| First Author | Vázquez A | Year | 2014 |
| Journal | Int J Biol Sci | Volume | 10 |
| Issue | 8 | Pages | 909-20 |
| PubMed ID | 25170304 | Mgi Jnum | J:309153 |
| Mgi Id | MGI:6755799 | Doi | 10.7150/ijbs.9214 |
| Citation | Vazquez A, et al. (2014) Mouse macrophage galactose-type lectin (mMGL) is critical for host resistance against Trypanosoma cruzi infection. Int J Biol Sci 10(8):909-20 |
| abstractText | The C-type lectin receptor mMGL is expressed exclusively by myeloid antigen presenting cells (APC) such as dendritic cells (DC) and macrophages (Mphi), and it mediates binding to glycoproteins carrying terminal galactose and alpha- or beta-N-acetylgalactosamine (Gal/GalNAc) residues. Trypanosoma cruzi (T. cruzi) expresses large amounts of mucin (TcMUC)-like glycoproteins. Here, we show by lectin-blot that galactose moieties are also expressed on the surface of T. cruzi. Male mMGL knockout (-/-) and wild-type (WT) C57BL/6 mice were infected intraperitoneally with 10(4) T. cruzi trypomastigotes (Queretaro strain). Following T. cruzi infection, mMGL-/- mice developed higher parasitemia and higher mortality rates compared with WT mice. Although hearts from T. cruzi-infected WT mice presented few amastigote nests, mMGL-/- mice displayed higher numbers of amastigote nests. Compared with WT, Mphi from mMGL-/- mice had low production of nitric oxide (NO), interleukin (IL)-12 and tumor necrosis factor (TNF)-alpha in response to soluble T. cruzi antigens (TcAg). Interestingly, upon in vitro T. cruzi infection, mMGL-/- Mphi expressed lower levels of MHC-II and TLR-4 and harbored higher numbers of parasites, even when mMGL-/- Mphi were previously primed with IFN-gamma or LPS/IFN-gamma. These data suggest that mMGL plays an important role during T. cruzi infection, is required for optimal Mphi activation, and may synergize with TLR-4-induced pathways to produce TNF-alpha, IL-1beta and NO during the early phase of infection. |
