Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P30536 (PBS)
 9,886 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The (NZB X NZW)F1 mouse is recognized as an important animal model of the human disease systemic lupus erythematosus (SLE). Groups of NZB/W F1 mice were treated either with IFN-gamma or with PBS. The results demonstrate that IFN-treated animals have accelerated development of fatal immune complex glomerulonephritis relative to age-matched controls. On the other hand, administration of mAbs specific for IFN-gamma to such mice from 4 to 7 mo of age resulted in significant remission. Development of both proteinuria and anti-DNA antibodies were delayed and survival at 11 mo was increased from less than 20% to 95% in treated mice relative to controls (p less than or equal to 0.001). These findings may have therapeutic implications for the treatment of SLE.
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PMID:In vivo treatment of (NZB X NZW)F1 lupus-like nephritis with monoclonal antibody to gamma interferon. 311 9

Conditions are described for the production of mouse interferon by L929 cells cultured as monolayer in roller tubes. Kinetics of interferon production are described. Release of interferon into the culture medium began at 9 h after induction. One hour earlier the nutrient medium (MEM with 10% calf serum) was replaced with serum-free medium (MEM or PBS). Longer time of intensive nutrition of cells influenced the IFN yield. Interferon titers obtained with this method were higher than those obtained with the routine method of interferon production in which the nutrient media were replaced into serum-free media immediately after induction.
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PMID:Increase in L929 cell interferon production in serum-free media. 714 25

Sixty C3H/He male mice were divided into 6 groups (10 mice per group). Control mice (group I) received three injections of PBS and drinking water. Mice of group II were injected with PBS but drinking water was substituted by ethanol solutions with increasing concentration of ethanol (w/v): 6% during the first week of experiment, 10% during the second and 20% during the third week. Group III received three intraperitoneal injections of CCl4 (1 ml of CCl4 per 1 kg of body weight) and water for drinking. Group IV was treated with CCl4 as group III, but drinking water was substituted by ethanol solutions with increasing concentrations as in the group II. Samples of blood, liver and spleen were taken 24 h after the third acute CCl4 intoxication. Group IIIa and IVa were treated as group III and IV, respectively, but samples of blood and organs were taken a week after the last CCl4 injection. A typical increase in serum ALT and necrosis of hepatocytes as confirmed by the histological examination, was observed 24 h after CCl4 injections (group III and IV). A week later (group IIIa and IVa) regenerative changes in the liver and a significant decrease in ALT serum activity was observed. Acute CCl4 intoxication (group III) significantly decreased IFN production in liver and spleen cells isolated 24 h after the last CCl4 injection. Combined CCl4 and ethanol administration affected very strongly IFN production (group IV).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of carbon tetrachloride intoxication and ethanol ingestion on interferon production in mice. 748 75

Our studies were undertaken to evaluate early events associated with IFN expression and IFN-induced cellular changes in the spleen. Polyinosinic-polycytidylic acid (poly(I:C)) was used to induce IFN in C57BL/6 mice. Biologically active IFN was present in spleens and sera of poly(I:C)-treated mice as early as 3 h and peaked at 6 to 12 h posttreatment. Neutralization assays and Northern blot analyses demonstrated that IFN-beta was the form of IFN preferentially induced in the spleens. Immunohistochemical staining and in situ hybridization studies of splenic tissue sections demonstrated that, although many cells were induced to express low levels of IFN-beta, low frequency cells were particularly potent expressers of IFN-beta. Perivascular cells expressed high levels of IFN-beta. Other positive cells were localized in red pulp at early times and in white pulp at later times posttreatment. Histologic examination of splenic sections showed that the IFN production was accompanied by dramatic architectural changes. There were significant 1.4-fold increases in the proportion of white pulp area and > 50% decreases in red pulp leukocyte number. These architectural changes appeared at 6 h and lasted through 36 h after poly(I:C) treatment. They were not due to increased cell proliferation as splenic weights and cell yields were not elevated. The changes in splenic leukocyte distribution were shown to be a result of IFN induction as: 1) treatment with anti-IFN antibodies inhibited poly(I:C)-induced depletion of red pulp leukocytes, and 2) administration of purified IFN-beta induced both an increase in white pulp area and a decrease in red pulp leukocytes. Splenic leukocytes were labeled with the lipophilic fluorescent dye, 1,1'-dioctadecyl-3,3,3',3'-tetramethyl indocarbocyanine perchlorate, to evaluate cell traffic after IFN induction. Poly(I:C) enhanced accumulation of cells in white pulp regions. In contrast to the 76 +/- 2 labeled cells that accumulated in 0.5 mm2 of white pulp area in control PBS-treated mice, 131 +/- 4 labeled cells accumulated in 0.5 mm2 of white pulp area in poly(I:C)-treated mice. The poly(I:C)-enhanced leukocyte accumulation in short term cell migration to white pulp regions was dependent on preexposure of both splenic leukocytes and recipient environments to the IFN inducer. These data demonstrate that poly(I:C) is a potent and rapid inducer of IFN-beta production by splenic cells and that IFN induces cellular redistribution in the spleen. The results suggest that margination of leukocytes into splenic white pulp may be another important immunoregulatory function of IFN.
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PMID:IFN induction and associated changes in splenic leukocyte distribution. 768 83

Expulsion of T. spiralis adult worms was accelerated in high-responder NIH mice vaccinated previously with complete Freund's adjuvant (CFA) emulsified in PBS, whereas the expulsion of this parasite from low-responder C57 BL/10 mice was unaffected. Incomplete Freund's adjuvant (IFA) did not induce protection and it was concluded that the mycobacterial component, present in CFA but absent from IFA, was responsible for inducing these non-specific protective effects. CFA did not induce T. spiralis-specific B- or T-cell responses, but high levels of IFN gamma from Con A-stimulated mesenteric lymph node cells of CFA-vaccinated NIH mice were detected. Such cytokine release was not produced by cells from the C57 BL/10 strain. It is therefore proposed that IFN gamma production is related to the mode of adjuvanticity and non-specific protective effects of CFA in this system.
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PMID:The mycobacterial component of complete Freund's adjuvant induces expulsion of the intestinal nematode Trichinella spiralis in mice. 857 44

The protective effects of recombinant IFN-alpha/beta on MHV-2cc-induced chronic and persistent hepatitis in athymic nude mice were examined. The mice intraperitoneally (ip) inoculated with MHV-2cc at day 0 of experiment were divided into 4 groups. Three of them were administered ip with recombinant IFN-alpha/beta at a daily dose of 1 x 10(3) IU from -1 (-1D-group), 0 (0D-group), and +1 day of experiment (+1D-group), respectively, for 3 consecutive weeks. The remaining one (control group) was given 0.1 ml/mouse of PBS from +1 day of the experiment in the same way. Three mice in each group were killed at 1, 2 and 3 weeks post inoculation (WPI) with MHV, respectively. The liver virus titer in the control group increased gradually and maintained high levels throughout the experimental period. In the IFN-groups, particularly in the -1D- and 0D-groups, the virus titers were significantly lower than that in control group. Histopathologically, focal hepatic lesions were observed at 1WPI and large irregular inflammatory lesions developed at 3WPI in the control group. Similar but somewhat less severe lesions were observed in the +1D-group. In the -1D- and 0D-groups, lesions were not observed at 1WPI and only small organized lesions with mononuclear cell infiltration were seen at 3WPI. In conclusion, it was clarified in the present study that the progression of MHV-2cc-induced chronic hepatitis in athymic nude mice was effectively prevented by extrinsic IFN-alpha/beta when administered from -1 day and 0 day of the virus infection.
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PMID:Protective effect of recombinant interferon (IFN)-alpha/beta on MHV-2cc-induced chronic hepatitis in athymic nude mice. 884 Jan 51

The role of endogenous interferon-gamma (IFN gamma) in the development of insulin-dependent diabetes mellitus (IDDM) in diabetes-prone BB rats was evaluated. Several groups of these animals were treated under different, experimental conditions with a purified polyclonal antibody (Ab), antirat IFN gamma. The results show that when administered at doses of 100 or 200 micrograms/week from the 30/33th until the 105th day of age, the anti-IFN gamma Ab reversibly reduced the incidence of IDDM compared to that in control rats treated with either irrelevant rabbit IgG or PBS. Moreover, when given up to the 105th day of age, these doses of anti-IFN gamma Abs exerted comparable preventive effects regardless of whether application started as early as within 24 h after birth or at the end of the prediabetic period (e.g. 70/75 days). In contrast, under none of the above experimental conditions did larger doses of anti-IFN gamma Ab (500 micrograms or 1 mg/week) exert antidiabetogenic effects in the BB rats. Apparently, this was due to the exuberant production of neutralizing Abs elicited by the large amount of the xenogeneic Ab injected. At histoimmunological analyses, the BB rats treated with 200 micrograms/ week anti-IFN gamma Abs from 30-80 days of age exhibited a milder insulitic process along with diminished spleen frequency of activated lymphoid cells (MHC class II and interleukin-2 receptor positive). Taken together, these results provide further in vivo evidence for the central pathogenic role of IFN gamma in BB rat IDDM and anticipate the usefulness of specific IFN gamma inhibitors in the prevention of the disease in the clinical setting. Defining novel and less immunogenic forms of specific IFN gamma inhibitors than xenogeneic Abs is important for improving the efficiency of anti-IFN gamma-oriented approaches.
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PMID:Prevention of spontaneous autoimmune diabetes in diabetes-prone BB rats by prophylactic treatment with antirat interferon-gamma antibody. 897 15

The innate immunity against murine cytomegalovirus (MCMV) at the early phase of infection is mediated by NK cells and macrophages. We studied the effects of hochu-ekki-to (HET), a traditional Chinese herbal medicine, on the regulation of innate immunity mediated by NK cells and macrophages. We found the oral administration of HET to increase both the number of leukocytes in the spleen and liver and the splenic NK cell cytotoxicity associated with the increased induction of serum IFN-alpha/beta after an MCMV infection but it had no effect on liver NK cells. However, no differences were found in the serum IL-12, IFN-gamma, TNF-alpha and nitric oxide (NO) production in the culture of macrophages between the HET- and PBS-treated mice on day 2 after MCMV infection. In addition, HET-treated splenic and peritoneal macrophages were found to show a higher intrinsic resistance against in vitro MCMV infection than that of PBS-treated mice. Therefore, the HET-induced effects on NK cells and macrophages selectively reduced the viral load in the spleen but not in the liver at an early phase of MCMV infection. HET may thus be useful in the treatment of human cytomegalovirus infection which commonly occurs in HIV-infected AIDS patients.
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PMID:Protective effects of hochu-ekki-to, a Chinese traditional herbal medicine against murine cytomegalovirus infection. 1042 45

Systemic lupus erythematosus (SLE)-prone female MRL-lpr / lpr (MRL-lpr) mice were treated with mouse or rat IFN-gamma under different experimental conditions, both prophylactically in 6- to 8 week-old animals and therapeutically in 12- to 18-week-old SLE-affected mice. It was found that IFN-gamma heterogeneously modulated the course of the disease in MRL-lpr mice. When administered prophylactically, IFN-gamma favorably modulated the histological, serological and clinical signs of the disease. Relative to untreated or PBS-treated control animals, the MRL-lpr mice which received IFN gamma were virtually free of inflammatory infiltration of the kidneys and the lungs, had lower levels of azotemia with reduction of both circulating IgG1, IgG2a and IgG3 and anti-double strand (ds) and single strand (ss) DNA antibodies, milder skin vasculitis, significantly reduced enlargement of their lymph nodes and lower weight of the spleens. IFN-gamma also lowered the rate of mortality of MRL-lpr mice. In contrast to these findings, therapeutically administered IFN-gamma worsened the course of the disease in MRL-lpr mice, which exhibited increased proteinuria, higher levels of IgG2a and IgG3 and anti-ds and -ss DNA antibodies, more aggressive nephritis and died at an earlier age than PBS-treated control mice. The dichotomic effect of IFN-gamma on disease manifestation in MRL-lpr mice offers new insights into the complex role of this cytokine in the regulation of systemic autoimmunity such as SLE.
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PMID:Dichotomic effects of IFN-gamma on the development of systemic lupus erythematosus-like syndrome in MRL-lpr / lpr mice. 1067 Nov 99

It has been reported that bacterial lipopolysaccharide (LPS) induces alveolar bone resorption and that the host immune system, especially activated T cells, plays a crucial role in osteoclastogenesis. On the other hand, interferon-gamma (IFN-g), which is produced by activated T cells, suppresses bone resorption both in vitro and in vivo. Thus, the question arises as to whether or not IFN-g production increases with increasing bone resorption. We previously demonstrated that repeated injections of Escherichia coli LPS into mouse gingiva causes osteoclast formation in alveolar bone. In the present study we observed changes in the IFN-g production of infiltrating cells in concurrence with bone resorption. Mice were repeatedly injected with 5 mg LPS 26 times every 48 hours. After the 16th injection, when the alveolar bone resorption reached a plateau, the concentration of LPS was altered (25 mg LPS or PBS alone). The level of bone resorption became significantly elevated, and the number of IFN-g- and interleukin-1 beta (IL-1b)-bearing cells also increased significantly in relation to bone resorption within the 25 mg LPS-injected group. On the other hand, few tartrate-resistant acid phosphatase positive cells, or IFN-g- and IL-1b-bearing cells, were seen in the PBS-injected group. These results suggest that alteration in IFN-g-bearing cells might play a role in counterbalancing LPS-induced bone resorption resulting from osteoclast activating cytokines such as IL-1b.
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PMID:Interferon-gamma production changes in parallel with bacterial lipopolysaccharide induced bone resorption in mice: an immunohistometrical study. 1204 12


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