Hypoxia aggravates lipopolysaccharide-induced lung injury

Overexpression of CREMα in T cells aggravates lipopolysaccharide-induced acute lung injury.

Transcription factor cAMP response element modulator (CREM)α contributes to various cellular and molecular abnormalities in T cells, including increased IL-17 and decreased IL-2 expression. For development of acute lung injury (ALI), the invasion and regulation of immune cells are highly important, but the role of T cells remains unclear. In this study, we show that CREMα is upregulated in LPS-...

Overexpression of CREMa in T Cells Aggravates Lipopolysaccharide-Induced Acute Lung Injury

Upregulation of hypoxia-induced mitogenic factor in bacterial lipopolysaccharide-induced acute lung injury.

Hypoxia-induced mitogenic factor (HIMF), also known as FIZZ1 (found in inflammatory zone), plays important roles in lung inflammation. We found that intraperitoneal injection of lipopolysaccharide (LPS) induced intensive HIMF production exclusively in mouse lung, but not in the heart, liver, spleen or kidney. This HIMF production, at least partly, contributes to LPS-induced vascular cell adhesi...

Zinc-deficient diet aggravates ventilation-induced lung injury in rats

We investigated the effects of zinc deficiency on acute lung injury (ALI) induced by mechanical ventilation. Male Sprague-Dawley rats were fed with a zinc-deficient or zinc-proficient diet for 4 weeks, and then received mechanical ventilation at normal frequency and pressure for 30 min. Total protein, cell count, the number of polymorphonuclear neutrophil (PMN) in the bronchoalveolar lavage (BA...

Time-dependent changes of autophagy and apoptosis in lipopolysaccharide-induced rat acute lung injury

Objective(s): Abnormal lung cell death including autophagy and apoptosis is the central feature in acute lung injury (ALI). To identify the cellular mechanisms and the chronology by which different types of lung cell death are activated during lipopolysaccharide (LPS)-induced ALI, we decided to evaluate autophagy (by LC3-II and autophagosome) and apoptosis (by caspase-3) at different time point...