Thymosin beta 4 regulation of actin in sepsis

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

Abstract

Introduction: 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.

Keywords: Actin; microcirculatory dysfunction; sepsis; thymosin beta 4.

Publication types

  • Review

MeSH terms

  • Actins / metabolism*
  • Animals
  • Humans
  • Microcirculation / drug effects
  • Oxidation-Reduction / drug effects
  • Rats
  • Reactive Oxygen Species / metabolism
  • Sepsis / drug therapy
  • Sepsis / metabolism*
  • Sepsis / pathology
  • Thymosin / pharmacology
  • Thymosin / physiology*
  • Thymosin / therapeutic use

Substances

  • Actins
  • Reactive Oxygen Species
  • thymosin beta(4)
  • Thymosin