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Mob-1 expression in IL-2-induced ARDS: regulation by TNF-alpha
L F Neville1, F Abdullah, P M McDonnell
1Department of Surgery, Jefferson Medical College, Philadelphia 19107, USA.
The American Journal of Physiology
|December 1, 1995
Summary
Researchers identified a novel gene, mob-1, highly induced in an animal model of acute respiratory distress syndrome (ARDS). This chemokine may play a role in the development of lung injury, offering new insights into ARDS pathogenesis.
Area of Science:
- Pulmonary Medicine
- Molecular Biology
- Inflammation Research
Background:
- Adult respiratory distress syndrome (ARDS) involves microvascular lung injury.
- Interleukin-2 (IL-2) infusion can elicit ARDS-like lung injury in animal models.
- Pro-inflammatory mediators are transcriptionally upregulated in IL-2-induced ARDS.
Purpose of the Study:
- To identify novel genes involved in IL-2-induced ARDS-like lung injury.
- To investigate the role of newly discovered genes in the pathogenesis of ARDS.
Main Methods:
- Establishment of an ARDS animal model using human interleukin-2 (IL-2) infusion.
- Differential display technique applied to total lung RNA from IL-2-challenged rats.
- Sequence homology analysis and Northern blot to characterize gene expression.
Main Results:
- A novel gene fragment, termed B1, was strongly induced in IL-2-treated rat lungs.
- B1 cDNA showed 99.14% homology to the 3'-UTR of mob-1, a C-X-C chemokine.
- Pulmonary mob-1 mRNA was upregulated before lung injury onset and suppressed by TNF-alpha inhibition.
Conclusions:
- Lung mob-1 is a novel, highly inducible gene in a clinically relevant ARDS model.
- As a chemokine, mob-1 may contribute to the development of ARDS.
- These findings provide potential targets for ARDS therapeutic strategies.