Peroxynitrite (PN) effects on small intestinal enterocytes (IEC-6) 1 1The Society of Black Academic Surgeons expresses its appreciation to Dr. Walter Pories and the editorial staff of Current Surgery for their interest in the Society and the publication of these abstracts.

1999 ◽  
Vol 56 (7-8) ◽  
pp. 382-383
Author(s):  
J.S. Upperman ◽  
P. Boyle ◽  
R. Hoffmann ◽  
S. Watkins ◽  
H.R. Ford
Keyword(s):  
Editorial Staff ◽  
Small Intestinal ◽  
Academic Surgeons ◽  
Intestinal Enterocytes

Small Intestinal Enterocytes

1993 ◽  
pp. 193-201
Author(s):  
Tak Yee Aw ◽  
Changli Bai ◽  
Dean P. Jones
Keyword(s):  
Small Intestinal ◽  
Intestinal Enterocytes

scholarly journals TMPRSS2 and TMPRSS4 promote SARS-CoV-2 infection of human small intestinal enterocytes

2020 ◽  
Vol 5 (47) ◽  
pp. eabc3582 ◽  
Author(s):  
Ruochen Zang ◽  
Maria Florencia Gomez Castro ◽  
Broc T. McCune ◽  
Qiru Zeng ◽  
Paul W. Rothlauf ◽  
...  
Keyword(s):  
Serine Proteases ◽  
Gastrointestinal Symptoms ◽  
Host Cells ◽  
Productive Infection ◽  
Intestinal Lumen ◽  
Fecal Shedding ◽  
Oral Transmission ◽  
Stool Specimens ◽  
Small Intestinal ◽  
Intestinal Enterocytes

Gastrointestinal symptoms and fecal shedding of SARS-CoV-2 RNA are frequently observed in COVID-19 patients. However, it is unclear whether SARS-CoV-2 replicates in the human intestine and contributes to possible fecal-oral transmission. Here, we report productive infection of SARS-CoV-2 in ACE2+ mature enterocytes in human small intestinal enteroids. Expression of two mucosa-specific serine proteases, TMPRSS2 and TMPRSS4, facilitated SARS-CoV-2 spike fusogenic activity and promoted virus entry into host cells. We also demonstrate that viruses released into the intestinal lumen were inactivated by simulated human colonic fluid, and infectious virus was not recovered from the stool specimens of COVID-19 patients. Our results highlight the intestine as a potential site of SARS-CoV-2 replication, which may contribute to local and systemic illness and overall disease progression.

scholarly journals Loss of myosin Vb promotes apical bulk endocytosis in neonatal enterocytes

2019 ◽  
Vol 218 (11) ◽  
pp. 3647-3662 ◽  
Author(s):  
Amy C. Engevik ◽  
Izumi Kaji ◽  
Meagan M. Postema ◽  
James J. Faust ◽  
Anne R. Meyer ◽  
...  
Keyword(s):  
Brush Border Membrane ◽  
Apical Membrane ◽  
Primary Mechanism ◽  
Neuronal Stimulation ◽  
Myosin Vb ◽  
Small Intestinal ◽  
Membrane Treatment ◽  
Activity Dependent ◽  
Intestinal Enterocytes ◽  
Inactivating Mutations

In patients with inactivating mutations in myosin Vb (Myo5B), enterocytes show large inclusions lined by microvilli. The origin of inclusions in small-intestinal enterocytes in microvillus inclusion disease is currently unclear. We postulated that inclusions in Myo5b KO mouse enterocytes form through invagination of the apical brush border membrane. 70-kD FITC-dextran added apically to Myo5b KO intestinal explants accumulated in intracellular inclusions. Live imaging of Myo5b KO–derived enteroids confirmed the formation of inclusions from the apical membrane. Treatment of intestinal explants and enteroids with Dyngo resulted in accumulation of inclusions at the apical membrane. Inclusions in Myo5b KO enterocytes contained VAMP4 and Pacsin 2 (Syndapin 2). Myo5b;Pacsin 2 double-KO mice showed a significant decrease in inclusion formation. Our results suggest that apical bulk endocytosis in Myo5b KO enterocytes resembles activity-dependent bulk endocytosis, the primary mechanism for synaptic vesicle uptake during intense neuronal stimulation. Thus, apical bulk endocytosis mediates the formation of inclusions in neonatal Myo5b KO enterocytes.

Sign in / Sign up

Export Citation Format

Share Document