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Eur J Immunol. 1999 Feb;29(2):643-9.
Combined effects of IL-12 and IL-18 on the clinical course and local cytokine production in murine pulmonary infection with Cryptococcus neoformans.

Qureshi MH, Zhang T, Koguchi Y, Nakashima K, Okamura H, Kurimoto M, Kawakami K.

The First Department of Internal Medicine, Faculty of Medicine, University of the Ryukyus, Nishihara, Okinawa, Japan.

We reported recently that interleukin (IL)-12 and IL-18 synergistically increased the fungicidal activity of mouse peritoneal exudate cells against Cryptococcus neoformans by inducing the production of interferon (IFN)-gamma by natural killer (NK) cells. To confirm these findings in vivo, we examined the effect of combined treatment using these two cytokines on the course of experimentally induced pulmonary and disseminated cryptococcosis in mice. IL-12 and IL-18 were used at subtherapeutic doses (0.005 and 2 microg/mouse/day, respectively). A single administration of either cytokine was not effective in protecting mice against the infection, while combined treatment significantly prolonged survival time of infected mice and reduced the lung and brain loads of organisms. These protective effects were associated with elevated IFN-gamma and reduced IL-4 levels in bronchoalveolar lavage fluid. Finally, depletion of NK and gammadelta T cells, but not of CD4+ T cells, by administration of specific antibodies, significantly reduced the production of IFN-gamma in lungs by IL-12/IL-18 treatment during the 7 days of infection. Our results demonstrated that IL-12 and IL-18 protected mice against cryptococcal infection in a synergistic manner by enhancing the local production of IFN-gamma by NK and gammadelta T cells in the early phase of infection and by suppressing the production of IL-4 in lungs.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10064081&dopt=Abstract

Am J Physiol. 1999 Mar;276(3 Pt 1):C700-10.
Chemokine expression in CF epithelia: implications for the role of CFTR in RANTES expression.

Schwiebert LM, Estell K, Propst SM.

Department of Physiology and Biophysics, University of Alabama, Birmingham, Alabama 35294, USA.

To delineate the mechanisms that facilitate leukocyte migration into the cystic fibrosis (CF) lung, expression of chemokines, including interleukin-8 (IL-8), monocyte chemoattractant protein-1 (MCP-1), and RANTES, was compared between CF and non-CF airway epithelia. The findings presented herein demonstrate that, under either basal conditions or tumor necrosis factor-alpha (TNF-alpha)- and/or interferon-gamma (IFN-gamma)-stimulated conditions, a consistent pattern of differences in the secretion of IL-8 and MCP-1 between CF and non-CF epithelial cells was not observed. In contrast, CF epithelial cells expressed no detectable RANTES protein or mRNA under basal conditions or when stimulated with TNF-alpha and/or IFN-gamma (P </= 0.05), unlike their non-CF counterparts. Correction of the CF transmembrane conductance regulator (CFTR) defect in CF airway epithelial cells restored the induction of RANTES protein and mRNA by TNF-alpha in combination with IFN-gamma (P </= 0.05) but had little effect on IL-8 or MCP-1 production compared with mock controls. Transfection studies utilizing RANTES promoter constructs suggested that CFTR activates the RANTES promoter via a nuclear factor-kappaB-mediated pathway. Together, these results suggest that 1) RANTES expression is altered in CF epithelia and 2) epithelial expression of RANTES, but not IL-8 or MCP-1, is dependent on CFTR.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10069998&dopt=Abstract

Clin Exp Allergy. 1999 Jan;29(1):124-32.
Comparison of cytokine secretion profiles provoked in mice by glutaraldehyde and formaldehyde.

Dearman RJ, Basketter DA, Evans P, Kimber I.

Zeneca Central Toxicology Laboratory, Alderley Park, Macclesfield, UK.

BACKGROUND: Glutaraldehyde and formaldehyde are commonly used sterilizing agents that are known skin sensitizers. There is some controversy, however, regarding their capacity to cause respiratory allergy. The authors have demonstrated previously that topical exposure of mice to chemical contact allergens such as 2,4-dinitrochlorobenzene (DNCB) or respiratory allergens such as trimellitic anhydride (TMA) induces characteristic cytokine secretion profiles consistent with the selective activation of T helper1 (TH1)- and TH2-type cells, respectively. OBJECTIVE: To investigate the quality of immune response provoked following topical exposure of mice to these materials. METHODS: BALB/c strain mice were exposed topically to 50% formaldehyde or to various concentrations of glutaraldehyde in acetone. Control animals were treated concurrently with the reference contact allergen DNCB (1% in acetone:olive oil [AOO]) or with the reference respiratory sensitizer TMA (10% in AOO). Thirteen days after the initiation of exposure, draining lymph node cells (LNCs) were cultured for 12-120h and cytokine content of supernatants analysed by cytokine-specific enzyme-linked immunosorbent assay. RESULTS: DNCB-alpha and formaldehyde-activated LNCs produced high levels of the TH1-type cytokine interferon gamma, but little of the TH2-type products interleukins 4 and 10. TMA- and glutaraldehyde-stimulated LNCs displayed the converse TH2-type pattern of cytokine expression. CONCLUSIONS: These data are consistent with glutaraldehyde, but not formaldehyde, having significant potential to cause allergic sensitization of the respiratory tract.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10051711&dopt=Abstract

Arch Mal Coeur Vaiss. 1999 Jan;92(1):53-6.
[Third degree atrio-ventricular block induced by interferon alpha. Report of a case]

[Article in French]

Parrens E, Chevalier JM, Rougier M, Douard H, Labbe L, Quiniou G, Broustet A, Broustet JP.

Service de cardiologie A, Hopital cardiologique du Haut-Leveque, Pessac.

Iatrogenic third degree atrioventricular block due to alpha interferon is rare. The authors present a case which occurred with low dosage, regressed when treatment was withdrawn and reappeared when treatment was reintroduced. The physiopathological mechanism of disease of the conduction pathways and its general cardiotoxicity is not yet understood. The secondary effects of this increasingly widely used anti-tumoral and anti-infectious drug should be recognised in order to prevent them. Initial cardiological investigation and follow-up are indicated to ensure this prevention.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10065282&dopt=Abstract

AIDS. 2003 Mar 7;17(4):495-504.
Interferon-alpha restores HIV-induced alteration of natural killer cell perforin expression in vivo.

Portales P, Reynes J, Pinet V, Rouzier-Panis R, Baillat V, Clot J, Corbeau P.

Laboratoire d'Immunologie, Hopital Saint Eloi, the Service des Maladies Infectieuses et Tropicales, Hopital Gui de Chauliac, Montpellier, France.

OBJECTIVE: The percentage and the activity of natural killer (NK) cells are known to be decreased in HIV-infected patients. However, the mechanisms responsible for this NK deficiency are poorly understood. Because of the role of NK cells in the host defence against microbial infections, this defect contributes to the virus-induced immune deficiency. The aim of the present study was to better understand this defect in order to be able to restore NK function in HIV infection. DESIGN AND METHODS: The expression of the cytolytic mediators perforin and granzyme A was analysed by flow cytometry, the lytic activity of peripheral blood NK cells of HIV-infected patients was analysed by cytotoxic assay, and the expression of perforin was followed during administration of interferon (IFN)alpha attached to polyethylene glycol (PEG)-IFNalpha. RESULTS: The lytic activity and the expression of perforin and granzyme A was low in NK cells of infected individuals in comparison with normal control volunteers. In both groups NK cytotoxic capacity was linked to perforin expression. The low perforin expression in HIV-infected subjects negatively correlated with HIV RNA plasma level. administration of PEG-IFNalpha restored perforin expression even in patients whose viral load was not reduced by this treatment. CONCLUSIONS: These results suggest that HIV-induced NK deficiency could be partly mediated by a defect in perforin and granzyme A expression, and that PEG-IFNalpha could be used in infected subjects to directly improve their natural immunity in addition to eventually reducing their viraemia.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12598769&dopt=Abstract

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