| First Author | Viladomiu M | Year | 2017 |
| Journal | J Immunol | Volume | 198 |
| Issue | 8 | Pages | 3195-3204 |
| PubMed ID | 28264969 | Mgi Jnum | J:252697 |
| Mgi Id | MGI:5927214 | Doi | 10.4049/jimmunol.1601902 |
| Citation | Viladomiu M, et al. (2017) Cooperation of Gastric Mononuclear Phagocytes with Helicobacter pylori during Colonization. J Immunol 198(8):3195-3204 |
| abstractText | Helicobacter pylori, the dominant member of the human gastric microbiota, elicits immunoregulatory responses implicated in protective versus pathological outcomes. To evaluate the role of macrophages during infection, we employed a system with a shifted proinflammatory macrophage phenotype by deleting PPARgamma in myeloid cells and found a 5- to 10-fold decrease in gastric bacterial loads. Higher levels of colonization in wild-type mice were associated with increased presence of mononuclear phagocytes and in particular with the accumulation of CD11b+F4/80hiCD64+CX3CR1+ macrophages in the gastric lamina propria. Depletion of phagocytic cells by clodronate liposomes in wild-type mice resulted in a reduction of gastric H. pylori colonization compared with nontreated mice. PPARgamma-deficient and macrophage-depleted mice presented decreased IL-10-mediated myeloid and T cell regulatory responses soon after infection. IL-10 neutralization during H. pylori infection led to increased IL-17-mediated responses and increased neutrophil accumulation at the gastric mucosa. In conclusion, we report the induction of IL-10-driven regulatory responses mediated by CD11b+F4/80hiCD64+CX3CR1+ mononuclear phagocytes that contribute to maintaining high levels of H. pylori loads in the stomach by modulating effector T cell responses at the gastric mucosa. |
