Defective ceramide response in C3H/HeJ (Lpsd) macrophages

Sheila A. Barber, Pin Yu Perera, Stefanie N. Vogel

Research output: Contribution to journalArticlepeer-review


Lipid second messengers are gaining recognition as important mediators of extracellular signals. One such lipid, ceramide, generated from membrane sphingomyelin following stimulation with TNF-α, IL-1β, or IFN-γ, activates ceramide-activated kinase (CAK). A recent study demonstrated that LPS activated CAK without generating ceramide, suggesting that the LPS stimulation of cells mimics the second messenger function of ceramide. To compare ceramide to LPS signaling, we assessed the ability of LPS-responsive (Lpsn) and LPS-hyporesponsive (Lpsd) macrophages to respond directly to ceramide for enhanced expression of LPS-inducible genes. In contrast to macrophages from C3H/OuJ (Lpsn) mice, C3H/ HeJ (Lpsd) macrophages failed to respond to cell-permeable analogues of ceramide (C2,C6,C16) or sphingomyelinase. These results suggest that a common critical molecule, encoded by the LPs gene, regulates both ceramide and LPS signaling pathways.

Original languageEnglish (US)
Pages (from-to)2303-2305
Number of pages3
JournalJournal of Immunology
Issue number5
StatePublished - 1995
Externally publishedYes

ASJC Scopus subject areas

  • Immunology

Fingerprint Dive into the research topics of 'Defective ceramide response in C3H/HeJ (Lpsd) macrophages'. Together they form a unique fingerprint.

Cite this