectins with intermediate DM (DM43/DM49) and high DB (DB60), but not with low DB (DB33), inhibit TLR2-1 as strongly as low DM. High DM pectins (DM84/88) with DB71 and DB91 do not inhibit TLR2-1 strongly. Pectin-binding to TLR2 was confirmed by capture-ELISA. In human macrophages, low DM and intermediate DM pectins with high DB inhibited TLR2-1 induced IL-6 secretion. Both high number and blockwise distribution of non-esterified GalA in pectins are responsible for the anti-inflammatory effects via inhibition of TLR2-1.

果胶通过以下方式具有抗炎作用Toll样受体（TLR）抑制的程度取决于甲基酯化（DM）。但是，果胶在半乳糖醛酸（GalA）主链上的甲酯分布也不同（嵌段度-DB），其对抗炎能力的影响尚不清楚。果胶主要抑制TLR2-1，但大小取决于DM和DB。具有低（DB86）和高DB（DB94）的低DM果胶（DM18 / 19）强烈抑制TLR2-1。但是，具有中等DM（DM43 / DM49）和高DB（DB60）但不具有低DB（DB33）的果胶与低DM一样强烈抑制TLR2-1。具有DB71和DB91的高DM果胶（DM84 / 88）不能强烈抑制TLR2-1。通过捕获-ELISA证实果胶与TLR2的结合。在人类巨噬细胞中，具有高DB的低DM和中等DM果胶可抑制TLR2-1诱导的IL-6分泌。通过抑制TLR2-1。