Insulin modulates cytokine release and selectin expression in the early phase of allergic airway inflammation in diabetic rats

<p>Abstract</p> <p>Background</p> <p>Clinical and experimental data suggest that the inflammatory response is impaired in diabetics and can be modulated by insulin. The present study was undertaken to investigate the role of insulin on the early phase of allergic airway inflammation.</p> <p>Methods</p> <p>Diabetic male Wistar rats (alloxan, 42 mg/Kg, i.v., 10 days) and controls were sensitized by s.c. injection of ovalbumin (OA) in aluminium hydroxide 14 days before OA (1 mg/0.4 mL) or saline intratracheal challenge. The following analyses were performed 6 hours thereafter: a) quantification of interleukin (IL)-1β, tumor necrosis factor (TNF)-α and cytokine-induced neutrophil chemoattractant (CINC)-1 in the bronchoalveolar lavage fluid (BALF) by Enzyme-Linked Immunosorbent Assay, b) expression of E- and P- selectins on lung vessels by immunohistochemistry, and c) inflammatory cell infiltration into the airways and lung parenchyma. NPH insulin (4 IU, s.c.) was given i.v. 2 hours before antigen challenge.</p> <p>Results</p> <p>Diabetic rats exhibited significant reduction in the BALF concentrations of IL-1β (30%) and TNF-α (45%), and in the lung expression of P-selectin (30%) compared to non-diabetic animals. This was accompanied by reduced number of neutrophils into the airways and around bronchi and blood vessels. There were no differences in the CINC-1 levels in BALF, and E-selectin expression. Treatment of diabetic rats with NPH insulin, 2 hours before antigen challenge, restored the reduced levels of IL-1β, TNF-α and P-selectin, and neutrophil migration.</p> <p>Conclusion</p> <p>Data presented suggest that insulin modulates the production/release of TNF-α and IL-1β, the expression of P- and E-selectin, and the associated neutrophil migration into the lungs during the early phase of the allergic inflammatory reaction.</p

THE BIPOLAR MOLECULAR OUTFLOW OF V645-CYGNI

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A flare in the millimetre to IR spectrum of 3C273

Over the past two years some of us (E.I.R., P.A.R.A., W.K.G., M.G.S., and I.G.N.) have been monitoring the millimetre and submillimetre spectrum of 3C273 (ref. 1). We have presented elsewhere a quiescent millimetre-to-far-IR spectrum2 with an index α = −0.7 (Sv α vα) connecting smoothly to the radio and mid-IR. Our discovery of a concurrent flare in the IR-to-near-millimetre spectrum of 3C273 implies that the emission over this range of frequency originates in the same region of the source. The flare was seen to propagate to longer wavelengths whilst decaying at shorter wavelengths. The time scale of the flare is suggestive of an event within the central 0.1 pc of the source. Millimetre wavelength variability of 3C273 has been reported3,4 but with very little temporal overlap with our data. Rieke and Lebofsky16 have reviewed the 2.2 and 10 µm variability