| First Author | McFarland-Mancini MM | Year | 2010 |
| Journal | J Immunol | Volume | 184 |
| Issue | 12 | Pages | 7219-28 |
| PubMed ID | 20483735 | Mgi Jnum | J:160966 |
| Mgi Id | MGI:4456451 | Doi | 10.4049/jimmunol.0901929 |
| Citation | McFarland-Mancini MM, et al. (2010) Differences in wound healing in mice with deficiency of IL-6 versus IL-6 receptor. J Immunol 184(12):7219-28 |
| abstractText | IL-6 modulates immune responses and is essential for timely wound healing. As the functions mediated by IL-6 require binding to its specific receptor, IL-6Ralpha, it was expected that mice lacking IL-6Ralpha would have the same phenotype as IL-6-deficient mice. However, although IL-6Ralpha-deficient mice share many of the inflammatory deficits seen in IL-6-deficient mice, they do not display the delay in wound healing. Surprisingly, mice with a combined deficit of IL-6 and IL-6Ralpha, or IL-6-deficient mice treated with an IL-6Ralpha-blocking Ab, showed improved wound healing relative to mice with IL-6 deficiency, indicating that the absence of the receptor contributed to the restoration of timely wound healing, rather than promiscuity of IL-6 with an alternate receptor. Wounds in mice lacking IL-6 showed delays in macrophage infiltration, fibrin clearance, and wound contraction that were not seen in mice lacking IL-6Ralpha alone and were greatly reduced in mice with a combined deficit of IL-6 and IL-6Ralpha. MAPK activation-loop phosphorylation was elevated in wounds of IL-6Ralpha-deficient mice, and treatment of wounds in these mice with the MEK inhibitor U0126 resulted in a delay in wound healing suggesting that aberrant ERK activation may contribute to improved healing. These findings underscore a deeper complexity for IL-6Ralpha function in inflammation than has been recognized previously. |
