Burn injury influences the T cell homeostasis in a butyrate-acid sphingomyelinase dependent manner

Teresa C. Rice; Stephanie M. Armocida; Joshua W. Kuethe; Emily F. Midura; Ayushi Jain; David A. Hildeman; Daniel P. Healy; Erich Gulbins; Charles C. Caldwell

doi:10.1016/j.cellimm.2016.12.004

Burn injury influences the T cell homeostasis in a butyrate-acid sphingomyelinase dependent manner

Teresa C. Rice, Stephanie M. Armocida, Joshua W. Kuethe, Emily F. Midura, Ayushi Jain, David A. Hildeman, Daniel P. Healy, Erich Gulbins, Charles C. Caldwell

Research output: Contribution to journal › Article › peer-review

11 Scopus citations

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	https://doi.org/10.1016/j.cellimm.2016.12.004
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

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10.1016/j.cellimm.2016.12.004

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5559081

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title = "Burn injury influences the T cell homeostasis in a butyrate-acid sphingomyelinase dependent manner",

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.",

keywords = "Acid sphingomyelinase, Apoptosis, Burn injury, Butyrate, T cells",

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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: {\textcopyright} 2016 Elsevier Inc.",

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AU - Rice, Teresa C.

AU - Armocida, Stephanie M.

AU - Kuethe, Joshua W.

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AU - Jain, Ayushi

AU - Hildeman, David A.

AU - Healy, Daniel P.

AU - Gulbins, Erich

AU - Caldwell, Charles C.

N1 - 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.

PY - 2017/3/1

Y1 - 2017/3/1

N2 - 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.

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Burn injury influences the T cell homeostasis in a butyrate-acid sphingomyelinase dependent manner

Abstract

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Keywords

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