tetano
Editor, Senior Moderator
J Interferon Cytokine Res
. 2022 Jun 8.
doi: 10.1089/jir.2022.0028. Online ahead of print.
Emergency Hematopoiesis in the Pathobiology of COVID-19: The Dark Side of an Early Innate Protective Mechanism
Juan Carlos Balandrán[SUP] 1 2 [/SUP], Gabriela Zamora-Herrera[SUP] 3 [/SUP], Rubí Romo-Rodríguez[SUP] 3 [/SUP], Rosana Pelayo[SUP] 3 [/SUP]
Affiliations
Abstract
The recognition of pathogens to which we are constantly exposed induces the immediate replenishment of innate immune cells from the most primitive stages of their development through emergency hematopoiesis, a central mechanism contributing to early infection control. However, as with other protective mechanisms, its functional success is at risk when the excess of inducing signals accelerates immunological catastrophes. Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection exhibits a clinical spectrum that ranges from completely asymptomatic states to fatal outcomes, with the amplification of inflammatory components being the critical point that determine the progress, complication, and severity of the disease. This review focuses on the most relevant findings that entail emergency hematopoiesis to SARS-CoV-2 infection response and revolutionize our understanding of the mechanisms governing the clinical prognosis of COVID-19. Of special interest are the metabolic or hyperinflammatory conditions in aging that exacerbate the phenomenon and favor the uncontrolled emergency myelopoiesis leading to the evolution of severe disease.
Keywords: COVID-19; TLR signaling; clonal hematopoiesis; emergency hematopoiesis; hematopoietic stem and progenitor cells; inflammation.
. 2022 Jun 8.
doi: 10.1089/jir.2022.0028. Online ahead of print.
Emergency Hematopoiesis in the Pathobiology of COVID-19: The Dark Side of an Early Innate Protective Mechanism
Juan Carlos Balandrán[SUP] 1 2 [/SUP], Gabriela Zamora-Herrera[SUP] 3 [/SUP], Rubí Romo-Rodríguez[SUP] 3 [/SUP], Rosana Pelayo[SUP] 3 [/SUP]
Affiliations
- PMID: 35675647
- DOI: 10.1089/jir.2022.0028
Abstract
The recognition of pathogens to which we are constantly exposed induces the immediate replenishment of innate immune cells from the most primitive stages of their development through emergency hematopoiesis, a central mechanism contributing to early infection control. However, as with other protective mechanisms, its functional success is at risk when the excess of inducing signals accelerates immunological catastrophes. Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection exhibits a clinical spectrum that ranges from completely asymptomatic states to fatal outcomes, with the amplification of inflammatory components being the critical point that determine the progress, complication, and severity of the disease. This review focuses on the most relevant findings that entail emergency hematopoiesis to SARS-CoV-2 infection response and revolutionize our understanding of the mechanisms governing the clinical prognosis of COVID-19. Of special interest are the metabolic or hyperinflammatory conditions in aging that exacerbate the phenomenon and favor the uncontrolled emergency myelopoiesis leading to the evolution of severe disease.
Keywords: COVID-19; TLR signaling; clonal hematopoiesis; emergency hematopoiesis; hematopoietic stem and progenitor cells; inflammation.