File:PMC3900397 pone.0084763.g006.png

English⧼Colon⧽ pone-0084763-g006: Model for changes in epithelial glucose handling in response to N. brasiliensis infection.(1) Infection induces a STAT6-dependent increase in mucosal permeability and (2) recruitment of alternatively activated macrophages (M2). (3) There is a M2-dependent inhibition of epithelial SGLT1 activity and M2-independent down-regulation of GLUT2. (4) This stresses the cell leading to activation of HIF-1α and up-regulation of the constitutive insulin-dependent GLUT1. This transporter serves as the major mechanism for glucose entry into the cell. Thus, parasitic nematode infection results in a “lean” epithelial phenotype as a result of a shift from insulin-dependent to insulin-independent glucose transporters. The increased permeability (1) enhances the contribution of paracellular absorption of glucose to maintain body weight during infection.