| First Author | McLaughlin PA | Year | 2019 |
| Journal | PLoS Pathog | Volume | 15 |
| Issue | 7 | Pages | e1007847 |
| PubMed ID | 31306468 | Mgi Jnum | J:282314 |
| Mgi Id | MGI:6358952 | Doi | 10.1371/journal.ppat.1007847 |
| Citation | McLaughlin PA, et al. (2019) Inflammatory monocytes provide a niche for Salmonella expansion in the lumen of the inflamed intestine. PLoS Pathog 15(7):e1007847 |
| abstractText | Salmonella exploit host-derived nitrate for growth in the lumen of the inflamed intestine. The generation of host-derived nitrate is dependent on Nos2, which encodes inducible nitric oxide synthase (iNOS), an enzyme that catalyzes nitric oxide (NO) production. However, the cellular sources of iNOS and, therefore, NO-derived nitrate used by Salmonella for growth in the lumen of the inflamed intestine remain unidentified. Here, we show that iNOS-producing inflammatory monocytes infiltrate ceca of mice infected with Salmonella. In addition, we show that inactivation of type-three secretion system (T3SS)-1 and T3SS-2 renders Salmonella unable to induce CC- chemokine receptor-2- and CC-chemokine ligand-2-dependent inflammatory monocyte recruitment. Furthermore, we show that the severity of the pathology of Salmonella- induced colitis as well as the nitrate-dependent growth of Salmonella in the lumen of the inflamed intestine are reduced in mice that lack Ccr2 and, therefore, inflammatory monocytes in the tissues. Thus, inflammatory monocytes provide a niche for Salmonella expansion in the lumen of the inflamed intestine. |
