scholarly journals Assessment of the levels of nitric oxide (NO) and cytokines (IL-5, IL-6, IL-13, TNF, IFN-gamma) in giardiosis

2011 ◽  
Vol 49 (2) ◽  
pp. 280-284 ◽  
Author(s):  
Joanna Matowicka-Karna ◽  
Maciej Kralisz ◽  
Halina Kemona
Keyword(s):  
Nitric Oxide ◽  
Ifn Gamma

scholarly journals Interleukin-4 stimulates cGMP production by IFN-gamma-activated human monocytes. Involvement of the nitric oxide synthase pathway

1994 ◽  
Vol 269 (13) ◽  
pp. 9811-9816
Author(s):  
J.P. Kolb ◽  
N. Paul-Eugene ◽  
C. Damais ◽  
K. Yamaoka ◽  
J.C. Drapier ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Interleukin 4 ◽  
Human Monocytes ◽  
Ifn Gamma ◽  
Cgmp Production ◽  
Oxide Synthase

scholarly journals The role of interleukin 12 and nitric oxide in the development of spontaneous autoimmune disease in MRL/MP-lpr/lpr mice.

1996 ◽  
Vol 183 (4) ◽  
pp. 1447-1459 ◽  
Author(s):  
F P Huang ◽  
G J Feng ◽  
G Lindop ◽  
D I Stott ◽  
F Y Liew
Keyword(s):  
Nitric Oxide ◽  
Autoimmune Disease ◽  
Cultured Cells ◽  
Daily Injection ◽  
Interleukin 12 ◽  
No Production ◽  
Necrosis Factor Alpha ◽  
Ifn Gamma ◽  
Peritoneal Cells ◽  
High Concentrations

MRL/MP-lpr/lpr (MRL/lpr) mice develop a spontaneous autoimmune disease. Serum from these mice contained significantly higher concentrations of nitrite/nitrate than serum from age-matched control MRL/MP-+/+ (MRL/+), BALB/c or CBA/6J mice. Spleen and peritoneal cells from MRL/lpr mice also produced significantly more nitric oxide (NO) than those from the control mice when cultured with interferon (IFN) gamma and lipopolysaccharide (LPS) in vitro. It is interesting to note that peritoneal cells from MRL/lpr mice also produced markedly higher concentrations of interleukin (IL) 12 than those from MRL/+ or BALB/c mice when cultured with same stimuli. It is striking that cells from MRL/lpr mice produced high concentrations of NO when cultured cells from MRL/+ or BALB/c mice. The enhanced NO synthesis induced by IFN-gamma/LPS was substantially inhibited by anti-IL-12 antibody. In addition, IL-12-induced NO production can also be markedly inhibited by anti-IFN-gamma antibody, but only weakly inhibited by anti-tumor necrosis factor alpha antibody. The effect of IL-12 on NO production was dependent on the presence of natural killer and possibly T cells. Serum from MRL/lpr mice contained significantly higher concentrations of IL-12 compared with those of MRL/+ or BALB/c control mice. Daily injection of recombinant IL-12 led to increased serum levels of IFN-gamma and NO metabolites, and accelerated glomerulonephritis in the young MRL/lpr mice (but not in the MRL/+ mice) compared with controls injected with phosphate-buffered saline alone. These data, together with previous finding that NO synthase inhibitors can ameliorate autoimmune disease in MRL/lpr mice, suggest that high capacity of such mice to produce IL-12 and their greater responsiveness to IL-12, leading to the production of high concentrations of NO, are important factors in this spontaneous model of autoimmune disease.

DOMINANT T CELL REGULATION ACHIEVED EX-VIVO VIA IFN-GAMMA/STAT-1 SIGNALING AND NITRIC OXIDE INDUCTION

2008 ◽  
Vol 86 (Supplement) ◽  
pp. 7
Author(s):  
G Feng ◽  
R Francis ◽  
W Gao ◽  
T Strom ◽  
M Oukka ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
T Cell ◽  
Ex Vivo ◽  
Cell Regulation ◽  
Ifn Gamma ◽  
T Cell Regulation

TNF-alpha and IFN-gamma induce expression of nitric oxide synthase in cultured rat medullary interstitial cells

1995 ◽  
Vol 269 (2) ◽  
pp. F212-F217 ◽  
Author(s):  
K. S. Lau ◽  
O. Nakashima ◽  
G. R. Aalund ◽  
L. Hogarth ◽  
K. Ujiie ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Smooth Muscle ◽  
Nitric Oxide Synthase ◽  
Vascular Smooth Muscle ◽  
Guanylyl Cyclase ◽  
Soluble Guanylyl Cyclase ◽  
Tnf Alpha ◽  
No Production ◽  
Ifn Gamma ◽  
Oxide Synthase

Cytokines increase the expression of the inducible (type II) nitric oxide synthase (NOS) in macrophages, liver, and renal epithelial cells. Previously, we found that cultured rat medullary interstitial cells (RMIC) contain high levels of soluble guanylyl cyclase. To determine whether these cells can also produce NO, we studied the effects of tumor necrosis factor-alpha (TNF-alpha) and interferon-gamma (IFN-gamma) on NO production, NOS II mRNA, and NOS II protein expression. Both TNF-alpha and IFN-gamma, in the presence of a low concentration of the other cytokine, caused dose-dependent increases in NO production. Exposure to TNF-alpha and IFN-gamma stimulated the production of NOS II mRNA, as determined by Northern blotting. Restriction mapping of reverse transcription-polymerase chain reaction products indicated that normal cells contained macrophage NOS II, whereas cytokine-stimulated cells contained primarily vascular smooth muscle NOS II and some macrophage NOS II. The appearance of NOS II protein was demonstrated by Western blotting. RMIC cell guanosine 3',5'-cyclic monophosphate accumulation increased 129-fold in response to the cytokines. NOS inhibitors decreased nitrite production. We conclude that 1) TNF-alpha and IFN-gamma induce the expression of vascular smooth muscle NOS II and production of NO in RMIC, and 2) NO acts as an autocrine activator of the soluble guanylyl cyclase in RMIC.

scholarly journals A hypoxia-responsive element mediates a novel pathway of activation of the inducible nitric oxide synthase promoter.

1995 ◽  
Vol 182 (6) ◽  
pp. 1683-1693 ◽  
Author(s):  
G Melillo ◽  
T Musso ◽  
A Sica ◽  
L S Taylor ◽  
G W Cox ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Inducible Nitric Oxide Synthase ◽  
Picolinic Acid ◽  
Transient Transfection ◽  
Ifn Gamma ◽  
Functional Studies ◽  
Inos Promoter ◽  
Oxide Synthase ◽  
Inducible Nitric Oxide

Picolinic acid, a catabolite of L-tryptophan, activates the transcription of the inducible nitric oxide synthase gene (iNOS) in IFN-gamma-treated murine macrophages. We performed functional studies on the 5' flanking region of the iNOS gene linked to a CAT reporter gene to identify the cis-acting element(s) responsible for the activation of iNOS transcription by picolinic acid. Transient transfection assays showed that the full-length iNOS promoter in the murine macrophage cell line ANA-1 was activated by the synergistic interaction between IFN-gamma and picolinic acid. Deletion or mutation of the iNOS promoter region from -227 to -209, containing a sequence homology to a hypoxia-responsive enhancer (iNOS-HRE), decreased picolinic acid- but not LPS-induced CAT activity by more than 70%. Functional studies using a tk promoter-CAT reporter gene plasmid demonstrated that the iNOS-HRE was sufficient to confer inducibility by picolinic acid but not by IFN-gamma or LPS. Electrophoretic mobility shift assays confirmed that picolinic acid alone induced a specific binding activity to the iNOS-HRE. Furthermore, we found that the iNOS-HRE activity was inducible by hypoxia and that hypoxia in combination with IFN-gamma activated the iNOS promoter in transient transfection assays and induced iNOS transcription and mRNA expression. These data establish that the iNOS-HRE is a novel regulatory element of the iNOS promoter activity in murine macrophages and provide the first evidence that iNOS is a hypoxia-inducible gene.

scholarly journals Mechanisms of innate resistance to Toxoplasma gondii infection

1997 ◽  
Vol 352 (1359) ◽  
pp. 1355-1359 ◽  
Author(s):  
J. Alexander ◽  
T. M. Scharton-Kersten ◽  
G. Yap ◽  
C. W. Roberts ◽  
F. Y. Liew ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Toxoplasma Gondii ◽  
Chronic Infection ◽  
Preliminary Evidence ◽  
Metabolic Inhibitors ◽  
Interleukin 12 ◽  
Tumour Necrosis Factor Receptor ◽  
Apparent Paradox ◽  
Ifn Gamma ◽  
Toxoplasma Gondii Infection

The interaction of protozoan parasites with innate host defences is critical in determining the character of the subsequent infection. The initial steps in the encounter of Toxoplasma gondii with the vertebrate immune system provide a striking example of this important aspect of the host–parasite relationship. In immunocompetent individuals this intracellular protozoan produces an asymptomatic chronic infection as part of its strategy for transmission. Nevertheless, T. gondii is inherently a highly virulent pathogen. The rapid induction by the parasite of a potent cell–mediated immune response that both limits its growth and drives conversion to a dormant cyst stage explains this apparent paradox. Studies with gene–deficient mice have demonstrated the interleukin–12 (IL–12)–dependent production of interferon gamma (IFN–gamma) to be of paramount importance in controlling early parasite growth. However, this seems to be independent of nitric oxide production as mice deficient in inducible nitric oxide synthase (iNOS) and tumour necrosis factor receptor were able to control early growth of T. gondii , although they later succumbed to infection. Nitric oxide does, however, seem to be important in controlling persistent infection; treating chronic infection with iNOS metabolic inhibitors results in disease reactivation. Preliminary evidence implicates neutrophils in effector pathways against this parasite distinct from that described for macrophages. Once initiated, IL–12–dependent IFN–gamma production in synergy with other proinflammatory cytokines can positively feed back on itself to induce ‘cytokine shock’. Regulatory cytokines, particularly IL–10, are essential to down–regulate inflammation and limit host pathology.

Differential nitric oxide production by microvascular and macrovascular endothelial cells

1997 ◽  
Vol 273 (1) ◽  
pp. L275-L281 ◽  
Author(s):  
M. Geiger ◽  
A. Stone ◽  
S. N. Mason ◽  
K. T. Oldham ◽  
K. S. Guice
Keyword(s):  
Nitric Oxide ◽  
Endothelial Cells ◽  
Endothelial Cell ◽  
Fold Increase ◽  
Cell Types ◽  
Microvascular Endothelial Cells ◽  
Tnf Alpha ◽  
Cell Populations ◽  
Ifn Gamma ◽  
Nitrite Production

Phenotypic heterogeneity among endothelial cell populations may account for important organ-specific behaviors. Experimental evidence suggests that endothelium-derived nitric oxide mediates certain of these unique responses. The purpose of these investigations was to compare rat pulmonary microvascular endothelial cells with pulmonary artery and aortic macrovascular endothelial cells in their ability to generate nitric oxide (NO). Cultures of these microvascular and macrovascular endothelial cells were incubated with interferon-gamma (IFN-gamma), tumor necrosis factor-alpha (TNF-alpha), and Salmonella typhimurium lipopolysaccharide (LPS) alone or in combination, and nitrite production was measured. Single-agent exposure with IFN-gamma (up to 1,000 U/ml), TNF-alpha (up to 60,000 U/ml), or LPS (up to 500 ng/ml) had little effect on nitrite generation. Nitrite production by rat aortic macrovascular endothelial cells (RAEC) was significantly greater than that by the rat lung microvascular endothelial cells (RLMVEC) when stimulated with TNF-alpha + IFN-gamma, LPS + IFN-gamma, or TNF-alpha + LPS. The maximal response by all endothelial cell types (approximately 15-fold increase in RAEC and 8-fold increase in RLMVEC) was observed with LPS + IFN-gamma. The nitrite generation from rat pulmonary artery endothelial cells was intermediate between RAEC and RLMVEC responses when stimulated with IFN-gamma + LPS or TNF-alpha. Similar patterns of heterogeneous inducible nitric oxide synthase mRNA induction occurred when Northern analysis of specimens from the cultured endothelial cell types was done. These data suggest that phenotypic heterogeneity between these endothelial cell populations is substantial and, by inference, that site-specific NO. generation may occur.

scholarly journals Tissue expression of inducible nitric oxide synthase is closely associated with resistance to Leishmania major.

1994 ◽  
Vol 180 (3) ◽  
pp. 783-793 ◽  
Author(s):  
S Stenger ◽  
H Thüring ◽  
M Röllinghoff ◽  
C Bogdan
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Inducible Nitric Oxide Synthase ◽  
Leishmania Major ◽  
Tissue Expression ◽  
Ifn Gamma ◽  
Oxide Synthase ◽  
Inducible Nitric Oxide

Previous studies with inhibitors of inducible nitric oxide synthase (iNOS) suggested that high-output production of nitric oxide (NO) is an important antimicrobial effector pathway in vitro and in vivo. Here, we investigated the tissue expression of iNOS in mice after infection with Leishmania major. Immunohistochemical staining with an iNOS-specific antiserum revealed that in the cutaneous lesion and draining lymph nodes (LN) of clinically resistant mice (C57BL/6), iNOS protein is found earlier during infection and in significantly higher amounts than in the nonhealing BALB/c strain. Similar differences were seen on the mRNA level as quantitated by competitive polymerase chain reaction. Anti-CD4 treatment of BALB/c mice not only induced resistance to disease, but also restored the expression of iNOS in the tissue. In situ, few or no parasites were found in those regions of the skin lesion and the draining LN which were highly positive for iNOS. By double labeling experiments, macrophages were identified as iNOS expressing cells in vivo. In the lesions of BALB/c mice, cells staining positively for transforming growth factor beta (TGF-beta), a potent inhibitor of iNOS in vitro, were strikingly more prominent than in C57BL/6, whereas no such difference was found for interleukin 4 or interferon gamma (IFN-gamma). In vitro, production of NO was approximately threefold higher in C57BL/6 than in BALB/c macrophages after stimulation with IFN-gamma. We conclude that the pronounced expression of iNOS in resistant mice is an important mechanism for the elimination of Leishmania in vivo. The relative lack of iNOS in susceptible mice might be a consequence of macrophage deactivation by TGF-beta and reduced responsiveness to IFN-gamma.

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