Subcellular Expression Pattern and role of IL-15 in Pneumococci induced Lung Epithelial Apoptosis

Hocke, AC; Hartmann, I.; Eitel, Julia; Suttorp, Norbert; Hippenstiel, Stefan

doi:10.1055/s-2008-1074122

Cited by 5 publications

(5 citation statements)

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“…However, given that transient augmentation of IL-15 mRNA expression immediately precedes the initial influx of T eff to the lung airways (Fig 1; T eff first detectable ~5.5 days p.i. (data not shown)), the documented chemotactic properties of IL-15, and the fact that lung parenchymal cells (including influenza-infected lung epithelial cells) can also express IL-15 (29), we hypothesized that in addition to supporting the survival anti-influenza CD8T eff , IL-15 could also participate in the recruitment of the T eff to the site of infection. To that end, IL-15 −/− and WT animals were infected i.n.…”

Section: Resultsmentioning

confidence: 99%

A Role for IL-15 in the Migration of Effector CD8 T Cells to the Lung Airways following Influenza Infection

Verbist

Cole

Field

et al. 2011

The Journal of Immunology

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The cytokines generated locally in response to infection play an important role in CD8 T cell trafficking, survival, and effector function, rendering these signals prime candidates for immune intervention. In this paper, we show that localized increases in the homeostatic cytokine IL-15 induced by influenza infection is responsible for the migration of CD8 effector T cells to the site of infection. Moreover, intranasal delivery of IL-15–IL-15Rα soluble complexes (IL-15c) specifically restores the frequency of effector T cells lost in the lung airways of IL-15–deficient animals after influenza infection. Exogenous IL-15c quantitatively augments the respiratory CD8 T cell response, and continued administration of IL-15c throughout the contraction phase of the anti-influenza CD8 T cell response magnifies the resultant CD8 T cell memory generated in situ. This treatment extends the ability of these cells to protect against heterologous infection, immunity that typically depreciates over time. Overall, our studies describe what to our knowledge is a new function for IL-15 in attracting effector CD8 T cells to the lung airways and suggest that adjuvanting IL-15 could be used to prolong anti-influenza CD8 T cell responses at mucosal surfaces to facilitate pathogen elimination.

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Section: Resultsmentioning

confidence: 99%

A Role for IL-15 in the Migration of Effector CD8 T Cells to the Lung Airways following Influenza Infection

Verbist

Cole

Field

et al. 2011

The Journal of Immunology

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“…IL-15 gene and protein expression have been previously reported in respiratory epithelial cells [22,23] and detected in bronchial biopsies from healthy controls as well as from patients with inflammatory lung diseases [22]. RSV upregulates IL-15 mRNA in a monocyte cell line but the effect of RSV on IL-15 production in respiratory epithelial cells has not been reported.…”

Section: Ifn-c Increases Rsv-induced Il-15 Levels But Downregulates Rmentioning

confidence: 99%

RSV infection modulates IL-15 production and MICA levels in respiratory epithelial cells

Zdrenghea¹,

Telcian²,

Laza-Stanca³

et al. 2011

Eur Respir J

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The cytokine interleukin (IL)-15, major histocompatibility complex (MHC) class I molecules and MHC class I chain-related proteins (MIC) A and B are involved in cellular immune responses to virus infections but their role in respiratory syncytial virus (RSV) infection has not been studied. We aimed to determine how RSV infection modulates IL-15 production, MHC class I and MICA expression in respiratory epithelial cells, the molecular pathways implicated in virusinduced IL-15 production and how interferon (IFN)-c alters RSV-induced IL-15 production and MHC class I and MICA expression.We infected respiratory epithelial cell lines (A549 and BEAS-2B cells) and primary bronchial epithelial cells with RSV and measured production of IL-15, expression of MHC I and MICA and the role of the transcription factor nuclear factor (NF)-kB.We report here that RSV increases IL-15 in respiratory epithelial cells via virus replication and NF-kB-dependent mechanisms. Therefore, IL-15 is likely to play a key role in the immune response to RSV infection but no data are available regarding RSV modulation of IL-15 production and MICA/B expression in human respiratory epithelial cells.We aimed to determine how RSV infection modulates IL-15 production in respiratory epithelial cells and the molecular pathways implicated in virus-induced IL-15 production. In addition, because RSV infection induces a type 1 immune response characterised by increased IFN-c production [11], we determined how IFN-c alters RSVinduced IL-15 production and the levels of MHC class I and MICA molecules in epithelial cells.

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“…Double immunofluorescence was performed, as described previously 30 31. Infected chondrocytes were grown on glass coverslips and fixed with 3% paraformaldehyde (pH 7.6) for 20 min.…”

Section: Methodsmentioning

confidence: 99%

“…A terminal deoxynucleotidyl transferase-mediated dUTP nick end labelling (TUNEL) technique (Roche, Mannheim, Germany) was used to detect chondrocyte cell apoptosis 30 33. Chondrocytes, grown on 24-well plates at a density of 2×10 4 per well, were infected with P gingivalis .…”

Section: Methodsmentioning

confidence: 99%

Effects of Porphyromonas gingivalis on cell cycle progression and apoptosis of primary human chondrocytes

Pischon

Röhner

Hocke

et al. 2008

Annals of the Rheumatic Diseases

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Subcellular Expression Pattern and role of IL-15 in Pneumococci induced Lung Epithelial Apoptosis

Cited by 5 publications

References 0 publications

A Role for IL-15 in the Migration of Effector CD8 T Cells to the Lung Airways following Influenza Infection

A Role for IL-15 in the Migration of Effector CD8 T Cells to the Lung Airways following Influenza Infection

RSV infection modulates IL-15 production and MICA levels in respiratory epithelial cells

Effects of Porphyromonas gingivalis on cell cycle progression and apoptosis of primary human chondrocytes

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