PubMed · 13960997
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H N HAUGEN. 1963-04-01. [Chronic pyelonephritis].. https://pubmed.ncbi.nlm.nih.gov/13960997/
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Disruption of periciliary fluid homeostasis is the main pathogenesis of otitis media with effusion (OME), one of the most common childhood diseases. Although the underlying molecular mechanisms are unclear, it has been suggested that the altered functions of ion channels and transporters are involved in the fluid collection of middle ear cavity of OME patients. In the present study, we analyzed the effects of a major cytokine interleukin (IL)-1beta, which was known to be involved in the pathogenesis of OME, on Na(+)-K(+)-2Cl(-) cotransporter (NKCC) in human middle ear cells. Intracellular pH (pH(i)) was measured in primary cultures of normal human middle ear epithelial (NHMEE) cells using a double perfusion chamber, which enabled us to analyze the membrane-specific transporter activities. NKCC activities were estimated by the pH(i) reduction due to bumetanide-sensitive intracellular uptake of NH(4) (+). In NHMEE cells, NKCC activities were observed only in the basolateral membrane, and immunoblotting using specific antibodies revealed the expression of NKCC1. Interestingly, IL-1beta treatments augmented the basolateral NKCC activities and increased NKCC1 expression. In addition, IL-1beta treatments stimulated bumetanide-sensitive fluid transport across the NHMEE cell monolayers. Furthermore, an elevated NKCC1 expression was observed in middle ear cells from OME patients when compared to those from control individuals. The above results provide in vitro and in vivo evidence that the inflammatory cytokine IL-1beta upregulates NKCC1 in middle ear epithelial cells, which would be one of the important underlying mechanisms of excess fluid collection in OME patients.
OBJECTIVE: Although hypercalciuria, a well-established adverse effect of vitamin D3, can be a risk factor of renal stone formation, the risk of nephrolithiasis has not been well defined. The consumption of a diet high in acid precursors is often cited as a risk factor for the development of calcium-based kidney stones. In the present study, we investigated the effect of chronic acid ingestion on kidney stone formation in rats treated with calcitriol (1-25[OH]2 D3). METHODS: Control rats (C-C), calcitriol-treated rats (C-V; three treatments of 0.5 microg of calcitriol per week) and acid-ingested (water containing 0.21 mol/L NH4Cl), calcitriol-treated (three treatments of 0.5 microg of calcitriol per week) rats (A-V) were fed in metabolic cages. After 1 month, urine, blood, kidney and bone samples were analyzed. RESULTS: The A-V rats exhibited elevated serum calcium concentrations, urinary calcium and phosphate excretion, urinary type I collagen cross-linked N-peptide (NTx)/creatinine values, mRNA expression of osteopontin in the kidney, and renal calcium contents as well as decreased bone mineral densities, compared with the C-C and C-V rats. Urinary citrate excretion was lower and NaDC-1 mRNA expression in the kidney was higher in the A-V rats than in the C-C and C-V rats. Calcium phosphate kidney stones were found in the A-V rats. CONCLUSIONS: The ingestion of NH4Cl, an acid precursor, promotes calcium phosphate kidney stone formation in calcitriol-treated rats. The chronic intake of a diet rich in acid precursors may be a risk factor for the development of kidney stones in subjects who are being treated with calcitriol.
Sperm hyperactivated motility is characterized by high flagellar bend amplitude and asymmetrical beating, which are detected by computer-assisted sperm motility analysis as increased curvilinear velocity and lateral head movement. It is required for sperm penetration of the oocyte zona pellucida during fertilization and is induced by an increase in flagellar Ca(2+). Our objective was to determine whether pH plays a role in promoting Ca signaling of hyperactivated motility. The cell-permeant weak base NH(4)Cl increased curvilinear velocity and amplitude of lateral head movement of bovine sperm, indicative of hyperactivation. Fluorometric recordings of sperm loaded with BCECF-AM or fluo3-AM, revealed that NH(4)Cl evoked elevations of intracellular pH and Ca(2+), respectively, with the rise in pH occurring more rapidly than that of Ca(2+). Single-cell image analysis showed increased Ca(2+) levels in the flagellum in response to NH(4)Cl. When extracellular Ca(2+) was lowered with BAPTA (1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid) prior to treatment with NH(4)Cl, intracellular pH was increased, but elevation of Ca(2+) and hyperactivation were diminished. This suggests that the rise in intracellular pH precedes an influx of Ca(2+). The Ca(2+) channel blocker Ni(2+) also diminished NH(4)Cl stimulation of hyperactivation, demonstrating that Ca(2+) entry is required for maximal expression of hyperactivation. Ca(2+) ionophore produced an increase in Ca(2+) that was 3-fold greater than that produced by NH(4)Cl; however, it produced a weaker hyperactivation response. These results indicate that a rise in pH increases intracellular Ca(2+)and promotes hyperactivation primarily by stimulating Ca(2+) influx, but also by other mechanisms.