Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0038002 (splenomegaly)
 9,873 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

An animal model of a sublethal infection, utilizing murine cytomegalovirus (MCMV), was developed to determine whether immunological factors could contribute to the establishment of a persistent viral infection. Adult female C3H mice inoculated intraperitoneally with 10(5) plaque-forming units of MCMV developed splenomegaly 5 to 12 days after infection. Virus replicated to peak titers (10(3) to 10(6) plaque-forming units per g of tissue) in liver, spleen, lung, kidney, and salivary gland tissue during the acute phase of the infection (3 to 12 days); it then decreased to undetectable levels in all tissues except salivary gland. Serum interferon was detected as early as 12 h after infection, peaked at 36 h (1,093 U/ml), and was undetectable by 4 days after infection. MCMV-infected animals were hyporeactive to interferon induction with New castle disease virus on days 5 to 9 of the infection. Splenic lymphocyte reactivity to phytohemagglutinin and lipopolysaccharide was normal early during the course of the infection, was suppressed during the acute phase of the infection, and had returned to normal by day 18. These data indicate that several parameters of host defense are transiently suppressed during the course of a MCMV infection. The capacity of cytomegaloviruses to alter host resistance may be one factor that contributes to the establishment of a persistent infection.
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PMID:Alteration of host defense mechanisms by murine cytomegalovirus infection. 20 66

Mice could be significantly protected against infection with herpes simplex virus (HSV) by i.p. or i.v. injection of killed Corynebacterium parvum 7 days before infection. This protection was seen in inbred strains of mice with a different degree of sensitivity to HSV and after both i.p. and i.v. infection. Resistant mice immunosuppressed by X-irradiation and showing an increased susceptibility to HSV could also be protected by a previous injection of C. parvum. Elevated levels of interferon were demonstrated in the serum of mice injected with C. parvum 5 to 12 days previously. Four different strains of anaerobic coryneforms were compared and only those which were able to induce a systemic activation of the lymphoreticular system (as reflected by splenomegaly) protected against HSV infection. Protection against HSV-infection could also be demonstrated by using killed Bordetella pertussis. C. parvum also protected against Semliki Forest virus infection in two different strains of mice.
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PMID:Protection of mice against viral infection by Corynebacterium parvum and Bordetella pertussis. 21 22

SN11841 [4'-(9-acridinylamino)-methanesulfon-m-aniside] is an antitumor compound discovered by B.F. Cain. The LD50 for BALB/c mice with single intraperitoneal dosage is approximately 25 mg/kg. RLV-(Rauscher leukemia virus)-induced splenomegaly, a disease indicator in BALB/c mice, is inhibited at SN11841 doses not causing acute mortality. The life span of RLV-infected mice increases at some SN11841 doses. SN11841 does not have direct, or virolytic effects on RLV under conditions approximating those of antiviral effectiveness. SN11841 is cytotoxic for cells in tissue culture, as measured by inhibition of growth rate or vital dye uptake. At nontoxic concentrations SN11841 has no effect on RLV infectivity for murine cells, as determined by XC-cell induced syncytium formation. SN11841 has antiviral activity against vaccinia virus in tissue culture but is inactive against herpes simplex (Type 1), vesicular stomatitis, encephalomyocarditis, or reoviruses. SN11841 apparently does not act by inducing interferon. SN11841 is chemically labile, particularly in the presence of sulfhydryl compounds, but the degradation products resulting from prolonged storage in media are neither cytotoxic nor antiviral.
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PMID:Antiviral activities of 4'-(9-acridinylamino)-methanesulfon-M-aniside (SN11841). 28 Jan 45

Daily subcutaneous injections of 5 to 10 million units of partially purified human leukocyte interferon were given to newborn rabbits for 2 weeks or 1 month. The control groups received mock interferon, saline or nothing. The interferon treatment had no overt effect on the development of the animals during the period of treatment. The rabbits treated with interferon had leukocytosis, splenomegaly and prolonged postnatal extramedullary hematopoiesis in the liver and spleen. Certain immune responses were also demonstrated in the rabbits treated with interferon and mock interferon preparations. Platelet counts and the serum-ASAT, -ALAT, -LD and alkaline phosphatase values were normal.
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PMID:Toxicity studies with human leukocyte interferon in newborn rabbits. 69 30

The prolonged adminstration of rabbit anti-mouse L cell interferon globulin had a marked potentiating effect on Rauscher Murine Leukemia Virus (MuLV-R) infection in BALB/c mice, as shown by spleen size. Normal rabbit globulin had a lesser, but still significant, augmenting effect on splenic enlargement. It was possible to discriminate quantitatively between the non-specific enhancement of splenomegaly in MuLV-R infected mice due to antigenic stimulation with normal rabbit globulin and the effects due to elimination of endogenous interferon by specific antibodies. The difference in the spleen-enlarging activity between the anti-interferon IgG and normal rabbit IgG was found to be maximal 3-4 weeks after infection when potent, diluted anti-interferon IgG (58 microgram protein per dose) was used. It would appear that the endogenous interferon, even prodcued in undetectable amounts, plays an essential role in controlling infection with an oncogenic virus.
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PMID:Enchancement of leukemogenesis in mice after prolonged administration of anti-interferon or normal rabbit globulin. 92 45

A female patient simultaneously developed hematologic evidence of hairy cell leukemia and marked but short-lived inflammatory involvement of a number of joints. Both these groups of symptoms resolved simultaneously and rapidly under alpha-2 interferon therapy. This course suggests that the arthritis was a rheumatologic manifestation of the hematologic disease. The concomitant occurrence in this patient of arthritis, splenomegaly and leukopenia was suggestive of Felty syndrome: these two conditions need to be differentiated.
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PMID:[Polyarthritis revealing hairy cell leukemia]. 130 95

Mice infected with LP-BM5 murine leukemia viruses develop a syndrome, termed mouse AIDS (MAIDS), characterized by increasingly severe immunodeficiency and progressive lymphoproliferation. Virus-infected mice were examined for the ability to resist acute infection and to control chronic infection with the protozoan Toxoplasma gondii, a major opportunistic pathogen of individuals infected with human immunodeficiency virus. Mice infected with the retroviruses for 2 or 4 weeks responded normally to challenge with the parasite, but mice inoculated with the protozoan 8 or 12 weeks after viral infection died with acute disease due to T. gondii. Increased sensitivity to acute infection was associated with a reduced ability to produce gamma interferon (IFN-gamma) and with established changes in CD4+ T-cell function. Mice latently infected with T. gondii and then inoculated with the retrovirus mixture were found to reactivate the parasite infection, with 30 to 40% of dually infected animals dying between 5 and 16 weeks after viral infection. Reactivation was associated with reduced proliferation and impaired production of IFN-gamma in response to stimulation with soluble T. gondii antigens or to concanavalin A. Continuing resistance to lethal reactivation in the remaining mice was shown to require CD8+ T cells and expression of IFN-gamma. In addition, it was found that chronic infection with T. gondii altered the course of MAIDS by inhibiting the progression of splenomegaly and immunodeficiency and reducing the expression of both the helper and etiologic defective viruses. These results support previous studies which indicate that infection with T. gondii is controlled by synergistic interactions between CD4+ and CD8+ T cells, the functions of which are progressively impaired during the course of MAIDS.
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PMID:Opportunistic infections and retrovirus-induced immunodeficiency: studies of acute and chronic infections with Toxoplasma gondii in mice infected with LP-BM5 murine leukemia viruses. 132 58

(B10.A x A/WySn)F1 mice, infected with the Friend virus (FV) complex, were used as a predictive therapeutic model for AIDS. These infected mice exhibit many of the viral and immunologic manifestations of AIDS. Bropirimine (2-amino-5-bromo-6-phenyl-4[3H]pyrimidinone, ABPP) is an immunomodulating compound which has been shown to inhibit other viral infections. Oral (per os treatment) dosages of ABPP ranging from 50 to 400 mg/kg/day for 3 days resulted in increased numbers of infectious centers in the infected mice and increased splenomegaly and percentage of Ig+ (B cells) in spleens of infected and uninfected mice. Decreased percentages of total Thy-1.2+ (total T) cells and L3T4+ (T-helper) cells were seen in both uninfected and infected mice and a slightly decreased percentage of Ly-2+ (T-suppressor/cytotoxic) cells was observed in spleens of the infected mice. No effect on Ly2+ cells in spleens of uninfected mice was found. Intraperitoneal injection, single or multiple, of 20-200 mg/kg ABPP prior to FV injection resulted in increased spleen weights but had no effect on numbers of infectious centers in the spleens or on FV antibody titers in the plasma. Intraperitoneal treatment of uninfected mice with ABPP resulted in slight or no changes in percentages of Thy-1.2+, L3T4+ and Ly-2+ cells. Mice receiving multiple exposures of ABPP had an increase in percentage of splenic B cells and a depressed response to the T cell mitogen PHA. Treatment with ABPP induced the production of interferon (IFN); however, a state of hyporesponsive IFN production was seen following multiple administrations of ABPP. These data suggest that the immunomodulator ABPP may have an enhancing effect on this retroviral disease.
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PMID:Murine retroviral disease-enhancing effects of a pyrimidinone immunomodulator. 144 28

We have followed for 33 months the changes that occurred in natural killer (NK) cell numbers and activity in a patient (A) with hairy cell leukaemia (HCL), using a single cell assay and a microcytotoxicity assay. The composition of the peripheral blood mononuclear cell population and malignant cell phenotype were also analysed. During this period he received treatment with interferon and his grossly enlarged spleen was removed. Four further patients were also studied, two were splenectomized and all had received treatment with interferon. In four of the five patients studied there was an apparent link between low NK activity and presence of a tumour-infiltrated spleen, and in the fifth patient, who was aleukemic and had no splenomegaly, NK function was related to disease activity. There was no correlation between NK activity and the number of target binding (TB) cells in these five patients. IFN had little direct effect on overall NK activity, but the proportion of killing cells among TB cells was increased. Three patients showed binding of several cells to a single target. Further analysis revealed that in the patients most of the TB cells were not CD56-positive NK cells, in contrast to TB cells from normal subjects. In patient A a large proportion (84%) of TB cells were identified as malignant cells and in patient E 15% of TB cells were malignant cells. The phenotype of the malignant cells was: CD19+, HLA-DR+ and CD25(Tac)+, except for patient A. In this patient the hairy cells were positive for the NK marker CD56 as well as the monocyte marker CD14. Furthermore, a change occurred in phenotype as only later samples carried CD25. It is concluded that the level of NK function correlates closely with disease activity in HCL and that competitive target cell binding by malignant cells may be one cause of depressed NK-cell function in hairy cell leukaemia.
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PMID:Natural killer cell function and malignant cell phenotype in hairy cell leukaemia. 153 17

A sarcomatoid renal cell carcinoma has been isolated from a patient with Stauffer's syndrome. The tumor, designated BA1119, has been established in tissue culture over 80 passages. Subcutaneous deposition of BA1119 in athymic mice induced splenomegaly and hepatic dysfunction which became fatal within four weeks without metastasis. Suramin is a synthetic polyanionic compound which is capable of altering the function of a number of biologic systems and inhibiting the activity of a variety of protein and growth factors. In this study we attempted to study the effect of suramin on growth of BA1119 in culture and in nude mice. Suramin, at 300 micrograms/ml., had a profound inhibitory effect on cell growth during a six-day culture period. Suramin given i.p. weekly to nude mice at clinically relevant doses (200 mg./kg.) caused significant shrinkage of subcapsular tumor deposits. Splenic hypertrophy secondary to BA1119-induced Stauffer's syndrome was inhibited by suramin. Synergistic effect with enhanced cytotoxicity on BA1119 cells was observed when suramin (100 micrograms/ml.) was used in combination with lymphokines, such as gamma interferon (500 units/ml.) and alpha tumor necrosis factor (300 ng./ml.). These results may suggest a therapeutic efficacy of suramin in renal cell carcinoma patients with Stauffer's syndrome.
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PMID:Inhibitory effects of suramin on a human renal cell carcinoma line, causing nephrogenic hepatic dysfunction. 155 13


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