ABSTRACT
The intestinal absorption of phosphate (Pi) takes place transcellularly through the active NaPi-cotransporters type IIb (NaPiIIb) and III (PiT1 and PiT2) and paracellularly by diffusion through tight junction (TJ) proteins. The localisation along the intestines and the regulation of Pi absorption differ between species and are not fully understood. It is known that 1,25-dihydroxy-vitamin D3 (1,25-(OH)2D3) and phosphorus (P) depletion modulate intestinal Pi absorption in vertebrates in different ways. In addition to the apical uptake into the enterocytes, there are uncertainties regarding the basolateral excretion of Pi. Functional ex vivo experiments in Ussing chambers and molecular studies of small intestinal epithelia were carried out on P-deficient goats in order to elucidate the transepithelial Pi route in the intestine as well as the underlying mechanisms of its regulation and the proteins, which may be involved. The dietary P reduction had no effect on the duodenal and ileal Pi transport rate in growing goats. The ileal PiT1 and PiT2 mRNA expressions increased significantly, while the ileal PiT1 protein expression, the mid jejunal claudin-2 mRNA expression and the serum 1,25-(OH)2D3 levels were significantly reduced. These results advance the state of knowledge concerning the complex mechanisms of the Pi homeostasis in vertebrates.
Subject(s)
Homeostasis , Intestinal Absorption , Intestinal Elimination , Phosphorus, Dietary/metabolism , Phosphorus/deficiency , Animals , Calcitriol/blood , Duodenum/metabolism , Goats , Ileum/metabolism , Intestinal Mucosa/metabolism , Male , Sodium-Phosphate Cotransporter Proteins/genetics , Sodium-Phosphate Cotransporter Proteins/metabolismABSTRACT
In January 2016, a large-scale outbreak of acute gastroenteritis was reported among French armed forces deployed in the Central African Republic. Challenging investigations, conducted from France, made it possible to identify a norovirus genogroup II in both stool and food samples, confirming a norovirus foodborne disease outbreak. Infected food handler management is discussed.
Subject(s)
Caliciviridae Infections/virology , Foodborne Diseases/virology , Gastroenteritis/virology , Norovirus/isolation & purification , Adult , Caliciviridae Infections/epidemiology , Central African Republic/epidemiology , Disease Outbreaks , Feces/virology , Female , Foodborne Diseases/epidemiology , Gastroenteritis/epidemiology , Genotype , Humans , Male , Military Facilities , Military Personnel/statistics & numerical data , Norovirus/genetics , RNA, Viral/genetics , Workforce , Young AdultABSTRACT
Bluetongue virus (BTV) is the cause of bluetongue (BT), an emerging, arthropod-transmitted disease of ungulates. The cellular tropism of BTV in ruminants includes macrophages, dendritic cells and endothelial cells (ECs), and fulminant infection is characterized by lesions consistent with those of so-called viral hemorrhagic fevers. Specifically, BT is characterized by vascular injury with hemorrhage, tissue infarction and widespread edema. To further investigate the pathogenesis of vascular injury in BT, we evaluated the responses of cultured bovine pulmonary artery EC (bPAEC) and monocyte-derived macrophages (bMDM) to BTV infection by measuring transcript levels of genes encoding molecules important in mediating EC activation and/or endothelial barrier dysregulation. The data confirm that BTV infection of bPAEC resulted in increased transcription of genes encoding chemokine ligand 2 (CCL2) and E-selectin, and BTV infection of bMDM resulted in increased transcription of genes encoding TNF-alpha, IL-1beta, IL-8, and inducible nitric oxide synthase (iNOS). The data from these in vitro studies provide further evidence that cytokines and other vasoactive substances produced in macrophages potentially contribute to vascular injury in BTV-infected ruminants, along with direct effects of the virus itself on ECs.
