Adaptive cellular mechanisms in response to glutamine-starvation.

Glutamine (Gln) utilising cells suffer from Gln-starvation during critical illness when plasma Gln levels are decreased. This study investigates whether such cells activate adaptive mechanisms. Monocytic U937 cells were cultured at 0.

Reduced stress tolerance of glutamine-deprived human monocytic cells is associated with selective down-regulation of Hsp70 by decreased mRNA stability.

In critically ill patients, clinicians observe a reverse correlation of survival and a decreased plasma concentration of the most abundant free amino acid, glutamine (Gln). However, in this context, the role of Gln remains largely elusive. Gln is used as an energy substrate by monocytes.

Increased susceptibility of glutamine-depleted monocytes to fever-range hyperthermia: the role of 70-kDa heat shock protein.

Objective: This study investigates the effect of fever-range hyperthermia on Gln-starving monocytes and the role of the 70-kDa heat shock protein Hsp70.

Summary Background Data: Fever is a protective acute-phase response to infection. However, in critically ill patients, the harmful effects of fever seem to be predominant.

Glutamine starvation of monocytes inhibits the ubiquitin-proteasome proteolytic pathway.

Peripheral blood monocytes utilize free glutamine (Gln) in addition to glucose as an important energy substrate. Although this demand increases upon activation, monocytes are commonly confronted with decreased plasma Gln during critical illness and thus suffer from Gln-starvation. Here we investigate the influence of Gln-starvation on protein stability and its effects on the monocyte proteome.

Glutamine depletion impairs cellular stress response in human leucocytes.

During sepsis and major trauma the blood glutamine (Gln) level is reduced. The administration of Gln can improve the outcome of these patients. However, the mechanism of this beneficial effect of Gln is poorly understood.

Glutamine deficiency renders human monocytic cells more susceptible to specific apoptosis triggers.

Background: After major trauma and sepsis, patients frequently show a decreased blood glutamine (Gln) level. Gln deprivation has been shown to induce apoptosis in intestinal epithelial cells. In this study, we investigated whether the Gln level also affects the susceptibility of monocytic cells to apoptosis.