scholarly journals The yin and yang of intestinal epithelial cells in controlling dendritic cell function

2007 ◽  
Vol 204 (10) ◽  
pp. 2253-2257 ◽  
Author(s):  
Iliyan D. Iliev ◽  
Gianluca Matteoli ◽  
Maria Rescigno

Recent work suggests that dendritic cells (DCs) in mucosal tissues are “educated” by intestinal epithelial cells (IECs) to suppress inflammation and promote immunological tolerance. After attack by pathogenic microorganisms, however, “non-educated” DCs are recruited from nearby areas, such as the dome of Peyer's patches (PPs) and the blood, to initiate inflammation and the ensuing immune response to the invader. Differential epithelial cell (EC) responses to commensals and pathogens may control these two tolorogenic and immunogenic functions of DCs.

2004 ◽  
Vol 1029 (1) ◽  
pp. 66-74 ◽  
Author(s):  
MONICA RIMOLDI ◽  
MARCELLO CHIEPPA ◽  
MARISA VULCANO ◽  
PAOLA ALLAVENA ◽  
MARIA RESCIGNO

Nutrients ◽  
2021 ◽  
Vol 13 (2) ◽  
pp. 328 ◽  
Author(s):  
Claudio Salaris ◽  
Melania Scarpa ◽  
Marina Elli ◽  
Alice Bertolini ◽  
Simone Guglielmetti ◽  
...  

SARS-CoV-2 is a newly emerging virus that currently lacks curative treatments. Lactoferrin (LF) is a naturally occurring non-toxic glycoprotein with broad-spectrum antiviral, immunomodulatory and anti-inflammatory effects. In this study, we assessed the potential of LF in the prevention of SARS-CoV-2 infection in vitro. Antiviral immune response gene expression was analyzed by qRT-PCR in uninfected Caco-2 intestinal epithelial cells treated with LF. An infection assay for SARS-CoV-2 was performed in Caco-2 cells treated or not with LF. SARS-CoV-2 titer was determined by qRT-PCR, plaque assay and immunostaining. Inflammatory and anti-inflammatory cytokine production was determined by qRT-PCR. LF significantly induced the expression of IFNA1, IFNB1, TLR3, TLR7, IRF3, IRF7 and MAVS genes. Furthermore, LF partially inhibited SARS-CoV-2 infection and replication in Caco-2 intestinal epithelial cells. Our in vitro data support LF as an immune modulator of the antiviral immune response with moderate effects against SARS-CoV-2 infection.


2013 ◽  
Vol 58 (2) ◽  
pp. 384-393 ◽  
Author(s):  
Mercedes Ortega-González ◽  
Borja Ocón ◽  
Isabel Romero-Calvo ◽  
Andrea Anzola ◽  
Emilia Guadix ◽  
...  

2009 ◽  
Vol 136 (5) ◽  
pp. A-702
Author(s):  
Els van Hoffen ◽  
Nicoline M. Korthagen ◽  
Sander de Kivit ◽  
Bastiaan Schouten ◽  
Bart Bardoel ◽  
...  

Cells ◽  
2020 ◽  
Vol 9 (8) ◽  
pp. 1847
Author(s):  
Gaku Nakato ◽  
Sohshi Morimura ◽  
Michael Lu ◽  
Xu Feng ◽  
Chuanjin Wu ◽  
...  

TROP1 (EpCAM) and TROP2 are homologous cell surface proteins that are widely expressed, and often co-expressed, in developing and adult epithelia. Various functions have been ascribed to EpCAM and TROP2, but responsible mechanisms are incompletely characterized and functional equivalence has not been examined. Adult intestinal epithelial cells (IEC) express high levels of EpCAM, while TROP2 is not expressed. EpCAM deficiency causes congenital tufting enteropathy (CTE) in humans and a corresponding lethal condition in mice. We expressed TROP2 and EpCAM in the IEC of EpCAM-deficient mice utilizing a villin promoter to assess EpCAM and TROP2 function. Expression of EpCAM or TROP2 in the IEC of EpCAM knockout mice prevented CTE. TROP2 rescue (T2R) mice were smaller than controls, while EpCAM rescue (EpR) mice were not. Abnormalities were observed in the diameters and histology of T2R small intestine, and Paneth and stem cell markers were decreased. T2R mice also exhibited enlarged mesenteric lymph nodes, enhanced permeability to 4 kDa FITC-dextran and increased sensitivity to detergent-induced colitis, consistent with compromised barrier function. Studies of IEC organoids and spheroids revealed that stem cell function was also compromised in T2R mice. We conclude that EpCAM and TROP2 exhibit functional redundancy, but they are not equivalent.


2010 ◽  
Vol 23 (6) ◽  
pp. 595-608 ◽  
Author(s):  
Alfonso Barreto ◽  
Luz-Stella Rodríguez ◽  
Olga Lucía Rojas ◽  
Marie Wolf ◽  
Harry B. Greenberg ◽  
...  

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