Abstract
ScopeIntestinal mucositis is a common side effect of the chemotherapeutic agent doxorubicin, which is characterized by severe Toll‐like receptor (TLR) 2‐mediated inflammation. The dietary fiber pectin is shown to prevent this intestinal inflammation through direct inhibition of TLR2 in a microbiota‐independent manner. Recent in vitro studies show that inhibition of TLR2 is determined by the number and distribution of methyl‐esters of pectins. Therefore, it is hypothesized that the degree of methyl‐esterification (DM) and the degree of blockiness (DB) of pectins determine attenuating efficacy on doxorubicin‐induced intestinal mucositis.Methods and ResultsFour structurally different pectins that differed in DM and DB are tested on inhibitory effects on murine TLR2 in vitro, and on doxorubicin‐induced intestinal mucositis in mice. These data demonstrate that low DM pectins or intermediate DM pectins with high DB have the strongest inhibitory impact on murine TLR2‐1 and the strongest attenuating effect on TLR2‐induced apoptosis and peritonitis. Intermediate DM pectin with a low DB is, however, also effective in preventing the induction of doxorubicin‐induced intestinal damage.ConclusionThese pectin structures with stronger TLR2‐inhibiting properties may prevent the development of doxorubicin‐induced intestinal damage in patients undergoing chemotherapeutic treatment with doxorubicin.
Highlights
Scope: Intestinal mucositis is a common side effect of the chemotherapeutic inflammation and ulceration of the intestinal lining.[1]
Anti-inflammatory agents have been used to suppress doxorubicininduced intestinal inflammation, but there is no effective treatment available doxorubicin-induced intestinal mucositis in mice. These data demonstrate besides stopping the chemotherapeutic that low degree of methyl-esterification (DM) pectins or intermediate DM pectins with high degree of blockiness (DB) have the treatment with severe consequences for strongest inhibitory impact on murine TLR2-1 and the strongest attenuating effect on TLR2-induced apoptosis and peritonitis
We addressed the impact of DM and DB on murine TLR2 (mTLR2) signaling
Summary
These pectin structures with stronger TLR2-inhibiting properties cositis is characterized by a fast inducmay prevent the development of doxorubicin-induced intestinal damage in patients undergoing chemotherapeutic treatment with doxorubicin. A. Schols Laboratory of Food Chemistry Wageningen University Bornse Weilanden 9, Wageningen, WG 6708, The Netherlands. In the unextracted cell walls of fruits and vegetables, the pectins contain additional domains including rhamogalacturonan I, rhamnogalacturonan II, and xylogalacturonan.[17] Homogalacturonan pectins consist mainly of α (1-4)-linked galacturonic acid (GalA) residues. These GalA residues within the galacturonan backbone can be methyl esterified, as quantified by the degree of methyl-esterification (DM). The anti-inflammatory effect of these pectin structures in mice with doxorubicin-induced intestinal mucositis was investigated by determining intestinal histology, intestinal apoptosis, intestinal barrier function, and peritoneal inflammation
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