Abstract
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.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 25-31 |
| Number of pages | 7 |
| Journal | Cellular Immunology |
| Volume | 313 |
| DOIs | |
| State | Published - Mar 1 2017 |
| Externally published | Yes |
Bibliographical note
Funding Information:This work was supported by the Shriners Hospitals for Children #85310-CIN-14 (CCC). The project described was supported by Award Number T32 GM08478 (TCR) from the National Institute of General Medical Sciences. The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Institute of General Medical Sciences or the National Institutes of Health.
Publisher Copyright:
© 2016 Elsevier Inc.
Keywords
- Acid sphingomyelinase
- Apoptosis
- Burn injury
- Butyrate
- T cells