Abstract
derived M2 populations failed to develop the characteristic MΦ dendrite morphology seen in control macrophages. Surface expression of CD40 in M2 CD-derived MΦs was 3.4-fold lower for M2a and 4.4fold lower for M2c compared to controls after E.coli challenge. CD163 was higher in M1 CD cells but reduced by 50% in M2 cells compared to healthy cells. After E.coli challenge, TNFα production by M2 but not M1 MΦs was significantly lower in CD than in controls (M2a 38%, M2c 27% respectively less than controls) but there were no differences in IL10 production. Prolonged intracellular survival of E.coli was demonstrated in CD M2 cells but effective killing occurred in all M1 CD MΦs and all control MΦs. In CD, M2 (but not M1) MΦs display abnormal morphological maturation, lower TNFα levels after E.coli challenge, prolonged intracellular bacterial survival and differences in surface marker expression. The results are consistent with an innate MΦ defect in CD relating particularly to a failure of the normal role of M2 MΦs to limit and control inflammation.
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