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Expert Opin Biol Ther. 2018 Jul;18(sup1):193-197. doi: 10.1080/14712598.2018.1448381. Epub 2018 Mar 6.

Thymosin beta 4 regulation of actin in sepsis.

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a Department of Emergency Medicine , Yale-New Haven Hospital , New Haven , CT , USA.
b Department of Emergency Medicine and Critical Care , Wayne State University , Detroit , MI , USA.
c Department of Emergency Medicine and Critical Care , Henry Ford Hospital , Detroit , MI , USA.
d Department of Emergency Medicine , Massachusetts General Hospital , Boston , MA , USA.
e Department of Internal Medicine, Yale-New Haven Hospital , The Anlyan Center , New Haven , CT , USA.
f Department of Emergency Medicine , Henry Ford Hospital , Detroit , MI , USA.


Sepsis is the dysregulated host response to an infection resulting in life-threatening organ damage. Thymosin Beta 4 is an actin binding protein that inhibits the polymerization of G-actin into F-actin and improves mortality when administered intravenously to septic rats. Thymosin Beta 4 decreases inflammatory mediators, lowers reactive oxygen species, up-regulates anti-oxidative enzymes, anti-inflammatory genes, and anti-apoptotic enzymes making it an interesting protein to study in sepsis. Areas covered: The authors summarize the current knowledge of actin and Thymosin Beta 4 as it relates to sepsis via a comprehensive literature search. Expert opinion: Sepsis results in measurable levels of F-actin in the circulation as well as a decreased concentration of Thymosin Beta 4. It is speculated that F-actinemia contributes to microcirculatory perturbations present in patients with sepsis by disturbing laminar flow. Given that Thymosin Beta 4 inhibits the polymerization of F-actin, it is possible that Thymosin Beta 4 decreases mortality in sepsis via the regulation of actin as well as its other anti-inflammatory properties and should be further pursued as a clinical trial in humans with sepsis.


Actin; microcirculatory dysfunction; sepsis; thymosin beta 4

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