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J Eur Acad Dermatol Venereol. 2003 Mar;17(2):193-5.
Lichen planus and leukocytoclastic vasculitis induced by interferon alpha-2b in a subject with HCV-related chronic active hepatitis.

Pinto JM, Marques MS, Correia TE.

University Clinic of Dermatology and Venereology, Faculty of Medical Sciences and H. de Pulido Valente, Lisbon, Portugal. jorgemspintetcabo.pt

Lichen planus (LP) has been reported in association with chronic active hepatitis, primary biliary cirrhosis and other chronic liver diseases. The occurrence of LP in persons with hepatitis C virus (HCV) was reported by Robert et al., and the possible relationship between LP and hepatitis virus has also been supported by cases of LP following hepatitis B vaccination. Exacerbation or appearance of LP during the treatment of chronic hepatitis C, lymphoproliferative diseases and melanoma with alpha-interferon (IFN-alpha) and improvement of these diseases after discontinuation of this drug indicate that IFN-alpha may possibly induce LP. We present a case of cutaneo-mucous LP in a woman with chronic active hepatitis treated with IFN-alpha and in whom local leukocytoclastic vasculitis was induced by the intradermal injection of a very low dose of IFN-alpha.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12705750&dopt=Abstract

Metabolism. 2001 Jan;50(1):99-106.
Effect of inflammatory cytokines on the metabolism of low-density lipoproteins by human vascular endothelial cells.

Klein RL, Ascencao JL, Mironova M, Huang Y, Lopes-Virella MF.

Research Service, Ralph H. Johnson Department of Veterans Affairs Medical Center, Charleston, SC 29401, USA.

Cytokines have been shown to activate multiple, varied metabolic pathways in endothelial cells. Little information is available concerning the effects of inflammatory cytokines on lipoprotein metabolism by vascular endothelial cells. Human umbilical vein endothelial cells (HuECs) and bovine aortic endothelial cells (BAECs) were incubated with the inflammatory cytokines recombinant human interleukin-1beta (IL-1), tumor necrosis factor alpha (TNF), interferon gamma (gamma-IF), and interferon beta (beta-IF) at increasing concentrations (0.1 to 1,000 U/mL), for increasing periods (6 to 72 hours). After the incubation period, the media were removed and replaced with serum-free media containing radiolabeled native or acetylated low-density lipoprotein (Ac-LDL) and the rates of degradation and accumulation of radiolabeled LDL were determined. The degradation and accumulation of 125I-LDL were significantly increased (P < .02) in HuECs preincubated with IL-1 (100 U/mL) compared with control incubations without the cytokine or incubations containing gamma-IF, beta-IF, or TNF. This resulted from a 38% increase in LDL receptor protein in cells incubated with IL-1. The increased rate of LDL catabolism by HuECs incubated with IL-1 was accompanied by a significant increase (P < .05) in the rate of cholesteryl ester synthesis in the cells. Cholesteryl ester synthesis rates in HuECs preincubated with gamma-IF, beta-IF, or TNF did not differ significantly from the rates in control incubations. The effect of preincubation with cytokine on the activity of the scavenger receptor was also determined. There were no significant differences in the rate of degradation or accumulation of radiolabeled Ac-LDL in control incubations compared with cultures preincubated with IL-1, gamma-IF, beta-IF, or TNF. There also were no significant differences in the rate of catabolism of native LDL or Ac-LDL in BAECs preincubated with cytokines. Although cytokines have been shown previously to alter the binding of monocytes to endothelial cells, there was no significant increase in the binding of monocytes to cultures incubated with IL-1 plus LDL compared with IL-1 alone. In summary, we now demonstrate that cytokines, specifically IL-1, may alter LDL metabolism by human vascular endothelial cells and alter endothelial cell cholesterol metabolism. These changes in endothelial cell metabolism provide additional evidence supporting the critical role of cytokines in atherogenesis.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11172482&dopt=Abstract

Int J Mol Med. 2001 Feb;7(2):149-54.
Interleukin-10 relieves the inhibitory effects of interferon-gamma on normal human lung fibroblasts.

Hashimoto T, Nakamura M, Oshika Y, Tsuchida T, Yamazaki H, Kijima H, Ueyama Y, Minoguchi K, Adachi M, Ota H.

Department of Pathology, Tokai University School of Medicine, Bohseidai, Isehara, Kanagawa 259-1193, Japan.

Interleukin-10 (IL-10) is an important cytokine that suppresses the production of cytokines and chemokines by immune cells. IL-10 has been suggested to be involved in chronic inflammatory responses including the remodeling process in the lung. We investigated the effects of IL-10 on proliferation, extracellular matrix and cytokine production in normal human lung fibroblasts (NHLF). Human IL-10 (hIL-10) complementary DNA (cDNA) was transfected into NHLF using an adenoviral vector. No significant changes were observed in proliferation, fibronectin or procollagen type I production in the NHLF transfected with hIL-10 cDNA. Interferon (IFN)-gamma significantly inhibited cell proliferation and extracellular matrix production in a dose-dependent manner. Transfection of hIL-10 cDNA significantly relieved the suppressive effects of IFN-gamma in NHLF. Transforming growth factor (TGF)-beta production was not significantly affected by either transfection of hIL-10 cDNA or the addition of IFN-gamma. The relief of the suppressive function of IFN-gamma by IL-10 suggested that IL-10 is indirectly involved in the remodeling process in the lung interstitium.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11172617&dopt=Abstract

Brain Res. 2001 Feb 23;892(2):380-5.
NO as an autocrine mediator in the apoptosis of activated microglial cells: correlation between activation and apoptosis of microglial cells.

Lee P, Lee J, Kim S, Lee MS, Yagita H, Kim SY, Kim H, Suk K.

Department of Herbal Pharmacology, Graduate School of East-West Medical Science, Kyung Hee University, Hoegi-dong, Tongdaemun-ku, 130-701, Seoul, South Korea.

Abnormal activation of microglial cells has been implicated in various neurodegenerative diseases. Microglial activation needs to be tightly regulated for physiological maintenance and normal functioning of the central nervous system. Potential mechanisms for the down-regulation of activated microglial cells are the deactivation or elimination of activated cells. We hypothesized that the elimination of activated microglial cells by apoptosis is one of the key mechanisms of auto-regulation of activated microglial cells. To test this hypothesis, we utilized BV-2 mouse microglial cells and rat primary microglial cultures exposed to activating agents such as lipopolysaccharide and interferon-gamma, and investigated a possible correlation between apoptosis and activation of these cells. We found that the activation of microglial cells led to apoptotic death, and the activation state of microglial cells inversely correlated with cell viability. We have also demonstrated that: (i) NO was produced by activated microglial cells in a manner dependent on time and dose of activating agents; (ii) inhibition of NO synthesis by iNOS inhibitor blocked the apoptosis of activated microglial cells; (iii) an exogenous NO donor induced apoptosis of microglial cells; and (iv) inhibition of TNFalpha or FasL using neutralizing antibodies did not affect activation-induced apoptosis of microglial cells. These results indicated that activation of microglial cells leads to the production of NO, which in turn acts as the major mediator of cellular apoptosis in an autocrine fashion. Our work suggests the presence of auto-regulatory mechanism for microglial activation, which may have relevance in the pathogenesis of various neurodegenerative diseases possibly resulting from 'over-activation' of microglial cells.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11172787&dopt=Abstract

FEMS Immunol Med Microbiol. 2001 Feb;30(1):1-7.
A model of the real-time correlation of viral titers with immune reactions in antibody-dependent enhancement of dengue-2 infections.

Chen RF, Yeh WT, Yang MY, Yang KD.

Chang Gung Children's Hospital at Kaohsiung, Chang Gung University, 123 Ta-Pei Road, Niau-Sung, 833, Kaohsiung, Taiwan.

We simultaneously assessed dengue-2 virus (DEN-2) titers by real-time quantitative reverse transcription-polymerase chain reaction (RT-PCR) and immune reactions including interleukin-4 (IL-4), interferon-gamma (IFN-gamma) and prostaglandin E(2) (PGE(2)) production by human mononuclear cells (MNLs) in a model of antibody-dependent enhancement (ADE). We found that DEN-1 immune sera at 1:100 and 1:250, but not those at 1:10 or control sera, enhanced DEN-2 infections in human MNLs as assessed by the fluorogenic RT-PCR technique. The enhanced profiles of DEN-2 infections determined by the RT-PCR in 6 h were reproducible by the standard plaque-forming unit (PFU) measurement established after 7 days. The ADE-enhanced DEN-2 titers determined by the RT-PCR were 5.5-33-fold higher than those detected by PFU assay, suggesting that total virions during infections were much higher than the viable ones detected by PFU assay. MNLs in response to DEN-2 infections had higher IFN-gamma and PGE(2) production. However, the enhancement of DEN-2 infections by DEN-1 immune sera in MNLs was not associated with further enhancement of IFN-gamma production. In contrast, the presence of subneutralizing DEN-1 immune sera that enhanced DEN-2 infections also enhanced PGE(2) but not IL-4 production. The results of this study suggest that ADE of DEN-2 infections associated with induction of immunosuppressive mediators such as PGE(2) and IL-4 can be simultaneously assessed in a real-time fashion.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11172984&dopt=Abstract

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