Effects of epidermal growth factor and Clostridium difficile toxin B in a model of mucosal injury.
Numerous factors have been advocated as being paramount to the development of necrotizing enterocolitis (NEC) including hypoxia, abnormal bacterial flora, and by products of enteral feedings. In an effort to better understand mechanisms involved at the level of the intestinal mucosal barrier the authors have chosen the CACO-2 cell line to model the neonatal intestinal epithelium. By growing CACO-2 cells in transwell inserts, the authors have investigated the ability of Clostridium difficile toxin B, epidermal growth factor (EGF), and a model of mechanical injury to alter transepithelial resistance of CACO-2 monolayers. The findings show that toxin B diminishes resistance in this setting, and EGF can alter that resistance drop.
Lawrence
J P
JP
Department of Surgery, University of Iowa Hospitals and Clinics, Iowa City 52242, USA.
Brevetti
L
L
Obiso
R J
RJ
Wilkins
T D
TD
Kimura
K
K
Soper
R
R
D000704:Analysis of Variance; D001427:Bacterial Toxins / Q000494:pharmacology*; D018938:Caco-2 Cells / Q000187:drug effects* / Q000378:metabolism; D002463:Cell Membrane Permeability; D016360:Clostridioides difficile; D017097:Electric Impedance; D004761:Enterocolitis, Pseudomembranous / Q000503:physiopathology*; D004815:Epidermal Growth Factor / Q000494:pharmacology*; D006801:Humans; D066298:In Vitro Techniques; D007413:Intestinal Mucosa / Q000187:drug effects* / Q000378:metabolism; D011897:Random Allocation
D001427:Bacterial Toxins; D004815:Epidermal Growth Factor