Disruption of guinea pig urinary bladder permeability barrier in noninfectious cystitis
Although most cell membranes permit rapid flux of water, small nonelectrolytes, and ammonia, the apical membranes of bladder epithelial umbrella cells, which form the bladder permeability barrier, exhibit strikingly low permeabilities to these substances. In cystitis, disruption of the bladder perme...
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Published in | American journal of physiology. Renal physiology Vol. 274; no. 1; pp. F205 - F214 |
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Main Authors | , , , , |
Format | Journal Article |
Language | English |
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United States
01.01.1998
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Abstract | Although most cell membranes permit rapid flux of water, small nonelectrolytes, and ammonia, the apical membranes of bladder epithelial umbrella cells, which form the bladder permeability barrier, exhibit strikingly low permeabilities to these substances. In cystitis, disruption of the bladder permeability barrier may irritate the bladder wall layers underlying the epithelium, causing or exacerbating inflammation, and increasing urinary frequency, urgency, and bladder pain. To determine the effects of inflammation on the integrity of the permeability barrier, guinea pigs were sensitized with ovalbumin, and the bladders were exposed subsequently to antigen by instillation on the urinary side. Inflammation of the bladder wall markedly reduced transepithelial resistance of dissected epithelium mounted in Ussing chambers and increased water and urea permeabilities modestly at 2 h and more strikingly at 24 h after induction of the inflammation. Transmission and scanning electron microscopy of bladders at 30 min and 24 h after antigen exposure revealed disruption of tight junctions, denuding of patches of epithelium, and occasional loss of apical membrane architecture. These permeability and structural effects did not occur in nonsensitized animals in which the bladders were exposed to antigen and in sensitized animals exposed to saline vehicle rather than antigen. These results demonstrate that inflammation of the underlying muscle and lamina propria can disrupt the bladder permeability barrier by damaging tight junctions and apical membranes and causing sloughing of epithelial cells. Leakage of urinary constituents through the damaged epithelium may then exacerbate the inflammation in the underlying muscle layers. |
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AbstractList | Although most cell membranes permit rapid flux of water, small nonelectrolytes, and ammonia, the apical membranes of bladder epithelial umbrella cells, which form the bladder permeability barrier, exhibit strikingly low permeabilities to these substances. In cystitis, disruption of the bladder permeability barrier may irritate the bladder wall layers underlying the epithelium, causing or exacerbating inflammation, and increasing urinary frequency, urgency, and bladder pain. To determine the effects of inflammation on the integrity of the permeability barrier, guinea pigs were sensitized with ovalbumin, and the bladders were exposed subsequently to antigen by instillation on the urinary side. Inflammation of the bladder wall markedly reduced transepithelial resistance of dissected epithelium mounted in Ussing chambers and increased water and urea permeabilities modestly at 2 h and more strikingly at 24 h after induction of the inflammation. Transmission and scanning electron microscopy of bladders at 30 min and 24 h after antigen exposure revealed disruption of tight junctions, denuding of patches of epithelium, and occasional loss of apical membrane architecture. These permeability and structural effects did not occur in nonsensitized animals in which the bladders were exposed to antigen and in sensitized animals exposed to saline vehicle rather than antigen. These results demonstrate that inflammation of the underlying muscle and lamina propria can disrupt the bladder permeability barrier by damaging tight junctions and apical membranes and causing sloughing of epithelial cells. Leakage of urinary constituents through the damaged epithelium may then exacerbate the inflammation in the underlying muscle layers. |
Author | Ruiz, W G Meyers, S A Zeidel, M L Apodaca, G Lavelle, J P |
Author_xml | – sequence: 1 givenname: J P surname: Lavelle fullname: Lavelle, J P organization: Department of Surgery, University of Pittsburgh Medical Center, Pennsylvania 15213, USA – sequence: 2 givenname: G surname: Apodaca fullname: Apodaca, G – sequence: 3 givenname: S A surname: Meyers fullname: Meyers, S A – sequence: 4 givenname: W G surname: Ruiz fullname: Ruiz, W G – sequence: 5 givenname: M L surname: Zeidel fullname: Zeidel, M L |
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References | B20 B10 B21 B12 B23 B13 B24 B14 B15 B18 B19 Zeidel M. L. (B26) 1996; 271 B1 B2 B3 B4 B5 B6 B7 B8 B9 Lattime E. C. (B11) 1992; 52 Molitoris B. A. (B16) 1991; 260 Negrete H. O. (B17) 1996; 271 |
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SubjectTerms | Animals Body Water - metabolism Chickens Cystitis - physiopathology Diffusion Epithelium - physiology Epithelium - physiopathology Epithelium - ultrastructure Guinea Pigs Microscopy, Electron Microscopy, Electron, Scanning Nystatin - pharmacology Ovalbumin Permeability Urea - pharmacokinetics Urinary Bladder - physiology Urinary Bladder - physiopathology Urinary Bladder - ultrastructure |
Title | Disruption of guinea pig urinary bladder permeability barrier in noninfectious cystitis |
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