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Printable Handouts
Navigable Slide Index
- Introduction
- Mediator paradigms in innate immunity
- Overview of eicosanoids
- Eicosanoids in antimicrobial immunity
- The leukotriene synthetic pathway
- Impaired bacterial clearance in 5-LO-/- mice
- LTB4 enhances phagocytosis in AMs
- Role of LTB4 in bacterial killing by AMs
- Pathway for NFκB activation upon PRR ligation
- Crosstalk between PRR and GPCR pathways?
- Dectin-1
- LTB4 enhances yeast binding via dectin-1
- Basal dectin-1 expression depends on LTB4
- LTB4 enhances cytokine generation
- Dectin-1 depends on an LTB4-PU.1 axis
- Pathway for NFκB activation upon TLR ligation
- NFκB translocation and LTB4/BLT1 signaling
- 5-LO and MyD88-dependent NFκB activity
- Role of 5-LO and LTB4 in MyD88 expression
- Role of STAT-1 and SOCS1 in MyD88 expression
- Effects of SOCS1 siRNA in 5-LO -/- MŘs
- PGE2 actions are context-dependent
- PGE2 synthesis and signaling
- PGE2-EP2 signaling
- PGE2 inhibits FcγR-mediated phagocytosis
- PGE2 inhibits AM ingestion of yeast via dectin-1
- PGE2 utilizes distinct cAMP effectors
- PGE2 inhibits bacterial killing
- PGE2 inhibits 2 NADPH oxidase carrier subunits
- PGE2 reduces AM expression of TLR4 protein
- PGE2 increases macrophage SOCS expression
- PGE2's opposite effect on TNF-alpha and IL-10
- Opposing actions of PGE2 versus LTB4 on PRR
- Eicosanoid imbalance in immunosuppression
- Summary
- Conclusion
- Acknowledgments
Topics Covered
- Mediator paradigms in innate immunity
- Eicosanoids
- Eicosanoids in antimicrobial immunity: Yin and Yang
- The leukotriene synthetic pathway
- Role of LTB4 in bacterial killing by AMs
- Pathway for NFκB activation upon PRR ligation
- Cross-talk between PRR and GPCR pathways?
- Dectin-1
- LTB4 enhances yeast binding via dectin-1
- Basal dectin-1 expression depends on constitutive LTB4 generation
- LTB4 enhances dectin-1-induced cytokine generation by elicited MΦ
- Dectin-1 expression in MΦ depends on an LTB4-PU.1 axis
- Pathway for NFκB activation upon TLR ligation
- LPS-induced nuclear translocation of NFκB subunits requires endogenous LTB4/BLT1 signaling
- 5-LO metabolism is required for MyD88-dependent NFkB activity in macrophages
- 5-LO and LTB4 are required for basal MyD88 expression in macrophages
- MyD88 expression is controlled by STAT-1 and SOCS1
- SOCS1 siRNA restores MyD88 expression and LPS responsiveness in 5-LO -/- MΦs
- PGE2 actions are context-dependent
- PGE2 synthesis and signaling
- Opposing actions of PGE2 vs. LTB4
- Eicosanoid imbalance in states of immunosuppression
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Talk Citation
Peters-Golden, M. (2014, March 5). Influence of eicosanoid lipid mediators on macrophage innate immune functions [Video file]. In The Biomedical & Life Sciences Collection, Henry Stewart Talks. Retrieved December 7, 2024, from https://doi.org/10.69645/SFWF5677.Export Citation (RIS)
Publication History
Financial Disclosures
- Prof. Marc Peters-Golden has not informed HSTalks of any commercial/financial relationship that it is appropriate to disclose.
Influence of eicosanoid lipid mediators on macrophage innate immune functions
Published on March 5, 2014
60 min
A selection of talks on Cell Biology
Transcript
Please wait while the transcript is being prepared...
0:00
This is Marc Peters-Golden
from the University of Michigan.
And I'm going to speak to you about
the influence of Eicosanoid Lipid
Mediators on macrophage
innate immune functions.
0:12
When we think about paradigms
to explain innate immunity,
the dominant paradigm sitting
at the center of the universe
is what I've termed
the land of cytokines.
A recent PubMed search on
cytokines and infection
yielded more than 66,000 references.
By contrast, out in the
corner of the universe
sits a much smaller
planet which I've
termed the land of lipid mediators.
In a recent PubMed search of
lipid mediators and infection
yielded just about 1,600 references.
So as you can see, lipid
mediators are much less well
studied in host defense
than our cytokines.
0:55
Let's look more closely at
the land of lipid mediators.
One particular family
of lipid mediators
that is going to be our
focus today are eicosanoids.
Eicosa is Greek for 20.
The term eicosanoids is used
to refer to an entire family
of oxygenated metabolites
of the 20 carbon parent
fatty acid, arachidonic acid.
The best known eicosanoids are
prostaglandins and leukotrienes.
These are lipid mediators which
are important participants
in many physiologic processes as
well as pathophysiologic processes,
such as inflammation,
fever, and pain.
Also, eicosanoids are
targets for the actions
of nonsteroidal anti-inflammatory
drugs, leukotriene modifiers that
are used in the treatment of
asthma, and omega 3 fatty acids.
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