Mob-1 expression in il-2-induced ards: regulation by
tnf[alpha].
Neville, L. F., Abdullah F., McDonnell, P. M., Young, P. R.,
Feuerstein G. Z. Andrabinovici, R.
Department of Surgery, Jefferson Medical College, Philadelphia, PA
19107, Departments of Molecular Immunology and Cardiovascular
Pharmacology, King of Prussia, PA 19406
APStracts 2:0159L, 1995.
We have recently established an animal model of adult respiratory
distress syndrome (ARDS)-like microvascular lung injury elicited by
infusion of human interleukin-2 (IL-2). Based on the pronounced,
transcriptional up-regulation of multiple pro-inflammatory mediators
in IL-2-induced ARDS, Differential Display was applied to search for
potentially novel genes in this paradigm of lung injury. Differential
Display on total lung RNA derived from IL-2-challenged rats presented
a highly reproducible 3' UTR fragment profile in which a band (
nearly equal to 250 bp), termed B1, was strongly induced. B1 cDNA
sequence exhibited 99.14% homology to the 3' UTR of mob-1, a recently
cloned gene belonging to the C-X-C chemokine superfamily.
Furthermore, Northern blot analysis showed that IL-2-induced
pulmonary mob-1 mRNA was expressed at time points prior to the onset
of lung injury and suppressed following TNF[alpha] inhibition. These
data implicate that lung mob-1 is a novel, highly inducible gene in a
clinically-relevant model of ARDS and based on its identification as
a chemokine, could participate in the development of lung injury.
Received 19 May 1995; accepted in final form 24 August 1995.
APS Manuscript Number L158-5.
Article publication pending Am. J. Physiol. (Lung Cell. Mol.
Physiology).
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 23 September 1995.