Double-walled carbon nanotubes trigger IL-1β release in human monocytes through Nlrp3 inflammasome activation.

Because of their outstanding physical properties, carbon nanotubes (CNTs) are promising new materials in the field of nanotechnology. It is therefore imperative to assess their adverse effects on human health. Monocytes/macrophages that recognize and eliminate the inert particles constitute the main target of CNTs.

PPARγ controls Dectin-1 expression required for host antifungal defense against Candida albicans.

We recently showed that IL-13 or peroxisome proliferator activated receptor gamma (PPARgamma) ligands attenuate Candida albicans colonization of the gastrointestinal tract. Here, using a macrophage-specific Dectin-1 deficient mice model, we demonstrate that Dectin-1 is essential to control fungal gastrointestinal infection by PPARgamma ligands. We also show that the phagocytosis of yeast and the release of reactive oxygen intermediates in response to Candida albicans challenge are impaired in macrophages from Dectin-1 deficient mice treated with PPARgamma ligands or IL-13.

Immunohistochemical distribution of activated nuclear factor kappaB and peroxisome proliferator-activated receptors in carbon tetrachloride-induced chronic liver injury in rats.

We investigated the immunohistochemical distribution of active NF-kappaB p65 and peroxisome proliferator-activated receptor (PPAR) subtypes alpha and gamma in the different phases of liver steatonecrosis and cirrhosis induced in rats after 3 and 9 weeks of carbon tetrachloride (CCl4) intoxication. CCl4 treatment can induce changes in the expression of NF-kappaB and PPARs. Immunohistochemical analysis of liver tissue sections from rats with steatonecrosis or cirrhosis demonstrated a significant increase in the number of NF-kappaB-positive and TNF-alpha-positive hepatocytes and Kupffer cells.