Stimulation of Cl permeability in colonic crypts of Lieberkuhn measured with a fluorescent indicator

1993 ◽  
Vol 265 (3) ◽  
pp. G423-G431 ◽  
Author(s):  
D. R. Halm ◽  
K. L. Kirk ◽  
K. C. Sathiakumar
Keyword(s):  
Epithelial Cell ◽  
Distal Colon ◽  
Cell Type ◽  
Fluorescent Indicator ◽  
Epithelial Cell Type ◽  
Colonic Crypts ◽  
Pg E2 ◽  
Crypt Cells ◽  
Stimulation Of ◽  
Cl Permeability

Crypts of Lieberkuhn were isolated from rabbit distal colon and the halide-sensitive dye 6-methoxy-N-[3-sulfopropyl]quinolinium was used to monitor changes in cell Cl by fluorescence microscopy. Distal colon from rabbits actively secretes Cl and K when stimulated with prostaglandin (PG) E2 but secretes only K in response to epinephrine. The secretagogues PGE2 and epinephrine each produced transient decreases of the apparent cell Cl concentration in about one-half of the crypt cells. Permeability to Cl was assessed by brief substitutions with gluconate or Br in the bath. After stimulation of secretion by PGE2 or epinephrine, Cl efflux and Br influx were increased but only in the cells that exhibited the decrease in cell Cl at the onset of stimulation. Although Cl efflux during gluconate substitution was stimulated similarly with either PGE2 or epinephrine, epinephrine stimulation led to a lower apparent Cl concentration after 2 min of gluconate substitution. Together these results support the concept that a particular epithelial cell type in the crypts responds to secretagogues and that the Cl permeability pathways differ between the secretory states induced by PGE2 and epinephrine.

On the Presence of a Ciliated Columnar Epithelial Cell Type within the Bovine Cervical Mucosa

1973 ◽  
Vol 36 (5) ◽  
pp. 936-940 ◽  
Author(s):  
R. J. Wordinger ◽  
J. B. Ramsey ◽  
J. F. Dickey ◽  
J. R. Hill
Keyword(s):  
Epithelial Cell ◽  
Cell Type ◽  
Epithelial Cell Type ◽  
Columnar Epithelial Cell ◽  
Cervical Mucosa

scholarly journals Phenotypic shift in human differentiated gastric cancers from gastric to intestinal epithelial cell type during disease progression

1998 ◽  
Vol 1 (2) ◽  
pp. 134-141 ◽  
Author(s):  
Akemi Yoshikawa ◽  
Ken-ichi Inada ◽  
Takasuke Yamachika ◽  
Nobuyuki Shimizu ◽  
Michio Kaminishi ◽  
...  
Keyword(s):  
Epithelial Cell ◽  
Disease Progression ◽  
Intestinal Epithelial Cell ◽  
Intestinal Epithelial ◽  
Cell Type ◽  
Epithelial Cell Type ◽  
Gastric Cancers ◽  
Phenotypic Shift

Differential localization of colonic H+-K+-ATPase isoforms in surface and crypt cells

1998 ◽  
Vol 274 (2) ◽  
pp. G424-G429 ◽  
Author(s):  
Vazhaikkurichi M. Rajendran ◽  
Satish K. Singh ◽  
John Geibel ◽  
Henry J. Binder
Keyword(s):  
Spatial Distribution ◽  
Atpase Activity ◽  
Distal Colon ◽  
Compelling Evidence ◽  
Α Subunit ◽  
Colonic Crypts ◽  
Rat Distal Colon ◽  
Acid Load ◽  
Apical Membranes ◽  
Crypt Cells

Two distinct colonic H+-K+-adenosinetriphosphatase (H+-K+-ATPase) isoforms can be identified in part on the basis of their sensitivity to ouabain. The colonic H+-K+-ATPase α-subunit (HKcα) was recently cloned, and its message and protein are present in surface (and the upper 20% of crypt) cells in the rat distal colon. These studies were performed to establish the spatial distribution of the ouabain-sensitive and ouabain-insensitive components of both H+-K+-ATPase activity in apical membranes prepared from surface and crypt cells and K+-dependent intracellular pH (pHi) recovery from an acid load both in isolated perfused colonic crypts and in surface epithelial cells. Whereas H+-K+-ATPase activity in apical membranes from surface cells was 46% ouabain sensitive, its activity in crypt apical membranes was 96% ouabain sensitive. Similarly, K+-dependent pHi recovery in isolated crypts was completely ouabain sensitive, whereas in surface cells K+-dependent pHi recovery was insensitive to ouabain. These studies provide compelling evidence that HKcα encodes the colonic ouabain-insensitive H+-K+-ATPase and that a colonic ouabain-sensitive H+-K+-ATPase isoform is present in colonic crypts and remains to be cloned and identified.

scholarly journals Heat-Killed Fusobacterium nucleatum Triggers Varying Heme-Related Inflammatory and Stress Responses Depending on Primary Human Respiratory Epithelial Cell Type

Molecules ◽  
2020 ◽  
Vol 25 (17) ◽  
pp. 3839
Author(s):  
Ryo Koike ◽  
Marni E. Cueno ◽  
Keiko Nodomi ◽  
Muneaki Tamura ◽  
Noriaki Kamio ◽  
...  
Keyword(s):  
Epithelial Cell ◽  
Inflammatory Response ◽  
Stress Responses ◽  
Inflammatory Responses ◽  
Fusobacterium Nucleatum ◽  
Alveolar Epithelial Cells ◽  
Cell Type ◽  
Alveolar Cells ◽  
Epithelial Cell Type ◽  
Alveolar Epithelial

Fusobacterium nucleatum (Fn) is generally an opportunistic oral pathogen that adheres to mammalian mucosal sites, triggering a host inflammatory response. In general, Fn is normally found within the human oral cavity; however, it was previously reported that Fn is a risk factor for certain respiratory diseases. Surprisingly, this was never fully elucidated. Here, we investigated the virulence potential of heat-killed Fn on primary human tracheal, bronchial, and alveolar epithelial cells. In this study, we measured the secretion of inflammatory- (IL-8 and IL-6), stress- (total heme and hydrogen peroxide), and cell death-related (caspase-1 and caspase-3) signals. We established that the inflammatory response mechanism varies in each epithelial cell type: (1) along tracheal cells, possible Fn adherence would trigger increased heme secretion and regulated inflammatory response; (2) along bronchial cells, potential Fn adherence would simultaneously initiate an increase in secreted H2O2 and inflammatory response (ascribable to decreased secreted heme amounts); and (3) along alveolar cells, putative Fn adherence would instigate the increased secretion of inflammatory responses attributable to a decrease in secreted heme levels. Moreover, regardless of the epithelial cell-specific inflammatory mechanism, we believe these are putative, not harmful. Taken together, we propose that any potential Fn-driven inflammation along the respiratory tract would be initiated by differing epithelial cell-specific inflammatory mechanisms that are collectively dependent on secreted heme.

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