| First Author | Lee PY | Year | 2011 |
| Journal | J Immunol | Volume | 186 |
| Issue | 3 | Pages | 1747-54 |
| PubMed ID | 21191074 | Mgi Jnum | J:168904 |
| Mgi Id | MGI:4939287 | Doi | 10.4049/jimmunol.1001328 |
| Citation | Lee PY, et al. (2011) IL-1alpha modulates neutrophil recruitment in chronic inflammation induced by hydrocarbon oil. J Immunol 186(3):1747-54 |
| abstractText | Exposure to naturally occurring hydrocarbon oils is associated with the development of chronic inflammation and a wide spectrum of pathological findings in humans and animal models. The mechanism underlying the unremitting inflammatory response to hydrocarbons remains largely unclear. The medium-length alkane 2,6,10,14 tetramethylpentadecane (also known as pristane) is a hydrocarbon that potently elicits chronic peritonitis characterized by persistent infiltration of neutrophils and monocytes. In this study, we reveal the essential role of IL-1alpha in sustaining the chronic recruitment of neutrophils following 2,6,10,14 tetramethylpentadecane treatment. IL-1alpha and IL-1R signaling promote the migration of neutrophils to the peritoneal cavity in a CXCR2-dependent manner. This mechanism is at least partially dependent on the production of the neutrophil chemoattractant CXCL5. Moreover, although chronic infiltration of inflammatory monocytes is dependent on a different pathway requiring TLR-7, type I IFN receptor, and CCR2, the adaptor molecules MyD88, IL-1R-associated kinase (IRAK)-4, IRAK-1, and IRAK-2 are shared in regulating the recruitment of both monocytes and neutrophils. Taken together, our findings uncover an IL-1alpha-dependent mechanism of neutrophil recruitment in hydrocarbon-induced peritonitis and illustrate the interactions of innate immune pathways in chronic inflammation. |
