Interfering with interferon-γ signalling in intestinal epithelial cells: selective inhibition of apoptosis-maintained secretion of anti-inflammatory interleukin-18 binding protein

Schuhmann, D.; Godoy, Pablo; Weiß, Christel; Gerloff, Andreas; Singer, Manfred V.; Dooley, Steven; Böcker, Ulrich

doi:10.1111/j.1365-2249.2010.04250.x

Cited by 24 publications

(18 citation statements)

References 43 publications

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“…Interferons have been shown to induce apoptosis of intestinal epithelial cells. Using human colon explant cultures, Jarry et al demonstrated that administration of IFN-α-2a rapidly induced IFN-γ production by lamina propria resident T cells and IFN-γ-dependent epithelial apoptosis, a direct effect of IFN-γ on the intestinal epithelium that has been reported previously ( 24 , 65 , 66 ). Katlinskaya et al also demonstrated a role for type I IFN in promoting apoptosis of the intestinal epithelium in a model of constitutive β-catenin signaling ( 63 ).…”

Section: Cytokine Actions On the Intestinal Epitheliummentioning

confidence: 66%

Cytokine Tuning of Intestinal Epithelial Function

2018

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The intestine serves as both our largest single barrier to the external environment and the host of more immune cells than any other location in our bodies. Separating these potential combatants is a single layer of dynamic epithelium composed of heterogeneous epithelial subtypes, each uniquely adapted to carry out a subset of the intestine’s diverse functions. In addition to its obvious role in digestion, the intestinal epithelium is responsible for a wide array of critical tasks, including maintaining barrier integrity, preventing invasion by microbial commensals and pathogens, and modulating the intestinal immune system. Communication between these epithelial cells and resident immune cells is crucial for maintaining homeostasis and coordinating appropriate responses to disease and can occur through cell-to-cell contact or by the release or recognition of soluble mediators. The objective of this review is to highlight recent literature illuminating how cytokines and chemokines, both those made by and acting on the intestinal epithelium, orchestrate many of the diverse functions of the intestinal epithelium and its interactions with immune cells in health and disease. Areas of focus include cytokine control of intestinal epithelial proliferation, cell death, and barrier permeability. In addition, the modulation of epithelial-derived cytokines and chemokines by factors such as interactions with stromal and immune cells, pathogen and commensal exposure, and diet will be discussed.

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Section: Cytokine Actions On the Intestinal Epitheliummentioning

confidence: 66%

Cytokine Tuning of Intestinal Epithelial Function

2018

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“…It is well documented that the immune modulatory activity of IDO1 is critical in limiting DSS-induced inflammation. 22 , 23 As IDO1 is expressed in mononuclear cells, especially in DCs, and in other cells such as epithelial cells, we first compared the levels of Ido1 expression between different LP DC subsets and colon IECs. At steady-state conditions, CD103 + CD11b − DCs are the major Ido1- expressing cells in the colon, but after DSS exposure, Ido1 mRNA expression in IECs exceeded by almost 10-fold the level of DC expression ( Figure 6c ).…”

Section: Resultsmentioning

confidence: 99%

Intestinal CD103+CD11b− dendritic cells restrain colitis via IFN-γ-induced anti-inflammatory response in epithelial cells

et al. 2016

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A crosstalk between commensals, gut immune cells, and colonic epithelia is required for a proper function of intestinal mucosal barrier. Here we investigated the importance of two distinct intestinal dendritic cell (DC) subsets in controlling intestinal inflammation. We show that Clec9A–diphtheria toxin receptor (DTR) mice after depletion of CD103+CD11b− DCs developed severe, low-dose dextran sodium sulfate (DSS)-induced colitis, whereas the lack of CD103+CD11b+ DCs in Clec4a4-DTR mice did not exacerbate intestinal inflammation. The CD103+CD11b− DC subset has gained a functional specialization that able them to repress inflammation via several epithelial interferon-γ (IFN-γ)-induced proteins. Among others, we identified that epithelial IDO1 and interleukin-18-binding protein (IL-18bp) were strongly modulated by CD103+CD11b− DCs. Through its preferential property to express IL-12 and IL-15, this particular DC subset can induce lymphocytes in colonic lamina propria and in epithelia to secrete IFN-γ that then can trigger a reversible early anti-inflammatory response in intestinal epithelial cells.

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“…Interferon, however, has been suggested to induce the death of virus infected epithelial cells (Schuhmann et al, 2010). To investigate whether cell shedding in response to virus infection is linked to interferon production of the epithelial cells, we compared the amounts of type I interferon produced by HAE infected with PIV5, PIV3, and RSV.…”

Section: Resultsmentioning

confidence: 99%

Comparison of differing cytopathic effects in human airway epithelium of parainfluenza virus 5 (W3A), parainfluenza virus type 3, and respiratory syncytial virus

et al. 2011

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Parainfluenza virus 5 (PIV5) infects a wide range of animals including dogs, pigs, cats, and humans; however, its association with disease in humans remains controversial. In contrast to parainfluenza virus 3 (PIV3) or respiratory syncytial virus (RSV), PIV5 is remarkably non-cytopathic in monolayer cultures of immortalized epithelial cells. To compare the cytopathology produced by these viruses in a relevant human tissue, we infected an in vitro model of human ciliated airway epithelium and measured outcomes of cytopathology. PIV5, PIV3 and, RSV all infected ciliated cells, and PIV5 and PIV3 infection was dependent on sialic acid residues. Only PIV5-infected cells formed syncytia. PIV5 infection resulted in a more rapid loss of infected cells by shedding of infected cells into the lumen. These studies revealed striking differences in cytopathology of PIV5 versus PIV3 or RSV and indicate the extent of cytopathology determined in cell-lines does not predict events in differentiated airway cells.

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Interfering with interferon-γ signalling in intestinal epithelial cells: selective inhibition of apoptosis-maintained secretion of anti-inflammatory interleukin-18 binding protein

Cited by 24 publications

References 43 publications

Cytokine Tuning of Intestinal Epithelial Function

Cytokine Tuning of Intestinal Epithelial Function

Intestinal CD103+CD11b− dendritic cells restrain colitis via IFN-γ-induced anti-inflammatory response in epithelial cells

Comparison of differing cytopathic effects in human airway epithelium of parainfluenza virus 5 (W3A), parainfluenza virus type 3, and respiratory syncytial virus

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