TY - JOUR
T1 - Abundance of ACVR1B transcript is elevated during septic conditions
T2 - Perspectives obtained from a hands-on reductionist investigation
AU - Preechanukul, Anucha
AU - Yimthin, Thatcha
AU - Tandhavanant, Sarunporn
AU - Brummaier, Tobias
AU - Chomkatekaew, Chalita
AU - Das, Sukanta
AU - Syed Ahamed Kabeer, Basirudeen
AU - Toufiq, Mohammed
AU - Rinchai, Darawan
AU - West, T. Eoin
AU - Chaussabel, Damien
AU - Chantratita, Narisara
AU - Garand, Mathieu
N1 - Publisher Copyright:
Copyright © 2023 Preechanukul, Yimthin, Tandhavanant, Brummaier, Chomkatekaew, Das, Syed Ahamed Kabeer, Toufiq, Rinchai, West, Chaussabel, Chantratita and Garand.
PY - 2023
Y1 - 2023
N2 - Sepsis is a complex heterogeneous condition, and the current lack of effective risk and outcome predictors hinders the improvement of its management. Using a reductionist approach leveraging publicly available transcriptomic data, we describe a knowledge gap for the role of ACVR1B (activin A receptor type 1B) in sepsis. ACVR1B, a member of the transforming growth factor-beta (TGF-beta) superfamily, was selected based on the following: 1) induction upon in vitro exposure of neutrophils from healthy subjects with the serum of septic patients (GSE49755), and 2) absence or minimal overlap between ACVR1B, sepsis, inflammation, or neutrophil in published literature. Moreover, ACVR1B expression is upregulated in septic melioidosis, a widespread cause of fatal sepsis in the tropics. Key biological concepts extracted from a series of PubMed queries established indirect links between ACVR1B and “cancer”, “TGF-beta superfamily”, “cell proliferation”, “inhibitors of activin”, and “apoptosis”. We confirmed our observations by measuring ACVR1B transcript abundance in buffy coat samples obtained from healthy individuals (n=3) exposed to septic plasma (n = 26 melioidosis sepsis cases)ex vivo. Based on our re-investigation of publicly available transcriptomic data and newly generated ex vivo data, we provide perspective on the role of ACVR1B during sepsis. Additional experiments for addressing this knowledge gap are discussed.
AB - Sepsis is a complex heterogeneous condition, and the current lack of effective risk and outcome predictors hinders the improvement of its management. Using a reductionist approach leveraging publicly available transcriptomic data, we describe a knowledge gap for the role of ACVR1B (activin A receptor type 1B) in sepsis. ACVR1B, a member of the transforming growth factor-beta (TGF-beta) superfamily, was selected based on the following: 1) induction upon in vitro exposure of neutrophils from healthy subjects with the serum of septic patients (GSE49755), and 2) absence or minimal overlap between ACVR1B, sepsis, inflammation, or neutrophil in published literature. Moreover, ACVR1B expression is upregulated in septic melioidosis, a widespread cause of fatal sepsis in the tropics. Key biological concepts extracted from a series of PubMed queries established indirect links between ACVR1B and “cancer”, “TGF-beta superfamily”, “cell proliferation”, “inhibitors of activin”, and “apoptosis”. We confirmed our observations by measuring ACVR1B transcript abundance in buffy coat samples obtained from healthy individuals (n=3) exposed to septic plasma (n = 26 melioidosis sepsis cases)ex vivo. Based on our re-investigation of publicly available transcriptomic data and newly generated ex vivo data, we provide perspective on the role of ACVR1B during sepsis. Additional experiments for addressing this knowledge gap are discussed.
KW - activin A
KW - blood transcriptomics
KW - innate immunity
KW - melioidosis
KW - sepsis
UR - http://www.scopus.com/inward/record.url?scp=85151792203&partnerID=8YFLogxK
U2 - 10.3389/fimmu.2023.1072732
DO - 10.3389/fimmu.2023.1072732
M3 - Article
C2 - 37020544
AN - SCOPUS:85151792203
SN - 1664-3224
VL - 14
JO - Frontiers in Immunology
JF - Frontiers in Immunology
M1 - 1072732
ER -