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J Interferon Cytokine Res. 2000 Dec;20(12):1077-82.
Tumor necrosis factor-alpha (TNF-alpha)-induced and interleukin-1 beta (IL-1 beta)-induced shedding of TNF receptors from gingival fibroblasts.

Ohe H, Takashiba S, Naruishi K, Chou HH, Yamada H, Nishimura F, Arai H, Murayama Y.

Department of Periodontology and Endodontology, Okayama University Dental School, Okayama, Japan.

Tumor necrosis factor-alpha (TNF-alpha) exerts its functions by binding two different receptors (TNFR55 and TNFR75). Both TNFR55 and TNFR75 exist in cell-associated and soluble forms. Soluble TNF receptors (sTNFR), sTNFR55 and sTNFR75, are proteolytically shed upon inflammatory stimuli and then modulate various TNF-alpha bioactivities. As human gingival fibroblasts (HGF) can be potential targets for TNF-alpha in inflamed gingiva, we hypothesized that HGF partially modulate the cellular responses to TNF-alpha by regulating their own TNFR. In this study, the kinetics of expression of cell-associated and soluble forms of both receptors from cultured HGF in response to proinflammatory cytokines TNF-alpha and interleukin-1 beta (IL-1 beta) were investigated in vitro. Both TNF-alpha and IL-1 beta upregulated the gene expression of TNFR75 and did not affect that of TNFR55. TNF-alpha and IL-1 beta decreased binding of [(125)I]TNF-alpha to HGF. Moreover, TNF-alpha and IL-1 beta upregulated the release of sTNFR75 from HGF but not that of sTNFR55. These results suggest that HGF under inflammatory conditions may contribute to the inactivation of circulating TNF-alpha through the preferential induction and shedding of TNFR75.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11152574&dopt=Abstract

J Interferon Cytokine Res. 2000 Dec;20(12):1083-90.
Effect of granulocyte colony-stimulating factor treatment on ex vivo neutrophil functions in nonneutropenic surgical intensive care patients.

Gerber A, Struy H, Weiss G, Lippert H, Ansorge S, Schulz HU.

Institute of Immunology, Otto von Guericke University Magdeburg, 39120 Magdeburg, Germany. annegret.gerbeedizin.uni-magdeburg.de

Granulocyte colony-stimulating factor (G-CSF) preferentially stimulates growth and differentiation of neutrophil precursors and activates neutrophil functions. The aim of the present study was to investigate the functional response of the neutrophil to exogenous recombinant human G-CSF (rHuG-CSF) in nonneutropenic patients. In 30 surgical intensive care unit patients with severely impaired wound healing, leukocyte differential count, plasma G-CSF level, and a broad spectrum of neutrophil functions were monitored before (day 0), throughout (days 1 and 5), and at days 1 and 5 after stopping G-CSF treatment. G-CSF application resulted in a 3.5-fold increase in peripheral blood granulocyte count at day 5 of treatment. The mean plasma G-CSF level rose from 48 to a maximum of 2314 pg/ml at day 1 of G-CSF therapy. Neutrophil chemotaxis and stimulated lysozyme release were decreased throughout G-CSF treatment, whereas respiratory burst activity, phagocytic activity, and intracellular calcium concentration were enhanced by G-CSF. Neutrophil membrane depolarization remained unaffected. The increased count and activation state of neutrophils were associated with clinical improvement in most of these patients. Thus, G-CSF may be a useful adjuvant treatment for nonneutropenic patients with severely impaired wound healing.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11152575&dopt=Abstract

J Interferon Cytokine Res. 2000 Dec;20(12):1091-100.
Caspase-dependent apoptosis by 2',5'-oligoadenylate activation of RNase L is enhanced by IFN-beta.

Rusch L, Zhou A, Silverman RH.

Department of Cancer Biology, Lerner Research Institute, Cleveland Clinic Foundation, Cleveland, OH 44195, USA.

The 2',5'-oligoadenylate (2-5A) system is an interferon (IFN)-regulated RNA decay pathway that provides innate immunity against viral infections. The biologic action of the 2-5A system is mediated by RNase L, an endoribonuclease that becomes enzymatically active after binding to 2-5A. RNase L is also implicated in mediating apoptosis in response to both viral and nonviral inducers. To study the cellular effects of RNase L activation directly, 2-5A was transfected into the human ovarian cancer cell line, Hey1B. Activation of RNase L by 2-5A resulted in specific 18S rRNA cleavage and induction of apoptosis, as measured by TUNEL and annexin V binding assays. In contrast, the dimeric form of 2-5A, ppA2'p5'A, neither activated RNase L nor caused apoptosis. Treatment with IFN-beta prior to 2-5A transfection enhanced cellular RNase L levels (< or = 2.2-fold) and increased the proportion of cells undergoing apoptosis (by < or =40%). However, rRNA cleavages after 2-5A transfections were not enhanced by IFN-beta pretreatments, indicating that basal levels of RNase L were sufficient for this activity. Apoptosis in response to RNase L activation was accompanied by cytochrome c release from mitochondria. Induction of apoptosis by either 2-5A alone or by the combination of 2-5A and IFN-beta was effectively blocked with either the pancaspase inhibitor, Z-VAD-fmk, or with the caspase 3 inhibitor, DEVD-fmk. Therefore, activation of RNase L by 2-5A leads to cytochrome c release into the cytoplasm and then to caspase activation and apoptosis. These results suggest potential uses for 2-5A in augmenting the anticancer activities of IFN.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11152576&dopt=Abstract

J Interferon Cytokine Res. 2000 Dec;20(12):1101-9.
Interferon-mediated block in cell cycle and altered integrin expression in a differentiated salivary gland cell line (HSG) cultured on Matrigel.

Daniels PJ, Gustafson SA, French D, Wang Y, DePond W, McArthur CP.

Department of Oral Biology, University of Missouri-Kansas City School of Dentistry, Kansas City, MO 64108, USA. pdanielumc.edu

Sjogren's syndrome (SS), an idiopathic, autoimmune exocrinopathy, is partly characterized by diminished salivary flow, acinar cell atrophy, and increased expression of several cytokines. Several in vivo characteristics of the sialoadenitis are also evident in a human salivary gland ductal epithelial cell line (HSG) treated with cytokines. HSG cells differentiate to the acinar phenotype when cultured on Matrigel (Becton Dickinson, Bedford, MA), a basement membrane extract. To elucidate mechanisms of salivary gland pathology, the effects of interferon-gamma (IFN-gamma) and tumor necrosis factor-alpha (TNF-alpha) on cell cycle progression and integrin expression were evaluated in HSG acinarlike cells. Flow cytometry experiments showed that cytokine treatment for 2 days arrested cells in G(1) phase of the cell cycle, and this preceded significant morphologic changes and decreased viability. Whereas only modest cytokine-mediated increases in protein expression for the alpha 3 and beta 1 integrin subunits were seen by immunoprecipitation, a form of alpha 3 integrin displaying enhanced electrophoretic mobility was evident after 6 days of cytokine treatment. To our knowledge, this is the first report demonstrating an IFN-mediated alteration in the electrophoretic mobility of integrin subunits. From this study, it was evident that the combination of IFN-gamma and TNF-alpha resulted in a block in G(1) phase for acinar cells before accumulation of the alpha 3 integrin variant or significant degenerative cellular changes. Information from the present and previous studies suggests that cytokines may alter the pattern of integrin expression and block cell cycle progression in salivary gland cells grown in three-dimensional acinarlike clusters. These experiments may provide a new cell culture model to study the effects of cytokines in normal and diseased salivary glands, including SS.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11152577&dopt=Abstract

J Interferon Cytokine Res. 2000 Dec;20(12):1111-20.
Suppression of interferon-induced antiviral activity in cells expressing hepatitis C virus proteins.

Aizaki H, Saito S, Ogino T, Miyajima N, Harada T, Matsuura Y, Miyamura T, Kohase M.

Department of Virology II, NIID, 1-23-1 Toyama, Tokyo 162-8640, Japan.

To elucidate the mechanism of the persistent nature of hepatitis C virus (HCV) infection, we examined whether the expression of HCV proteins affect the antiviral activity of interferon (IFN). Antiviral activity of IFN in HepG2 cells expressing all HCV (type 1b) proteins was much lower than vector control (VC) HepG2 cells when encephalomyocarditis virus (EMCV) was used as a challenge virus. Lesser sensitivity to IFN was also observed in cells expressing NS3, NS4, and NS5 and in cells expressing only NS5A. In contrast, HepG2 cells expressing core, E1, E2, NS2, and NS3 proteins were equally sensitive to IFN as VC cells. We then tested the antiviral activity by IFN in two human amnion-derived FL cell lines expressing NS5A from two different clones, one with an intact sequence of IFN sensitivity-determining region (ISDR) and the other with a mutated ISDR sequence. They were almost equally insensitive to IFN treatment when EMCV was challenged. HCV thus has functional protein(s), possibly NS5A, to suppress IFN-induced antiviral activity and plays an important role in virus-cell interaction and regulation of viral replication.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11152578&dopt=Abstract

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