Inflammation-induced Generation of Splenic Erythroblast-like Ter-Cells Inhibits the Progression of Acute Lung Injury via Artemin.
Summary
The study identifies a splenic erythroblast‑like cell population (Ter‑cells) arising from megakaryocyte‑erythroid progenitors that limits ALI progression through the neurotrophic factor artemin. This work expands ALI biology beyond leukocytes, implicating distal organ, non‑leukocyte responders as protective modulators.
Key Findings
- Identification of splenic erythroblast‑like Ter‑cells derived from megakaryocyte‑erythroid progenitors (Ter‑119+ phenotype).
- Ter‑cells mitigate ALI progression via secretion/action of artemin.
- Highlights a protective non‑leukocyte, distal organ cellular response in inflammatory lung injury.
Clinical Implications
Therapeutic augmentation of artemin signaling or harnessing Ter‑cells could represent novel strategies to prevent or attenuate ALI progression, pending translational validation.
Why It Matters
Reveals a previously unappreciated spleen–lung axis mediated by erythroblast‑like cells and artemin, opening avenues for cell‑ or factor‑based therapies in ALI/ARDS.
Limitations
- Preclinical evidence with incomplete mechanistic details in abstract; species translation unknown
- Extent of human relevance and therapeutic window require validation
Future Directions
Define artemin receptor pathways in lung targets, evaluate Ter‑cell/artermin augmentation in diverse ALI etiologies, and explore human correlates.
Study Information
- Study Type
- Case-control
- Research Domain
- Pathophysiology
- Evidence Level
- IV - Preclinical mechanistic study with comparative in vivo models and molecular analyses
- Study Design
- OTHER