| First Author | Cho JS | Year | 2012 |
| Journal | PLoS Pathog | Volume | 8 |
| Issue | 11 | Pages | e1003047 |
| PubMed ID | 23209417 | Mgi Jnum | J:195003 |
| Mgi Id | MGI:5475424 | Doi | 10.1371/journal.ppat.1003047 |
| Citation | Cho JS, et al. (2012) Neutrophil-derived IL-1beta is sufficient for abscess formation in immunity against Staphylococcus aureus in mice. PLoS Pathog 8(11):e1003047 |
| abstractText | Neutrophil abscess formation is critical in innate immunity against many pathogens. Here, the mechanism of neutrophil abscess formation was investigated using a mouse model of Staphylococcus aureus cutaneous infection. Gene expression analysis and in vivo multispectral noninvasive imaging during the S. aureus infection revealed a strong functional and temporal association between neutrophil recruitment and IL-1beta/IL-1R activation. Unexpectedly, neutrophils but not monocytes/macrophages or other MHCII-expressing antigen presenting cells were the predominant source of IL-1beta at the site of infection. Furthermore, neutrophil-derived IL-1beta was essential for host defense since adoptive transfer of IL-1beta-expressing neutrophils was sufficient to restore the impaired neutrophil abscess formation in S. aureus-infected IL-1beta-deficient mice. S. aureus-induced IL-1beta production by neutrophils required TLR2, NOD2, FPR1 and the ASC/NLRP3 inflammasome in an alpha-toxin-dependent mechanism. Taken together, IL-1beta and neutrophil abscess formation during an infection are functionally, temporally and spatially linked as a consequence of direct IL-1beta production by neutrophils. |
