79 research outputs found
Susceptibility to ozone-induced airway inflammation is associated with decreased levels of surfactant protein D
BACKGROUND: Ozone (O(3)), a common air pollutant, induces exacerbation of asthma and chronic obstructive pulmonary disease. Pulmonary surfactant protein (SP)-D modulates immune and inflammatory responses in the lung. We have shown previously that SP-D plays a protective role in a mouse model of allergic airway inflammation. Here we studied the role and regulation of SP-D in O(3)-induced inflammatory changes in the lung. METHODS: To evaluate the effects of O(3 )exposure in mouse strains with genetically different expression levels of SP-D we exposed Balb/c, C57BL/6 and SP-D knockout mice to O(3 )or air. BAL cellular and cytokine content and SP-D levels were evaluated and compared between the different strains. The kinetics of SP-D production and inflammatory parameters were studied at 0, 2, 6, 12, 24, 48, and 72 hrs after O(3 )exposure. The effect of IL-6, an O(3)-inducible cytokine, on the expression of SP-D was investigated in vitro using a primary alveolar type II cell culture. RESULTS: Ozone-exposed Balb/c mice demonstrated significantly enhanced acute inflammatory changes including recruitment of inflammatory cells and release of KC and IL-12p70 when compared with age- and sex-matched C57BL/6 mice. On the other hand, C57BL/6 mice had significantly higher levels of SP-D and released more IL-10 and IL-6. Increase in SP-D production coincided with the resolution of inflammatory changes. Mice deficient in SP-D had significantly higher numbers of inflammatory cells when compared to controls supporting the notion that SP-D has an anti-inflammatory function in our model of O(3 )exposure. IL-6, which was highly up-regulated in O(3 )exposed mice, was capable of inducing the expression of SP-D in vitro in a dose dependent manner. CONCLUSION: Our data suggest that IL-6 contributes to the up-regulation of SP-D after acute O(3 )exposure and elevation of SP-D in the lung is associated with the resolution of inflammation. Absence or low levels of SP-D predispose to enhanced inflammatory changes following acute oxidative stress
Metalloenzyme-Mimicking Supramolecular Catalyst for Highly Active and Selective Intramolecular Alkyne Carboxylation
Ozone toxicity in the rat. I. Effect of changes in ambient temperature on extrapulmonary physiological parameters
Elucidating the Mechanism of the Halide-Induced Ligand Rearrangement Reaction
The formation of heteroligated Rh<sup>I</sup> complexes
containing two different hemilabile phosphinoalkyl ligands, (κ<sup>2</sup>-Ph<sub>2</sub>PCH<sub>2</sub>CH<sub>2</sub>S-Aryl)Â(κ<sup>1</sup>-Ph<sub>2</sub>PCH<sub>2</sub>CH<sub>2</sub>O-C<sub>6</sub>H<sub>5</sub>)ÂRhCl, through a halide-induced ligand rearrangement
(HILR) reaction has been studied mechanistically. The half-life of
this rearrangement reaction depends heavily on the Rh<sup>I</sup> precursor
used and the chelating ability of the phosphinoalkyl thioether (PS)
ligand, while the chelating ability of the phosphinoalkyl ether (PO)
ligand has less of an effect. An intermediate complex which contains
two PO ligands, (nbd)Â(κ<sup>1</sup>-Ph<sub>2</sub>PCH<sub>2</sub>CH<sub>2</sub>O-C<sub>6</sub>H<sub>5</sub>)<sub>2</sub>RhCl (nbd
= norbornadiene), converts to (nbd)Â(κ<sup>1</sup>-Ph<sub>2</sub>PCH<sub>2</sub>CH<sub>2</sub>O-C<sub>6</sub>H<sub>5</sub>)ÂRhCl resulting
in a free PO ligand. The free PO ligand can then react with a homoligated
PS complex [(κ<sup>2</sup>-Ph<sub>2</sub>PCH<sub>2</sub>CH<sub>2</sub>S-Aryl)<sub>2</sub>Rh]<sup><b>+</b></sup>Cl<sup>–</sup> producing the heteroligated product. The PS ligand generated during
the reaction pathway can be trapped by the monoligated PO complex
(nbd)Â(κ<sup>1</sup>-Ph<sub>2</sub>PCH<sub>2</sub>CH<sub>2</sub>O-C<sub>6</sub>H<sub>5</sub>)ÂRhCl, leading to the formation of the
same heteroligated product. In this study, some of the key intermediates
and reaction steps underlying the HILR reaction have been identified
by variable temperature <sup>31</sup>PÂ{<sup>1</sup>H} NMR spectroscopy
and in two cases by single-crystal X-ray diffraction studies. Significantly,
this work provides mechanistic insight into the HILR process, which
is a key reaction used to prepare a large class of highly sophisticated
three-dimensional metallosupramolecular architectures and allosteric
catalysts
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