A Bifidobacterium probiotic strain and its soluble factors alleviate chloride secretion by human intestinal epithelial cells.

Previous studies indicate that certain probiotic bacterial strains or their soluble products can alleviate proinflammatory cytokine secretion by intestinal epithelial cells (IEC), but their impact on epithelial chloride (Cl(-)) secretion remains elusive. To further decipher the mechanisms of the cross-talk between bacteria/soluble factors and epithelial cells, we analyzed the capacity of the probiotic strain Bifidobacterium breve C50 (Bb C50), its conditioned medium, and other commensal Gram (+) bacteria to modulate epithelial Cl(-) secretion. The effect of Bb C50 on carbachol- (CCh) or forskolin (Fsk)-induced Cl(-) secretion was measured in an IEC line in Ussing chambers.

Regulation of ROMK (Kir 1.1) channel expression in kidney thick ascending limb by hypertonicity: role of TonEBP and MAPK pathways.

The present study assessed the mechanisms by which hypertonicity caused by NaCl enhances the renal outer medullary potassium channel (ROMK) mRNA abundance in rat kidney medullary thick ascending limb (MTAL) and in cultured mouse TAL cells. Using the run-off technique, we observed that the ROMK gene transcription rate in nuclei isolated from MTAL fragments was enhanced approximately 40% by a high NaCl medium. In MTAL fragments, hypertonicity (450 mosm) caused by NaCl, not by mannitol or urea, enhanced both ROMK mRNA abundance and tonicity-responsive enhancer binding protein (TonEBP) total abundance and nuclear localization.

Exploring the role of galectin 3 in kidney function: a genetic approach.

Galectin 3 belongs to a family of glycoconjugate-binding proteins that participate in cellular homeostasis by modulating cell growth, adhesion, and signaling. We studied adult galectin 3 null mutant (Gal 3-/-) and wild-type (WT) mice to gain insights into the role of galectin 3 in the kidney. By immunofluorescence, galectin 3 was found in collecting duct (CD) principal and intercalated cells in some regions of the kidney, as well as in the thick ascending limbs at lower levels.

Renal handling of NH3/NH4+: recent concepts.

To be appropriately excreted in urine, NH4+, the major component of urinary acid excretion, must be synthesized by proximal tubular cells, secreted into the proximal tubular fluid, reabsorbed by the medullary thick ascending limb (MTAL) to be accumulated in the medullary interstitium, and finally secreted in medullary collecting ducts. Several targets have been identified to account at the gene expression level for the adaptation of renal NH4+ synthesis and transport in response to a chronic acid load. These targets are the key enzymes of ammoniagenesis (mitochondrial glutaminase and glutamate dehydrogenase) and gluconeogenesis (phosphoenolpyruvate carboxykinase) and the Na+/H+(NH4+) exchanger NHE3 in the proximal tubule, the apical Na+-K+(NH4+)-2Cl- cotransporter of the MTAL, the basolateral Na+-K+(NH4+)-2Cl- cotransporter, and likely the epithelial Rh B and C glycoproteins in the collecting ducts.

Increased activity of the diastrophic dysplasia sulfate transporter in otosclerosis and its inhibition by sodium fluoride.

Hypothesis: This study investigates the function of the diastrophic dysplasia sulfate transporter (DTDST) in otosclerotic bone and the effect on it of sodium fluoride (NaF).

Background: Otosclerosis is a localized bone dystrophy with increased bone turnover. DTDST is implicated in the regulation of the bone turnover.

Acid pH increases the stability of BSC1/NKCC2 mRNA in the medullary thick ascending limb.

Chronic metabolic acidosis enhances the ability of the medullary thick ascending limb (MTAL) to absorb NH(4)(+) at least in part by stimulating the mRNA and protein expression of BSC1/NKCC2, the MTAL apical Na(+)-K(+)(NH(4)(+))-2Cl(-) co-transporter. For assessing the mechanism by which an acid pH enhances the BSC1 mRNA abundance, MTAL were harvested from adrenalectomized rats and incubated in control (pH 7.35) and acid (pH 7.

Regulation by glucocorticoids and osmolality of expression of ROMK (Kir 1.1), the apical K channel of thick ascending limb.

Mechanisms of regulation of ROMK channel mRNA and protein expression in medullary thick ascending limb (MTAL) were assessed in rat MTAL fragments incubated for 7 h. ROMK mRNA was quantified by quantitative RT-PCR and ROMK protein by immunoblotting analysis of crude membranes. Medium hyperosmolality (450 mosmol/kgH(2)O; NaCl plus urea added to isoosmotic medium) increased ROMK mRNA (P < 0.

Renal handling of NH4+ in relation to the control of acid-base balance by the kidney.

The major component of urinary acid excretion is NH4+. To be appropriately excreted in urine, NH4+ must be synthesized by proximal tubular cells, secreted into the proximal tubular fluid, reabsorbed by the medullary thick ascending limb (MTAL) to be accumulated in the medullary interstitium, and finally secreted in medullary collecting ducts. Each step of this renal pathway is highly regulated and, in addition to acute events mediated by peptide hormones such as parathyroid hormone, the control of gene expression explains how the renal handling of NH4+ fully adapts to chronic changes in the acid-base status.