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           Search results for: Recombinant Human IL-32 alpha Proteins    

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IL-32γ attenuates airway fibrosis by modulating the integrin-FAK signaling pathway in fibroblasts.

Fibrosis in severe asthma often leads to irreversible organ dysfunction. However, the mechanism that regulates fibrosis remains poorly understood. Interleukin (IL)-32 plays a role in several chronic inflammatory diseases, including severe asthma. In this study, we investigated whether IL-32 is involved in fibrosis progression in the lungs.

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Interleukin-32 plays an essential role in human calcified aortic valve cells.

Interleukin-32 (IL-32) is an inflammatory cytokine produced mainly by T, natural killer, and epithelial cells. Previous studies on IL-32 have primarily investigated its proinflammatory properties. The IL-32 also has been described as an activator of the p38 mitogen-activated protein kinase (MAPK) and NF-κB, and induces several cytokines. In this study, we hypothesized that the inflammatory regulators NF-κB, MAP kinase, STAT1, and STAT3 are associated with the expression of the IL-32 protein in human calcified aortic valve cells. This study comprised aortic valve sclerotic patients and control group patients without calcified aortic valve. Increased IL-32 expression in calcified aortic valvular tissue was shown by immunohistochemical staining and western blotting. There was an increase in NF-κB p65 level, p-ERK, p-JNK, and p-p38 MAPK activation underlying IL-32 expression in the study. The level of p-STAT3 but not p-STAT1 was found to be increased in calcified aortic valve tissue. In cultured primary human aortic valve interstitial cells, inhibition of NF-κB or MAPK kinase pathways results in a decrease of IL-32 expression. Treatment of recombinant IL-32 induced the levels of TNF-α, IL-6, IL-1β, and IL-8. Our findings demonstrate that IL-32 may be an important pro-inflammatory molecule involved in calcific aortic valve disease.

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Role of interleukin-32 in the pathogenesis of endometriosis: in vitro, human and transgenic mouse data.

Does interleukin-32 (IL-32) play a role in the pathogenesis of endometriosis?

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Role of Interleukin 32 in Human Immunodeficiency Virus Reactivation and Its Link to Human Immunodeficiency Virus-Herpes Simplex Virus Coinfection.

Herpes simplex virus type 2 (HSV-2; herpes) exacerbates human immunodeficiency virus type 1 (HIV) by unclear mechanisms. These studies tested the impact of HSV-2 on systemic T-cells and HIV reservoirs.

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c-Jun N-terminal kinase and Akt signalling pathways regulating tumour necrosis factor-α-induced interleukin-32 expression in human lung fibroblasts: implications in airway inflammation.

Airway inflammatory diseases such as chronic obstructive pulmonary disease (COPD) and asthma are associated with elevated expression of interleukin-32 (IL-32), a recently described cytokine that appears to play a critical role in inflammation. However, so far, the regulation of pulmonary IL-32 production has not been fully established. We examined the expression of IL-32 by tumour necrosis factor-α (TNF-α) in primary human lung fibroblasts. Human lung fibroblasts were cultured in the presence or absence of TNF-α and/or other cytokines/Toll-like receptor (TLR) ligands or various signalling molecule inhibitors to analyse the expression of IL-32 by quantitative RT-PCR and ELISA. Next, activation of Akt and c-Jun N-terminal kinase (JNK) signalling pathways was investigated by Western blot. Interleukin-32 mRNA of four spliced isoforms (α, β, γ and δ) was up-regulated upon TNF-α stimulation, which was associated with a significant IL-32 protein release from TNF-α-activated human lung fibroblasts. The combination of interferon-γ and TNF-α induced enhanced IL-32 release in human lung fibroblasts, whereas IL-4, IL-17A, IL-27 and TLR ligands did not alter IL-32 release in human lung fibroblasts either alone, or in combination with TNF-α. Furthermore, the activation of Akt and JNK pathways regulated TNF-α-induced IL-32 expression in human lung fibroblasts, and inhibition of the Akt and JNK pathways was able to suppress the increased release of IL-32 to nearly the basal level. These data suggest that TNF-α may be involved in airway inflammation via the induction of IL-32 by activating Akt and JNK signalling pathways. Therefore, the TNF-α/IL-32 axis may be a potential therapeutic target for airway inflammatory diseases.

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Inducible interleukin 32 (IL-32) exerts extensive antiviral function via selective stimulation of interferon λ1 (IFN-λ1).

Interleukin (IL)-32 has been recognized as a proinflammatory cytokine that participates in responses to viral infection. However, little is known about how IL-32 is induced in response to viral infection and the mechanisms of IL-32-mediated antiviral activities. We discovered that IL-32 is elevated by hepatitis B virus (HBV) infection both in vitro and in vivo and that HBV induced IL-32 expression at the level of both transcription and post-transcription. Furthermore, microRNA-29b was found to be a key factor in HBV-regulated IL-32 expression by directly targeting the mRNA 3'-untranslated region of IL-32. Antiviral analysis showed that IL-32 was not sufficient to alter HBV replication in HepG2.2.15 cells. To mimic the viremic phase of viral infection, freshly isolated peripheral blood mononuclear cells were treated with IL-32γ, the secretory isoform, and the supernatants were used for antiviral assays. Surprisingly, these supernatants exhibited extensive antiviral activity against multiplex viruses besides HBV. Thus, we speculated that the IL-32γ-treated peripheral blood mononuclear cells produced and secreted an unknown antiviral factor. Using antibody neutralization assays, we identified the factor as interferon (IFN)-λ1 and not IFN-α. Further studies indicated that IL-32γ effectively inhibited HBV replication in a hydrodynamic injection mouse model. Clinical data showed that elevated levels of IFN-λ1 both in serum and liver tissue of HBV patients were positively correlated to the increased levels of IL-32. Our results demonstrate that elevated IL-32 levels during viral infection mediate antiviral effects by stimulating the expression of IFN-λ1.

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Interleukin-32 gamma specific monoclonal antibody and developing IL-32 specific ELISA.

Cytokines are essential coordinators of defensive immune responses for resolving the invasion of pathogens such as bacteria, virus, and fungi. However, dysregulated cytokines are the main cause of various autoinflammatory immune disorders such as rheumatoid arthritis, inflammatory bowel disease, and psoriasis. Interleukin-32 (IL-32) is a recently described cytokine and characterized as a proinflammatory cytokine. IL-32 stimulates monocytes and macrophages to induce important proinflammatory cytokines (IL-1β, IL-6, and TNFα) and chemokines (IL-8 and MIP-2) by activating the NF-κB and p38 mitogen-activated protein (MAP) kinase pathways. The biological activities of IL-32 are associated with epidemic pathogens, Mycobacterium tuberculosis, influenza A virus, and human immunodeficiency virus (HIV). IL-32 is transcribed as six alternative splice variants (α, β, γ, δ, ɛ, and ζ), with IL-32γ being the most active isoform. However, it is unclear which isoform is related to specific disease activities since there are no high quality antibodies available to measure circulating IL-32 in biological samples of patients. Therefore, we developed specific anti-human IL-32γ monoclonal antibodies from recombinant human IL-32γ, which was expressed in Escherichia coli. The IL-32γ specific monoclonal antibodies recognized IL-32 in cell culture supernatants and serum of IL-32γ transgenic mice. The newly developed IL-32γ monoclonal antibodies will be a useful tool to measure IL-32 level in serum samples of various inflammatory diseases. These monoclonal antibodies will be helpful in investigating the precise function of IL-32 in immune responses and in autoinflammatory diseases.

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The effects of IL-32 on the inflammatory activation of cultured rat primary astrocytes.

A new family of cytokine IL-32 has been implicated in pro-inflammatory immune responses several human diseases such as rheumatoid arthritis, inflammatory bowel diseases and vasculitis. In this study, we investigated the role of IL-32 in the inflammatory activation of cultured rat primary astrocytes. Treatment of IL-32 increased ROS production and augmented lipopolysaccharide-induced increased production of nitric oxide as well as the expression of iNOS. IL-32 also induced the expression of MMP-9 but not MMP-2 in rat primary astrocytes. The increased expression of these inflammatory mediators was accompanied by the increased mRNA expression encoding iNOS, MMP-9 and TNF-α. ERK1/2 and p38, two essential regulators of pro-inflammatory signaling in rat primary astrocytes were activated by IL-32 as evidenced by increased phosphorylation. The results from the present study suggest that IL-32 may play a role in the regulation of neuroinflammatory responses in several neurological disease conditions such as ischemia and Alzheimer's disease.

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Proteinase 3-processed form of the recombinant IL-32 separate domain.

Interleukin-32 (IL-32) induces a variety of proinflammatory cytokines and chemokines. The IL-32 transcript was reported originally in activated T cells; subsequently, it was demonstrated to be abundantly expressed in epithelial and endothelial cells upon stimulation with inflammatory cytokines. IL-32 is regulated robustly by other major proinflammatory cytokines, thereby suggesting that IL-32 is crucial to inflammation and immune responses. Recently, an IL-32alpha-affinity column was employed in order to isolate an IL-32 binding protein, neutrophil proteinase 3 (PR3). Proteinase 3 processes a variety of inflammatory cytokines, including TNFalpha, IL-1beta, IL-8, and IL-32, thereby enhancing their biological activities. In the current study, we designed four PR3-cleaved IL-32 separate domains, identified by potential PR3 cleavage sites in the IL-32alpha and gamma polypeptides. The separate domains of the IL-32 isoforms alpha and gamma were more active than the intrinsic alpha and gamma isoforms. Interestingly, the N-terminal IL-32 isoform gamma separate domain evidenced the highest levels of biological activity among the IL-32 separate domains.

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Detection of expressed IL-32 in human stomach cancer using ELISA and immunostaining.

Interleukin (IL)-32 is a recently identified proinflammatory cytokine that is one of the IL-18 inducible genes, and plays an important role in autoimmune and inflammatory diseases. We produced antibodies against IL-32 and studied the expression of IL-32 in human stomach cancer. We detected IL-32 secreted from K-562 cells that werw stably transfected with IL-32 and in the sera of stomach cancer patients, by a sandwich ELISA using a monoclonal antibody KU32-52 and a polyclonal antibody. In order to optimize a sandwich immunoassay, recombinant IL-32alpha was added, followed by the addition of a biotinylated KU32-52 into microtiter plate wells precoated with a goat anti-IL-32 antibody. The bound biotinylated KU32-52 was probed with a streptavidin conjugated to HRP. This sandwich ELISA was highly specific and had a minimal detection limit of 80 pg/ml (mean+/-SD of zero calibrator) and measuring up to 3,000 pg/ml. This ELISA showed no cross-reaction with other cytokines such as hIL-1alpha, hIL-1beta, hIL-2, hIL-6, hIL-8, hIL-10, hIL-18, and hTNF-alpha. Intra-assay coefficients of variation were 18.5% to 4.6% (n=10), and inter-assay coefficients were 23% to 9% (n=10). The average IL-32 level in the sera of 16 stomach cancer patients (189 pg/ml) was higher than that of 12 healthy control men (109 pg/ml). Our results indicate that serum IL-32 level can be detected by using an established ELISA, and that this immunoassay and mAb KU32-09 specific for immunohistochemistry can be used in the detection of expressed and secreted IL- 32 in stomach cancer patients.

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