Interleukin-26 in Antibacterial Host Defense of Human Lungs. Effects on Neutrophil Mobilization

Fru, Karlhans; Tengvall, Sara; Levänen, Bettina; Silverpil, Elin; Smith, Melanie H.; Awad, Muhammed; Vikström, Max; Palmberg, Lena; Qvarfordt, Ingemar; Sköld, Magnus; Lindén, Anders

doi:10.1164/rccm.201404-0689oc

Cited by 62 publications

(150 citation statements)

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“…We also demonstrated that IL-26 enhances the chemotactic response of neutrophils toward a bacterial stimulus and toward IL-8, while at the same time inhibiting the chemokinesis in these innate effector cells (9)(10)(11). Moreover, we demonstrated that alveolar macrophages constitute a prominent source of IL-26, in addition to Th17 cells and other lymphocyte subsets.…”

mentioning

confidence: 54%

“…Given the abundance of IL-26 protein in the human airway lumen and its referred involvement in the immune response to bacterial (9,10) and viral stimulation (7,12,13), we hypothesized that IL-26 is involved in pulmonary host defense against viruses by being produced in bronchial epithelial cells after stimulation with a viral stimulus and that this production is modulated by additional Th17 cytokines. We also hypothesized that the intracellular signaling pathways leading to IL-26 release involves mitogen-activated protein (MAP) kinases and the nuclear transcription factor NF-κB.…”

Section: Interleukin-26 Production In Human Primary Bronchial Epithelmentioning

confidence: 99%

“…PhosphoTracer ELISA Intracellular activation/phosphorylation of p38, JNK1-3, ERK1/2 and NF-κB was measured according to manufacturer's instructions (Abcam ® ) (9). In brief, cell lysates were transferred in duplicates (50 mL/well) to the plates.…”

Section: Cell Culture and Stimulationmentioning

confidence: 99%

“…The primer sequences were obtained from the literature (9,21), and purchased from Cybergene. RT-PCR was performed as previously described (9).…”

Section: Rt-pcr Analysesmentioning

confidence: 99%

“…In a recent in vivo study (9), we forwarded evidence that endogenous IL-26 is abundant and involved in the local immune response against a bacterial stimulus, a toll-like receptor (TLR) 4 agonist, in healthy human airways. We also demonstrated that IL-26 enhances the chemotactic response of neutrophils toward a bacterial stimulus and toward IL-8, while at the same time inhibiting the chemokinesis in these innate effector cells (9)(10)(11).…”

mentioning

confidence: 99%

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Interleukin-26 Production in Human Primary Bronchial Epithelial Cells in Response to Viral Stimulation: Modulation by Th17 cytokines

Fru

Kaarteenaho

Lappi‐Blanco

et al. 2017

Mol Med

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Interleukin (IL)-26 is abundant in human airways and this cytokine is involved in the local immune response to a bacterial stimulus in vivo. Specifically, local exposure to the toll-like receptor (TLR) 4 agonist endotoxin does increase IL-26 in human airways and this cytokine potentiates chemotactic responses in human neutrophils. In addition to T-helper (Th) 17 cells, alveolar macrophages can produce IL-26, but it remains unknown whether this cytokine can also be produced in the airway mucosa per se in response to a viral stimulus. Here, we evaluated whether this is the case using primary bronchial epithelial cells from the airway epithelium in vitro and explored the signaling mechanisms involved, including the modulatory effects of additional Th17 cytokines. Finally, we assessed IL-26 and its archetype signaling responses in healthy human airways in vivo. We found increased transcription and release of IL-26 protein after stimulation with the viral-related double stranded (ds) RNA polyinosinic-polycytidylic acid (poly-IC) and showed that this IL-26 release involved mitogen-activated protein (MAP) kinases and nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB). The release of IL-26 in response to a viral stimulus was modulated by additional Th17 cytokines. Moreover, there was transcription of IL26 mRNA and expression of the protein in epithelial cells of bronchial brush and tissue biopsies respectively after harvest in vivo. In addition, the extracellular IL-26 protein concentrations in bronchoalveolar lavage (BAL) samples did correlate with increased epithelial cell transcription of an archetype intracellular signaling molecule downstream of the IL-26-receptor complex, STAT1, in the bronchial brush biopsies. Thus, our study suggests that viral stimulation causes the production of IL-26 in lining epithelial cells of human airways, structural cells that constitute a critical immune barrier and that this production is modulated by Th17 cytokines.

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mentioning

confidence: 54%

Section: Interleukin-26 Production In Human Primary Bronchial Epithelmentioning

confidence: 99%

Section: Cell Culture and Stimulationmentioning

confidence: 99%

“…The primer sequences were obtained from the literature (9,21), and purchased from Cybergene. RT-PCR was performed as previously described (9).…”

Section: Rt-pcr Analysesmentioning

confidence: 99%

mentioning

confidence: 99%

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Interleukin-26 Production in Human Primary Bronchial Epithelial Cells in Response to Viral Stimulation: Modulation by Th17 cytokines

Fru

Kaarteenaho

Lappi‐Blanco

et al. 2017

Mol Med

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IL-26 promotes the pathogenesis of malignant pleural effusion by enhancing CD4+IL-22+ T-cell differentiation and inhibiting CD8+ T-cell cytotoxicity

Niu

Peng

et al. 2021

Journal of Leukocyte Biology

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IL‐26 is a newly discovered IL‐10 cytokine family member mainly secreted by Th17 cells. However, the relationship between IL‐26 and lung cancer remains unclear. The present study reported that IL‐26 is involved in the production and promotion of malignant pleural effusion (MPE) for the first time. The concentrations of IL‐26 and several Th17‐related cytokines in MPE and peripheral blood (PB) from MPE patients were measured. IL‐26, IL‐10, and IL‐6 were elevated in MPE compared to PB. The cell resource of IL‐26 was primary Th17 cells measured by flow cytometry, whereas Tc17 cells and macrophages could also contribute to higher concentration of IL‐26 in MPE. Abundant IL‐6 and IL‐23 in MPE could promote the frequency of IL‐26 expressed by CD4+ T cells through phosphorylating STAT3 signaling pathway and promoting the expression of a specific Th17 lineage marker RORγt subsequently. IL‐26 could selectively increase Th22 proportion through up‐regulating the percentage of Ki‐67 expressed by CD4+ T cells and the expression of IL‐22 secreted by memory CD4+ T cells. In addition, IL‐26 could decrease secretion of granzyme B. The tumor‐killing activity of CD8+ T cells were inhibited as well when cocultured with malignant cells. Furthermore, the accumulation of IL‐26 protein in MPE predicted poor patient survival. In summary, our results indicated that IL‐26 was involved in the pathogenesis of MPE by exerting its impacts on both CD4+ T cells and CD8+ T cells.

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Synovial cell production of IL-26 induces bone mineralization in spondyloarthritis

et al. 2017

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Interleukin-26 in Antibacterial Host Defense of Human Lungs. Effects on Neutrophil Mobilization

Abstract: This study implies that alveolar macrophages produce IL-26, which stimulates receptors on neutrophils and focuses their mobilization toward bacteria and accumulated immune cells in human lungs.

Cited by 62 publications

References 44 publications

Interleukin-26 Production in Human Primary Bronchial Epithelial Cells in Response to Viral Stimulation: Modulation by Th17 cytokines

Interleukin-26 Production in Human Primary Bronchial Epithelial Cells in Response to Viral Stimulation: Modulation by Th17 cytokines

IL-26 promotes the pathogenesis of malignant pleural effusion by enhancing CD4+IL-22+ T-cell differentiation and inhibiting CD8+ T-cell cytotoxicity

Synovial cell production of IL-26 induces bone mineralization in spondyloarthritis

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