Interleukin (IL)-4/IL-9 and Exogenous IL-16 Induce IL-16 Production by BEAS-2B Cells, a Bronchial Epithelial Cell Line

Yoshida, Naruo; Arima, Masafumi; Cheng, Gang; Eda, Fukiko; Hirata, Hirokuni; Honda, K.; Fukushima, Fumiya; Fukuda, Takeshi

doi:10.1006/cimm.2000.1745

Cited by 11 publications

(6 citation statements)

References 18 publications

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“…The absence of IL-9 responsiveness in BEAS-2B cells is consistent with our inability to detect IL-9R mRNA in these cells by RT-PCR. A recent investigation also found BEAS-2B cells to be unresponsive to IL-9 stimulation alone (27). IL-9R transcripts have been detected by RT-PCR in primary murine (7), immortalized human, and primary human airway epithelial cells (9) in culture.…”

Section: Discussionmentioning

confidence: 89%

IL-9 Stimulates Release of Chemotactic Factors from Human Bronchial Epithelial Cells

Little

Cruikshank

Center

2001

Am J Respir Cell Mol Biol

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Interleukin (IL)-9 is a T helper 2 cytokine implicated as a candidate gene and contributor to human asthma. We hypothesized that the inflammatory potential of bronchial epithelium is affected by its local environment and explored this hypothesis with respect to the effect of IL-9 on bronchial epithelium. We investigated the response of primary and immortalized human bronchial epithelial cells to IL-9 stimulation with respect to the release of T-cell chemoattractant factors. In response to IL-9, the HBE4-E6/E7 cell line, but not BEAS-2B cells, released the T-cell chemoattractants IL-16 and regulated on activation, normal T cells expressed and secreted (RANTES) in a dose-dependent fashion. We found a similar dose response to IL-9 in primary cells from bronchial brushings of healthy subjects and that nearly all of the T-cell chemoattraction was attributable to IL-16 and RANTES. Reverse transcriptase/polymerase chain reaction of BEAS-2B, HBE4-E6/E7, and primary cells from two subjects revealed messenger RNA for IL-9 receptor (IL-9R) alpha but not in BEAS-2B cells. Fluorescence-activated cell sorter analysis of HBE4-E6/E7 and primary cells confirmed surface expression of the IL-9 receptor. Costimulation of both cell types with IL-9 and antibody to either gamma-common chain or IL-9Ralpha completely blocked the release of T-cell chemoattractant activity, confirming the primary role of a functioning IL-9 receptor for IL-9 signaling in HBE4-E6/E7 and primary bronchial epithelial cells. We conclude that IL-9 is a stimulus for airway epithelial cell release of T-cell chemoattractant factors, which in turn may modulate the immune response in allergic airway inflammation.

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Section: Discussionmentioning

confidence: 89%

IL-9 Stimulates Release of Chemotactic Factors from Human Bronchial Epithelial Cells

Little

Cruikshank

Center

2001

Am J Respir Cell Mol Biol

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“…Yoshida et al (2001) have shown that IL-4, IL-9, IL-16, and TNF-α alone do not exhibit any significant effect on the expression of IL-16 mRNA or IL-16 protein in bronchial epithelial cell line. However, this same cell line produces IL-16 after synergistic stimulation by either (IL-4 + IL-16) or (IL-9 + IL-16).…”

Section: Discussionmentioning

confidence: 92%

“…IL-16 expression is cell specific and is regulated at multiple levels. Furthermore, several reports indicate that only activated microglia in the CNS express IL-16 mRNA and protein (Engel et al, 2000; Schwab et al, 2001a,b; Yoshida et al, 2001). Though mitogens and antigens can activate transcription of IL-16 in T-cells, but the stimulus that induces the expression of IL-16 in macrophages/microglia has not been defined.…”

Section: Discussionmentioning

confidence: 99%

IL-12 p40 homodimer, but not IL-12 p70, induces the expression of IL-16 in microglia and macrophages

Jana

Pahan

2009

Molecular Immunology

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IL-16, a leukocyte chemoattractant factor (LCF), is involved in the disease process of multiple sclerosis and other autoimmune disorders. However, mechanisms by which this LCF is expressed are poorly understood. The present study underlines the importance of IL-12 p40 homodimer (p40 2 ), the so-called biologically inactive molecule, in inducing the expression of IL-16 in primary mouse and human microglia, mouse BV-2 microglial cells, mouse peritoneal macrophages, and RAW264.7 cells. In contrast, IL-12 p70, the bioactive heterodimeric cytokine, was unable to induce the expression of IL-16 in any of these cell types. Similarly IL-12 p40 2 also induced the activation of IL-16 promoter in microglia. Among various stimuli tested, p40 2 was the most potent one followed by p40 monomer, IL-16 and IL-23 in inducing the activation of IL-16 promoter in microglial cells. Furthermore, induction of IL-16 mRNA expression by over-expression of p40, but not p35, cDNA and induction of IL-16 expression by p40 2 in microglia isolated from IL-12p35 (−/−) mice confirm that p40, but not p35, is responsible for the induction of IL-16. Finally, by using primary microglia isolated from IL-12Rβ1 (−/−) and IL-12Rβ2 (−/−) mice, we demonstrate that p40 2 induces the expression of this LCF via IL-12Rβ1 but not IL-12Rβ2. These results delineate a novel biological function of p40 2 and raise the possibility that biological function of IL-12 p40 2 maybe different from IL-12 p70.

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“…Interleukin 16 (IL16), initially identified as lymphocyte chemoattractant factor, is a novel interleukin with no significant homology to other interleukins and cytokines [1]. It is constitutively expressed in a variety of cells, such as T cells, B cells, mast cells, eosinophils, and epithelial cells [1][2][3][4][5][6]. Human IL16 is initially translated into a 631 amino acid precursor protein that can be cleaved to generate an N-terminal pro-IL16 and a 121-residue C-terminal peptide, the cleaved C-terminal peptide is subsequently released into supernatant to become aggregate and bioactive form of mature IL16 [7].…”

Section: Introductionmentioning

confidence: 99%

Interleukin 16 contributes to gammaherpesvirus pathogenesis by inhibiting viral reactivation

Liu

Lei

et al. 2020

PLoS Pathog

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Gammaherpesviruses have evolved various strategies to take advantage of host cellular factors or signaling pathways to establish a lifelong latent infection. Like the human gammaherpesvirus Epstein-Barr virus, murine gammaherpesvirus 68 (MHV68) establishes and maintains latency in the memory B cells during infection of laboratory mice. We have previously shown that MHV68 can immortalize fetal liver-derived B cells that induce lymphomas when injected into immunodeficient mice. Here we identify interleukin 16 (IL16) as a most abundantly expressed cytokine in MHV68-immortalized B cells and show that MHV68 infection elevates IL16 expression. IL16 is not important for MHV68 lytic infection but plays a critical role in MHV68 reactivation from latency. IL16 deficiency increases MHV68 lytic gene expression in MHV68-immortalized B cells and enhances reactivation from splenic latency. Correlatively, IL16 deficiency increases the frequency of MHV68-infected plasma cells that can be attributed to enhanced MHV68 reactivation. Furthermore, similar to TPA-mediated lytic replication of Kaposi's sarcoma-associated herpesvirus, IL16 deficiency markedly induces Tyr705 STAT3 de-phosphorylation and elevates p21 expression, which can be counteracted by the tyrosine phosphatase inhibitor orthovanadate. Importantly, orthovanadate strongly blocks MHV68 lytic gene expression mediated by IL16 deficiency. These data demonstrate that virus-induced IL16 does not directly participate in MHV68 lytic replication, but rather inhibits virus reactivation to facilitate latent infection, in part through the STAT3-p21 axis.

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Interleukin (IL)-4/IL-9 and Exogenous IL-16 Induce IL-16 Production by BEAS-2B Cells, a Bronchial Epithelial Cell Line

Cited by 11 publications

References 18 publications

IL-9 Stimulates Release of Chemotactic Factors from Human Bronchial Epithelial Cells

IL-9 Stimulates Release of Chemotactic Factors from Human Bronchial Epithelial Cells

IL-12 p40 homodimer, but not IL-12 p70, induces the expression of IL-16 in microglia and macrophages

Interleukin 16 contributes to gammaherpesvirus pathogenesis by inhibiting viral reactivation

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