Lipopolysaccaride induces autophagic signaling in macrophages via a TLR4, heme oxygenase-1 dependent pathway

Paul Waltz; Evie H. Carchman; Atalie C. Young; Jayashree Rao; Matthew R. Rosengart; David Kaczorowski; Brian S. Zuckerbraun

doi:10.4161/auto.7.3.14044

Lipopolysaccaride induces autophagic signaling in macrophages via a TLR4, heme oxygenase-1 dependent pathway

Paul Waltz
, Evie H. Carchman
, Atalie C. Young
, Jayashree Rao
, Matthew R. Rosengart
, David Kaczorowski
, Brian S. Zuckerbraun

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

113 Scopus citations

Abstract

Toll-like receptor (TLR) signaling is an important part of the innate immune response. One of the downstream responses to TLR4 signaling upon lipopolysaccharide (LPS) stimulation is the induction of autophagy, which is a key response to multiple stressors. An additional adaptive signaling molecule that is involved in the response to stress is heme oxygenase-1 (HO-1). HO-1 signaling is essential to limit inflammation and restore homeostasis. We found that LPS induced autophagic signaling in macrophages via a TLR4, HO-1 dependent pathway in macrophages. These data add to the developing contribution of autophagic signaling as part of the inflammatory response.

Original language	English
Pages (from-to)	315-320
Number of pages	6
Journal	Autophagy
Volume	7
Issue number	3
DOIs	https://doi.org/10.4161/auto.7.3.14044
State	Published - Mar 2011

Keywords

Peritoneal macrophages
RAW 264.7
Sepsis
Tumor necrosis factoralpha

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title = "Lipopolysaccaride induces autophagic signaling in macrophages via a TLR4, heme oxygenase-1 dependent pathway",

abstract = "Toll-like receptor (TLR) signaling is an important part of the innate immune response. One of the downstream responses to TLR4 signaling upon lipopolysaccharide (LPS) stimulation is the induction of autophagy, which is a key response to multiple stressors. An additional adaptive signaling molecule that is involved in the response to stress is heme oxygenase-1 (HO-1). HO-1 signaling is essential to limit inflammation and restore homeostasis. We found that LPS induced autophagic signaling in macrophages via a TLR4, HO-1 dependent pathway in macrophages. These data add to the developing contribution of autophagic signaling as part of the inflammatory response.",

keywords = "Peritoneal macrophages, RAW 264.7, Sepsis, Tumor necrosis factoralpha",

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AU - Waltz, Paul

AU - Carchman, Evie H.

AU - Young, Atalie C.

AU - Rao, Jayashree

AU - Rosengart, Matthew R.

AU - Kaczorowski, David

AU - Zuckerbraun, Brian S.

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N2 - Toll-like receptor (TLR) signaling is an important part of the innate immune response. One of the downstream responses to TLR4 signaling upon lipopolysaccharide (LPS) stimulation is the induction of autophagy, which is a key response to multiple stressors. An additional adaptive signaling molecule that is involved in the response to stress is heme oxygenase-1 (HO-1). HO-1 signaling is essential to limit inflammation and restore homeostasis. We found that LPS induced autophagic signaling in macrophages via a TLR4, HO-1 dependent pathway in macrophages. These data add to the developing contribution of autophagic signaling as part of the inflammatory response.

AB - Toll-like receptor (TLR) signaling is an important part of the innate immune response. One of the downstream responses to TLR4 signaling upon lipopolysaccharide (LPS) stimulation is the induction of autophagy, which is a key response to multiple stressors. An additional adaptive signaling molecule that is involved in the response to stress is heme oxygenase-1 (HO-1). HO-1 signaling is essential to limit inflammation and restore homeostasis. We found that LPS induced autophagic signaling in macrophages via a TLR4, HO-1 dependent pathway in macrophages. These data add to the developing contribution of autophagic signaling as part of the inflammatory response.

KW - Peritoneal macrophages

KW - RAW 264.7

KW - Sepsis

KW - Tumor necrosis factoralpha

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EP - 320

JO - Autophagy

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ER -

Lipopolysaccaride induces autophagic signaling in macrophages via a TLR4, heme oxygenase-1 dependent pathway

Abstract

Keywords

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