Hypobaric hypoxia in 3000 m altitude leads to a significant decrease in circulating plasmacytoid dendritic cells in humans.

Introduction: Hypoxia is known to affect the immune system. It leads to an increase in pro-inflammatory cytokines such as interleukin-6 and influences the number of different inflammatory cells. This study investigates the effect of hypoxia on the number of different subsets of circulating human dendritic cells (DCs) as professional antigen-presenting cells.

Impact of Systemic Normobaric Short-Term Hypoxia on Pro-Inflammatory and Anti-Inflammatory Cytokines in Healthy Volunteers.

Background: Hypoxia has been shown to induce a microvascular inflammation, affect the cell count of different types of immune cells, and influence cytokine production in blood. In the present study, serum levels of different cytokines were investigated to achieve insights into the effect of hypoxia on the balance of inflammation and anti-inflammation.

Methods: Pro- (IL-8) and anti-inflammatory (IL-10) cytokines were measured in an experiment exposing 12 healthy subjects (35 ± 9 yr, 176 ± 7 cm, 73 ± 16 kg, BMI 23 ± 4 kg/m2) to systemic, normobaric hypoxia in a hypoxic chamber.

Conserved gene regulatory function of the carboxy-terminal domain of dictyostelid C-module-binding factor.

C-module-binding factor A (CbfA) is a jumonji-type transcription regulator that is important for maintaining the expression and mobility of the retrotransposable element TRE5-A in the social amoeba Dictyostelium discoideum. CbfA-deficient cells have lost TRE5-A retrotransposition, are impaired in the ability to feed on bacteria, and do not enter multicellular development because of a block in cell aggregation. In this study, we performed Illumina RNA-seq of growing CbfA mutant cells to obtain a list of CbfA-regulated genes.