Thymosin beta 4 regulation of actin in sepsis. (31st May 2018)

• Record Type: Journal Article
• Authors: Belsky, Justin B.; Rivers, Emanuel P.; Filbin, Michael R.; Lee, Patty J.; Morris, Daniel C.
• Is Part Of: Expert opinion on biological therapy. Volume 18(2018)Supplement 1
• Page Start: 193
• Page End: 197
• Publication Date: 2018-05-31
• Subjects: Actin -- microcirculatory dysfunction -- sepsis -- thymosin beta 4; Gene therapy -- Periodicals; Protein drugs -- Periodicals; Peptide drugs -- Periodicals; Immunotherapy -- Periodicals; Drug delivery systems -- Periodicals; 615.5
• DOI: 10.1080/14712598.2018.1448381
• Languages: English
• ISSNs: 1471-2598

Abstract

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.