| First Author | Wang G | Year | 2018 |
| Journal | Eur J Immunol | Volume | 48 |
| Issue | 9 | Pages | 1470-1480 |
| PubMed ID | 29935120 | Mgi Jnum | J:265779 |
| Mgi Id | MGI:6200501 | Doi | 10.1002/eji.201847491 |
| Citation | Wang G, et al. (2018) IFN-gamma protects from apoptotic neutrophil-mediated tissue injury during acute Listeria monocytogenes infection. Eur J Immunol 48(9):1470-1480 |
| abstractText | Listeria monocytogenes (LM) is a foodborne Gram-positive intracellular pathogen that can cause listeriosis in humans and animals. Although phagocytes are known to be involved in the response to this infection, the role of neutrophils is not entirely clear. Here, we have demonstrated that soon after LM infection, a large number of IFN-gamma-producing neutrophils quickly accumulated in the spleen, blood, and peritoneal cavity. Both in vivo and in vitro experiments demonstrated that neutrophils were an important source of IFN-gamma. IFN-gamma played a critical protective role against acute LM infection, as demonstrated by the poor survival of Ifng(-/-) mice. Moreover, IFN-gamma promoted bacterial clearance by the neutrophils, thereby inhibiting LM-induced neutrophil apoptosis and spleen damage. In addition to this, IFN-gamma could effectively drive macrophage-mediated phagocytosis of apoptotic neutrophils, which was accompanied with TGF-beta secretion and was involved in protection against tissue injury. Importantly, by phagocytizing apoptotic neutrophils, macrophages obtained myeloperoxidase, an important bactericidal molecule only produced by neutrophils, which further promoted the antibacterial activity of macrophages. These findings demonstrate that neutrophils are an important source of IFN-gamma at the early stage of LM infection, which is characterized by both LM elimination and tissue-protective effects. |
