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GAS6 in systemic inflammatory diseases: with and without infection
Begoña Hurtado1, Pablo García de Frutos
1Department of Cell Death and Proliferation, Institute for Biomedical Research of Barcelona (IIBB-CSIC-IDIBAPS), C/Roselló 161-6°, 08036 Barcelona, Spain. bego.hurtado@iibb.csic.es
Critical Care (London, England)
|November 12, 2010
Summary
Systemic inflammation, not infection, elevates Gas6 levels in sepsis patients. This suggests Gas6 is a key regulator of the innate immune response during inflammation.
Area of Science:
- Biochemistry
- Immunology
- Critical Care Medicine
Background:
- Vitamin K-dependent proteins play roles beyond blood coagulation.
- Investigated levels of GAS6 and its soluble receptor Axl in sepsis patients.
- Sepsis involves systemic inflammation, often triggered by infection.
Discussion:
- GAS6 levels are elevated in septicemia, but also in non-infectious inflammatory conditions.
- This indicates inflammation, rather than infection, drives GAS6 synthesis.
- The soluble Axl receptor showed less induction than GAS6.
Key Insights:
- GAS6 and Axl form an inactive complex in plasma.
- Elevated GAS6 during inflammation suggests a functional form may be synthesized.
- GAS6 is proposed as a regulator of the innate immune response.
Outlook:
- GAS6 synthesis is likely a regulatory mechanism in systemic inflammation.
- Further research is needed to understand the GAS6-Axl system.
- Genetic screening tools are available for future studies.
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