| First Author | Rice TC | Year | 2017 |
| Journal | Cell Immunol | Volume | 313 |
| Pages | 25-31 | PubMed ID | 28063598 |
| Mgi Jnum | J:274979 | Mgi Id | MGI:6295317 |
| Doi | 10.1016/j.cellimm.2016.12.004 | Citation | Rice TC, et al. (2017) Burn injury influences the T cell homeostasis in a butyrate-acid sphingomyelinase dependent manner. Cell Immunol 313:25-31 |
| abstractText | Following burn injury, a key factor for patients susceptible to opportunistic infections is immune suppression. Butyrate levels are important in maintaining a functional immune system and these levels can be altered after injury. The acid sphingomyelinase (Asm) lipid signaling system has been implicated in a T cell actions with some evidence of being influenced by butyrate. Here, we hypothesized that burn-injury changes in butyrate levels would mediate Asm activity and, consequently, T cell homeostasis. We demonstrate that burn injury temporally decreases butyrate levels. We further determined that T cell Asm activity is increased by butyrate and decreased after burn injury. We additionally observed decreased T cell numbers in Asm-deficient, burn-injured, and microbiota-depleted mice. Finally, we demonstrate that butyrate reduced T cell death in an Asm-dependent manner. These data suggest that restoration of butyrate after burn injury may ameliorate the T cell lost observed in burn-injured patients by Asm regulation. |
