scholarly journals Goblet cell compound exocytosis in the defense against bacterial invasion in the colon exposed to ischemia-reperfusion

Gut Microbes ◽  
2013 ◽  
Vol 4 (3) ◽  
pp. 232-235 ◽  
Author(s):  
Joep Grootjans ◽  
Inca H. Hundscheid ◽  
Wim A. Buurman
Keyword(s):  
Goblet Cell ◽  
Ischemia Reperfusion ◽  
Bacterial Invasion ◽  
Compound Exocytosis

Goblet Cell — Compound Exocytosis

2010 ◽  
pp. 90-91
Author(s):  
Margit Pavelka ◽  
Jürgen Roth
Keyword(s):  
Goblet Cell ◽  
Compound Exocytosis

Both crypt and villus intestinal goblet cells secrete mucin in response to cholinergic stimulation

1992 ◽  
Vol 262 (2) ◽  
pp. G327-G331 ◽  
Author(s):  
T. E. Phillips
Keyword(s):  
Goblet Cell ◽  
Morphometric Analysis ◽  
Secretory Granules ◽  
Goblet Cells ◽  
Computer Assisted ◽  
Cholinergic Stimulation ◽  
Compound Exocytosis ◽  
Apical Membranes

Computer-assisted morphometric analysis was used to quantify the effects of cholinergic stimulation on intestinal goblet cells. Within 5 min of stimulation (250 micrograms/kg carbachol sc), many crypt goblet cells were depleted of mucin secretory granules and their apical membranes had the deep cavitation that accompanies recent compound exocytotic activity. The percentage of crypt epithelial volume occupied by mucin secretory granules was decreased by 58.4% at 5 min and 45.9% at 60 min. Although villus goblet cells never showed signs of recent compound exocytosis, morphometric analysis revealed a 22.4% decrease in the percentage of villus epithelial volume occupied by mucin secretory granules within 5 min of stimulation and a 32.4% decrease by 60 min. The decrease in villus mucin stores was due to both a reduction in the volume of mucin in an average villus goblet cell and a drop in the number of recognizable goblet cells per square micrometer of villus epithelium. Mucin stores in both the crypt and villus regions were largely replenished by 4 h poststimulation.

Regulation of intestinal goblet cell secretion. I. Role of parasympathetic stimulation

1982 ◽  
Vol 242 (4) ◽  
pp. G370-G379 ◽  
Author(s):  
R. D. Specian ◽  
M. R. Neutra
Keyword(s):  
Molecular Weight ◽  
High Molecular Weight ◽  
Goblet Cell ◽  
Gel Filtration ◽  
Goblet Cells ◽  
Mucus Secretion ◽  
Cell Secretion ◽  
Intestinal Mucus ◽  
Compound Exocytosis

The in vivo effects of the parasympathomimetic drug pilocarpine on rat intestinal goblet cells were analyzed by autoradiography, light microscopy (LM), and electron microscopy (EM). Pilocarpine accelerated the release of mucus by compound exocytosis from crypt (but not surface) goblet cells throughout the small and large intestine. Pilocarpine-induced mucus secretion was blocked by atropine alone in ileum and colon, but total inhibition in proximal small intestine required a combination of atropine and tubocurarine. The sensitivity of morphological-autoradiographic methods for detection of goblet cell secretion was compared with that of a biochemical detection method, separation of labeled high-molecular-weight glycoproteins by Sepharose 4B gel filtration of luminal washings. Even when secretion of labeled mucus by compound exocytosis was clearly demonstrated by LM, EM, and autoradiography, gel filtration assay of luminal washings from pilocarpine-injected rats failed to reveal an increase in labeled high-molecular-weight glycoproteins. Autoradiographs of mucosal tissue after luminal washing showed that newly secreted, labeled mucus was retained in the crypts and was thus unavailable to the biochemical assay. Thus, direct observation of exocytosis in individual goblet cells provides a qualitative, but sensitive, assay for short-term acceleration of intestinal mucus secretion.

scholarly journals Ischemia/Reperfusion Injury Alters Sphingolipid Metabolism in the Gut

2016 ◽  
Vol 39 (4) ◽  
pp. 1262-1270 ◽  
Author(s):  
Richard S. Hoehn ◽  
Aaron P. Seitz ◽  
Peter L. Jernigan ◽  
Erich Gulbins ◽  
Michael J. Edwards
Keyword(s):  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Bacterial Overgrowth ◽  
Sphingolipid Metabolism ◽  
Bacterial Invasion ◽  
Proximal Jejunum ◽  
Dependent Manner ◽  
Upper Respiratory Tract ◽  
Bacterial Membranes

Background: Intestinal ischemia/reperfusion injury (I/R) is a significant cause of morbidity and mortality in surgical patients. Ceramide is a mediator of apoptosis and has been implicated as increasing bacterial infection susceptibility. The metabolite of ceramide, sphingosine, was recently shown to play an important role in the cell-autonomous, innate immune response of the upper respiratory tract by killing bacterial pathogens. The role of ceramide and/or sphingosine after mesenteric I/R is unknown. We investigated the specific effects of intestinal I/R on tissue ceramide and sphingosine concentration and resulting susceptibility to bacterial invasion. Methods: To simulate intestinal I/R, C57BL/6 mice underwent 30 minutes of vascular clamp-induced occlusion of the superior mesenteric artery followed by variable reperfusion times. Jejunum segments and intraluminal contents were analyzed for ceramide, sphingosine and bacteria using immunohistochemistry. Jejunum samples were also homogenized and cultured to quantify bacterial presence in the proximal intestine. Results: We hypothesized that I/R induces an increase of ceramide in the intestine resulting in increased permeability, while a concomitant decrease of sphingosine may permit bacterial overgrowth. Control mice had no measurable bacteria in their proximal jejunum as measured by tissue culture and immunohistochemistry. After I/R, bacterial counts in the jejunum increased in a time-dependent manner, reaching a peak at 12 hours after reperfusion. Immunohistochemical analysis revealed a marked increase in ceramide in the vasculature of jejunal villi. In contrast, while ceramide concentrations in the epithelial cells decreased after I/R, sphingosine levels appeared to remain unchanged. Surprisingly, bacteria present in the jejunal lumen following I/R contained a ceramide coat. Conclusion: These data indicate that intestinal I/R leads to small intestine bacterial overgrowth as well as ceramide formation in the jejunal vasculature, which may contribute to the gut permeability associated with this injury. Moreover, our novel finding of ceramide in bacterial membranes represents a new opportunity to investigate the dynamic pathogenicity of the gut microbiome. The hypothesis that a decrease of sphingosine after I/R permits bacterial overgrowth in the intestine was not confirmed.

Changes in hepatic and pulmonary leukotriene concentrations following ischemia-reperfusion of rat liver

2001 ◽  
Vol 120 (5) ◽  
pp. A379-A379
Author(s):  
Y TAKAMATSU ◽  
K SHIMADA ◽  
K CHIJIWA ◽  
M TANAKA
Keyword(s):  
Rat Liver ◽  
Ischemia Reperfusion

1618: Real-Time Monitoring of Nitric Oxide and Blood Flow During Ischemia-Reperfusion in the Rat Testis

2006 ◽  
Vol 175 (4S) ◽  
pp. 521-521
Author(s):  
Motoaki Saito ◽  
Tomoharu Kono ◽  
Yukako Kinoshita ◽  
Itaru Satoh ◽  
Keisuke Satoh
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Real Time ◽  
Ischemia Reperfusion ◽  
Real Time Monitoring ◽  
Rat Testis

1843: Role of Cxcr2 in Renal Ischemia/Reperfusion Injury

2004 ◽  
Vol 171 (4S) ◽  
pp. 487-487
Author(s):  
Motoo Araki ◽  
Masayoshi Miura ◽  
Hiromi Kumon ◽  
John Belperio ◽  
Robert Strieter ◽  
...  
Keyword(s):  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Renal Ischemia ◽  
Renal Ischemia Reperfusion Injury
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