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Citrate modulates lipopolysaccharide-induced monocyte inflammatory responses.

M J Ashbrook¹, K L McDonough², J J Pituch¹

¹Divisions of Pediatric Nephrology, University of Michigan, Ann Arbor, MI, USA.

Clinical and Experimental Immunology

|January 27, 2015

Summary

Citrate, an anticoagulant, can both inhibit and enhance inflammatory responses by affecting gene transactivation. Its effects depend on calcium levels and metabolism by ATP-citrate lyase, influencing immune function.

Keywords:

citrate epigenetics inflammation monocytes

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Area of Science:

Biochemistry
Immunology
Cell Biology

Background:

Citrate is a key metabolic intermediate and anticoagulant.
ATP-citrate lyase is crucial for inflammation, but exogenous citrate's role is unclear.
Citrate's dual role as metabolite and calcium chelator suggests modulation of inflammatory signaling.

Purpose of the Study:

To investigate how citrate affects monocyte inflammatory responses to lipopolysaccharide (LPS).
To determine the impact of clinically relevant citrate levels on pro-inflammatory cytokine production.
To elucidate the mechanisms underlying citrate's modulation of inflammatory signaling cascades.

Main Methods:

Utilized THP-1 human acute monocytic leukemia cell line.
Assessed LPS-induced tumor necrosis factor-alpha (TNF-α) and interleukin-8 (IL-8) transcript levels.
Employed IL-8-luciferase reporter assays and histone acetylation analysis.
Investigated the role of ATP-citrate lyase using tricarballylic acid.

Main Results:

Citrate inhibited TNF-α and IL-8 in normal calcium conditions (0.4 mM).
Citrate augmented TNF-α and IL-8 in high calcium conditions (1.4 mM), independent of chelation.
Augmentation was linked to ATP-citrate lyase metabolism and involved transcriptional regulation and histone acetylation.
Citrate demonstrated a dual role, inhibiting or augmenting cytokine production.

Conclusions:

Citrate modulates inflammatory gene transactivation, leading to both inhibition and augmentation of pro-inflammatory cytokine production.
The observed effects are dependent on calcium concentration and citrate metabolism via ATP-citrate lyase.
Citrate's anticoagulant use may influence immune function through complex interactions with inflammatory pathways.