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Background  Toll-like receptor 4 (TLR4), an innate immune receptor, is suspected to play a key role in the postprandial inflammation that is induced by a high-fat meal rich in saturated fatty acids (SFA). Our objective was to test this hypothesis by using a specific competitive inhibitor of TLR4 (INH) vs vehicle (VEH) administered immediately before a high-SFA meal in rats.    Methods  First, in a cross-over kinetic study of 12 rats receiving INH and VEH  i.v.  10 min before the test meal, we measured plasma inflammatory and vascular markers for 6 h. Then, in 20 rats, 3 h after INH or VEH followed by the test meal (parallel study), we measured the mRNA level of a set of cytokines ( Il1-β ,  Il-6 ,  Tnfα ,  Mcp-1 ,  Pai-1 ), and of  Tlr4  and  Tlr2  in the adipose tissue and the liver, and that of adhesion molecules ( Icam-1  and  Vcam-1 ) in the aorta.    Results  Plasma IL-6 and PAI-1 increased >4-fold at 3–4 h after test-meals, very similarly after INH as compared to VEH. The expression of TLR2 and of all measured cytokine genes in the adipose tissue was dramatically higher after INH (vs VEH). In the liver, gene expression of  Il1-β ,  Tnfα ,  Mcp-1  and  Tlr2 , was also higher after INH, though more moderately, whereas that of  Il-6  and  Pai-1  was similar between groups. INH did not affect mRNA level of  Icam-1  and  Vcam-1  in the aorta.    Conclusion  TLR4 activation is not specifically required to mediate systemic postprandial inflammation and we propose that TLR2 and TLR4 exert a dual and interdependent mediation of the postprandial inflammatory response, at least in the adipose tissue.

Postprandial low-grade inflammation does not specifically require TLR4 activation in the rat