Shigella interaction with intestinal epithelial cells determines the innate immune response in shigellosis

Lactobacillus delbrueckii subsp. lactis CRL 581 beneficially modulates the intestinal antiviral innate immune response triggered by the Toll-like receptor 3 (TLR3) agonist poly(I:C) in vivo. This study aimed to characterize further the immunomodulatory properties of the technologically relevant starter culture L. delbrueckii subsp. lactis CRL 581 by evaluating its interaction with intestinal epithelial cells and macrophages in the context of innate immune responses triggered by TLR3. Our results showed that the CRL 581 strain was able to adhere to porcine intestinal epithelial (PIE) cells and mucins. The CRL 581 strain also augmented the expression of antiviral factors (IFN-α, IFN-β, Mx1, OAS1, and OAS2) and reduced inflammatory cytokines in PIE cells triggered by TLR3 stimulation. In addition, the influence of L. delbrueckii subsp. lactis CRL 581 on the response of murine RAW macrophages to the activation of TLR3 was evaluated. The CRL 581 strain was capable of enhancing the expression of IFN-α, IFN-β, IFN-γ, Mx1, OAS1, TNF-α, and IL-1β. Of note, the CRL 581 strain also augmented the expression of IL-10 in macrophages. The results of this study show that the high proteolytic strain L. delbrueckii spp. lactis CRL 581 was able to beneficially modulate the intestinal innate antiviral immune response by regulating the response of both epithelial cells and macrophages relative to TLR3 activation.

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Lactobacilli stimulate the innate immune response and modulate the TLR expression of HT29 intestinal epithelial cells in vitro

International Journal of Food Microbiology ◽

10.1016/j.ijfoodmicro.2009.05.013 ◽

2009 ◽

Vol 133 (1-2) ◽

pp. 86-93 ◽

Cited By ~ 77

Author(s):

María G. Vizoso Pinto ◽

Manuel Rodriguez Gómez ◽

Stephanie Seifert ◽

Bernhard Watzl ◽

Wilhelm H. Holzapfel ◽

...

Keyword(s):

Immune Response ◽

Epithelial Cells ◽

Innate Immune Response ◽

Intestinal Epithelial Cells ◽

Innate Immune ◽

Intestinal Epithelial

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Colostrum and bioactive, colostral peptides differentially modulate the innate immune response of intestinal epithelial cells

Journal of Peptide Science ◽

10.1002/psc.1190 ◽

2009 ◽

Vol 16 (1) ◽

pp. 21-30 ◽

Cited By ~ 23

Author(s):

Ann Louise Worsøe Jørgensen ◽

Helle Risdahl Juul-Madsen ◽

Jan Stagsted

Keyword(s):

Immune Response ◽

Epithelial Cells ◽

Innate Immune Response ◽

Intestinal Epithelial Cells ◽

Innate Immune ◽

Intestinal Epithelial

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1000 Gliadin Elicits An Innate Immune Response in Monocytic and Intestinal Epithelial Cells Via the MyD88 Pathway

Gastroenterology ◽

10.1016/s0016-5085(08)60700-3 ◽

2008 ◽

Vol 134 (4) ◽

pp. A-150-A-151

Author(s):

Yvonne Junker ◽

Detlef Schuppan

Keyword(s):

Immune Response ◽

Epithelial Cells ◽

Innate Immune Response ◽

Intestinal Epithelial Cells ◽

Innate Immune ◽

Intestinal Epithelial ◽

Myd88 Pathway

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Protective Effects of Lactoferrin against SARS-CoV-2 Infection In Vitro

Nutrients ◽

10.3390/nu13020328 ◽

2021 ◽

Vol 13 (2) ◽

pp. 328 ◽

Cited By ~ 1

Author(s):

Claudio Salaris ◽

Melania Scarpa ◽

Marina Elli ◽

Alice Bertolini ◽

Simone Guglielmetti ◽

...

Keyword(s):

Immune Response ◽

Epithelial Cells ◽

Intestinal Epithelial Cells ◽

Plaque Assay ◽

Immune Response Gene ◽

Intestinal Epithelial ◽

Antiviral Immune Response ◽

Qrt Pcr ◽

Anti Inflammatory

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.

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Innate immune response in CF airway epithelia: hyperinflammatory?

AJP Cell Physiology ◽

10.1152/ajpcell.00605.2005 ◽

2006 ◽

Vol 291 (2) ◽

pp. C218-C230 ◽

Cited By ~ 123

Author(s):

Terry E. Machen

Keyword(s):

Immune Response ◽

Epithelial Cells ◽

Innate Immune Response ◽

Cellular Signaling ◽

Basolateral Membrane ◽

Airway Epithelial Cells ◽

Innate Immune ◽

Airway Epithelial ◽

Airway Epithelia ◽

Intracellular Ca

The lack of functional cystic fibrosis (CF) transmembrane conductance regulator (CFTR) in the apical membranes of CF airway epithelial cells abolishes cAMP-stimulated anion transport, and bacteria, eventually including Pseudomonas aeruginosa, bind to and accumulate in the mucus. Flagellin released from P. aeruginosa triggers airway epithelial Toll-like receptor 5 and subsequent NF-κB signaling and production and release of proinflammatory cytokines that recruit neutrophils to the infected region. This response has been termed hyperinflammatory because so many neutrophils accumulate; a response that damages CF lung tissue. We first review the contradictory data both for and against the idea that epithelial cells exhibit larger-than-normal proinflammatory signaling in CF compared with non-CF cells and then review proposals that might explain how reduced CFTR function could activate such proinflammatory signaling. It is concluded that apparent exaggerated innate immune response of CF airway epithelial cells may have resulted not from direct effects of CFTR on cellular signaling or inflammatory mediator production but from indirect effects resulting from the absence of CFTRs apical membrane channel function. Thus, loss of Cl−, HCO3−, and glutathione secretion may lead to reduced volume and increased acidification and oxidation of the airway surface liquid. These changes concentrate proinflammatory mediators, reduce mucociliary clearance of bacteria and subsequently activate cellular signaling. Loss of apical CFTR will also hyperpolarize basolateral membrane potentials, potentially leading to increases in cytosolic [Ca2+], intracellular Ca2+, and NF-κB signaling. This hyperinflammatory effect of CF on intracellular Ca2+and NF-κB signaling would be most prominently expressed during exposure to both P. aeruginosa and also endocrine, paracrine, or nervous agonists that activate Ca2+signaling in the airway epithelia.

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