Table 1 Agouti (endogenous MC1R inverse agonist) inhibits the effects of MECO-1 and alpha-MSH on endotoxin-stimulated TNF release

From: New melanocortin-like peptide of E. coli can suppress inflammation via the mammalian melanocortin-1 receptor (MC1R): possible endocrine-like function for microbes of the gut

Agouti (pM) TNF-accumulated (% of control)
  MECO-1 (10-12 M) Alpha-MSH (10-12 M)
0 52.9 ± 11.2 67.05 ± 10.2
10 134.3 ± 14.5** 132.6 ± 4.9*
103 172.9 ± 10.1** 138.6 ± 12.4*
105 152.4 ± 6.1** 122.2 ± 4.3*
  1. The experiment was as described in the legend of Fig. 3 except that HMGB1 were replaced by LPS (10 ng/ml) and anti-receptor antibody was replaced by agouti, the endogenous peptide that is an inverse agonist of alpha-MSH action via MC1R. TNF release by LPS (10 ng/ml) alone was set at 100%
  2. **p<0.01 vs. MECO-1, *p<0.05 vs. alpha-MSH