| First Author | Alam MS | Year | 2014 |
| Journal | Sci Rep | Volume | 4 |
| Pages | 4486 | PubMed ID | 24670982 |
| Mgi Jnum | J:210462 | Mgi Id | MGI:5571222 |
| Doi | 10.1038/srep04486 | Citation | Alam MS, et al. (2014) Ecto-5'-nucleotidase (CD73) regulates host inflammatory responses and exacerbates murine salmonellosis. Sci Rep 4:4486 |
| abstractText | Food-borne Salmonella spp., are a major cause of hospitalization and death. Adenosine, an important immune regulator of inflammation, limits tissue damage during infection. CD39 (nucleoside triphosphate dephosphorylase) combined with ecto-5'-nucleotidase (CD73) metabolizes ATP to adenosine. We studied the expressions of CD39 and CD73 in tissues, and T helper cells in mice after Salmonella infection and evaluated the role of CD73 in regulating immune responses and bacterial clearance in wild-type and CD73-deficient (CD73(-/-)) mice. Both CD39 and CD73 transcript levels declined in the infected wild-type mice. Compared to wild-type mice, tissues from infected CD73(-/-) mice had significantly higher expression of pro-inflammatory cytokines and reduced anti-inflammatory responses. CD73(-/-) mice were more resistant to infection and had a greater inflammatory responses and a significantly lower bacterial load in the liver compared to wild-type mice. Thus, CD73 expression attenuates inflammation during murine Salmonellosis and impairs immunity, leading to increased bacterial colonization and prolonged infection. |
