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

Infection with Listeria monocytogenes stimulates T cell proliferation and T cell-derived lymphokine production. The release of lymphokines, in turn, "activates" macrophages, enhancing their bactericidal capacity. Because prior studies suggest that I-A+ accessory cells play a critical role in this pathway, we assessed the effects of an anti-I-A antibody on the murine host resistance to listerial infection. To this end, we infused Listeria into control C57BL/6 mice (I-Ab haplotype) and mice of the same strain which had been pretreated 18 hr earlier with D3137 (a monoclonal IgG2a anti-I-Ab,d antibody). Preliminary studies demonstrated that this antibody can markedly inhibit antigen-induced proliferation of Listeria-dependent T cells in vitro and (at a dose of 1 mg/animal) can markedly reduce I-A expression on splenocytes in vivo. Even though D3137 pretreatment prevented the splenomegaly normally observed after Listeria infusion into mice, it protected animals infused with otherwise lethal concentrations of Listeria. Because antibody-treated animals had sevenfold fewer organisms in their spleens 18 hr after infection and 1000-fold fewer organisms than control animals 3 days after infection, improved survival resulted from an antibody-induced increase in the bactericidal capacity of the MPS. Protection was not noted when C1.18.4 (an IgG2a myeloma protein without known antibody activity) was infused into C57BL/6 mice or when D3137 was infused in B10.BR (I-Ak) mice. D3137 also protected (B10 X B10.BR)F1 mice (which are hybrids bearing I-Ab and I-Ak), suggesting that complete blockade of antigen presentation is not a prerequisite for its protective action. Further studies into the mechanism for these effects may provide new insights into the pathophysiology of MPS activation in response to immunologic challenge.
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PMID:The effects of an anti-I-Ab antibody on murine host resistance to Listeria monocytogenes. 349 82

Immunization with avirulent Salmonella typhimurium strain SL3235, a smooth, aroA- derivative, was shown to induce high levels of resistance to challenge with virulent S. typhimurium in innately hypersusceptible C3H/HeJ mice and inherently resistant C3H/HeNCrlBR mice. Strain SL3235 is one of a class of avirulent aroA- derivatives made from various strains and species of Salmonella that are being considered as vaccine candidates for cattle and humans. This paper supports their efficacy and potential utility in this regard. In C3H/HeJ mice, immunity against over 1,000 50% lethal doses of virulent S. typhimurium was evident as early as 3 days after immunization and persisted for at least 7 months. Further, the vaccine was effective over a broad spectrum of doses, ranging from 10(4) to 10(6) organisms. Infection with SL3235 led to marked splenomegaly in both mouse strains. The relationship of splenomegaly to the growth kinetics and colonization by SL3235 in the spleens of infected C3H/HeJ and C3H/HeNCrlBR mice was followed. SL3235 initially multiplied slowly in the spleens of both mouse strains and then was rapidly cleared. Less multiplication was seen in the resistant C3H/HeNCrlBR mice than in C3H/HeJ mice. Maximum splenomegaly occurred after clearance of the organism had begun. Protection against virulent S. typhimurium persisted after virtually all of the SL3235 vaccine strain had been cleared from the spleen. Cross-protection against Listeria monocytogenes was evident, but had a later onset, waned by 21 days, and was not detectable by 1 month after vaccination. Demonstration of this cross-protection is consistent with the interpretation that SL3235 induces cellular immunity. One-week immune spleen cells adoptively transferred anti-S. typhimurium and anti-L. monocytogenes immunity. T cell-enriched fractions were ineffective in adoptive transfer, as were spleen cells taken 2 weeks or later after immunization. Protective capacity was in the adherent cell fraction and seemed to be associated with macrophages. Evidence for induction of a population of sensitized T cells was obtained by using a peritoneal exudate T-lymphocyte proliferation assay on peritoneal T lymphocytes collected 1 to 3 months after SL3235 infection.
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PMID:Immunity to Salmonella typhimurium infection in C3H/HeJ and C3H/HeNCrlBR mice: studies with an aromatic-dependent live S. typhimurium strain as a vaccine. 388 60

Infection of adult BALB/c mice with Friend disease virus results in a leukemia-like disease characterized by erythropoietic changes and splenomegaly. A marked depression of formation of cellular and serum antibody occurs in infected animals. Electron-microscopic examination of the ultrastructure of spleen sections from infected mice with depressed immunity revealed that virus particles can be detected only in immature blastlike lymphoid cells and not in plasmocytes characteristic of the immune response in spleens of noninfected mice immunized with sheep erythrocytes.
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PMID:Leukemia virus suppression of antibody-forming cells: ultrastructure of infected spleens. 563 63

We had shown previously that the prevalence of human T-cell leukemia/lymphoma virus type I (HTLV-I)-antibody positivity is high in Jamaican non-Hodgkin's lymphoma (NHL) patients and that virus-positive patients have the clinical features and poor prognosis of adult T-cell leukemia/lymphoma (ATL). Sixty-two % of 45 NHL patients diagnosed consecutively between 2/1/82 and 1/31/84 and studied prospectively were HTLV-I-antibody positive. Skin involvement (38%), hypercalcemia (44%), and leukemia (40%) were unusually prevalent and there was a strong association (p less than 0.05) with HTLV-I-antibody positivity. Fifty-two % of the patients had bone marrow infiltration, and 74% of these patients were HTLV-I-antibody positive (p = 0.06). Lymphadenopathy (96%), hepatomegaly (60%), and splenomegaly (25%) were detected with about the same frequency as in other series of NHL patients with advanced disease, and 61-88% of these patients were HTLV-I-antibody positive. Patients were classified into those with "typical ATL" (NHL associated with 2 of the 4 features i) hypercalcemia; ii) histologically proven skin infiltration; iii) leukemia; and iv) bone marrow infiltration, providing that the morphology of infiltrating or leukemic cells was characteristic of ATL; those "consistent with ATL" (NHL associated with 1 of these 4 features); and "non-ATL" (NHL without any of these 4 additional features). Thirty-two (71%) of the NHL patients were ATL patients, i.e., had features typical of or consistent with ATL, and 78% of these were HTLV-I-antibody positive. HTLV-I provirus was detected in tumour cells of all HTLV-I-antibody positive patients tested. Three (23%) of the non-ATL patients were HTLV-I-antibody positive. There was no correlation between histopathological features and the clinical classification or HTLV-I-antibody positivity. Median survival of ATL and non-ATL patients was 16 and 53 weeks. Although the disease was usually fulminant, 34% of the ATL patients had a subacute or chronic course. Skin involvement and leukemia were prominent in these patients. Hypercalcemia was the chief prognostic determinant. Median survival of hypercalcemic and normocalcemic ATL patients was 13 and 86 weeks (p less than 0.05). Hypercalcemia caused 10 deaths, infections 12, and death was due to tumour progression in 4 patients. Infections were usually due to pyogenic organisms and only 2 patients had systemic opportunistic infections. Six (27%) of 22 chronic lymphocytic leukemic (CLL) patients were HTLV-I-antibody positive.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Adult T-cell leukemia/lymphoma in Jamaica and its relationship to human T-cell leukemia/lymphoma virus type I-associated lymphoproliferative disease. 610 Jun 52

Infection of A/J mice with Trypanosoma cruzi results in the polyclonal activation of B lymphocytes in vivo as assessed by the spontaneous plaque-forming cell (PFC) response to trinitrophenyl and to goat, equine, and sheep erythrocytes. The peak response to these antigens is found at 5 to 6 days of infection. Additionally, a polyclonal response to syngeneic erythrocytes can be detected in infected mice by using aged but not fresh indicator cells. Polyclonally stimulated PFC to human gamma-PFC found late in infection during a period of marked splenomegaly and parasitemia. This trypanosoma-induced polyclonal B cell activation may well be responsible for the abnormalities in immunoglobulin synthesis and secretion that have been reported to occur during human infection with T. cruzi.
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PMID:Polyclonal B lymphocyte activation during Trypanosoma cruzi infection. 615 88

Infection of mice with Brucella abortus strain 19 provides a most useful and interesting model in which to study chronic infection with intracellular bacteria. Most strains of mice develop a chronic infection. However, certain strains are better able to handle their infection. Long term bone marrow chimeras showed this to be due to bone marrow derived cells, rather than host physiology, although whether it is due T or B lymphocytes, macrophages or polymorphs is yet to be determined. In vitro treatment of lymphocytes from infected donors showed that the subpopulations transferring protection to naive mice was Thy 1+ 2+ Ia-. i.e. the same T cell which induces cell mediated immunity to Listeria. In vivo injection of an optimal regime of anti Ly1 monoclonal antibody exacerbated infection and removed the population of cells transferring immunity. Sub-optimal amounts of anti-Ly-1 abrogated IgG Brucella agglutinating antibody without affecting bacterial numbers, thus confirming the T dependence of IgG antibody and suggesting that it is not important in recovery from infection. Marked splenomegaly occurred about 3 weeks after infection of the mice. It was transferred by T lymphocytes and involved marked influx of macrophages, increased haemopoiesis, fibrin deposition and fluid in the spleen. Although the macrophages were immunosuppressive in vitro they did not appear to account for chronicity of infection. In seeking to account for this chronicity we have compared a number of aspects of the immune response in chronically infected mice and in mice which were able to control their infection. Although we have ruled out a number of possibilities, we have not yet established the basis of chronicity.
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PMID:Pathogenesis and cellular immunity in experimental murine brucellosis. 633 62

Patients with HCL are subject to a variety of medical problems. Many of these complications are caused by the cytopenias and splenomegaly produced by proliferating neoplastic cells. Infection is a common cause of morbidity in HCL, but it is not clear whether there is an inherent defect in the immune system. The incidence of infection is related to neutropenia and is increased by the administration of cytotoxic drugs and corticosteroids; such drugs should be used cautiously in these patients. Opportunistic or unusual pathogens occur frequently in HCL, but recovery from such infections is the rule if the diagnosis is made early. Marrow hypoplasia is not infrequently seen and may present diagnostic difficulties. Such patients may have a lower tumor burden and clinically milder anemia. Hemorrhagic complications are unusual in HCL, though many patients have platelet function abnormalities. Other medical problems occur with increased frequency in HCL, and failure to recognize them leads to increased morbidity in this disease. Autoimmune disease is seen in up to one fourth of patients. It takes the form of self-limited skin and joint disease, or a more progressive, systemic of patients. It takes the form of self-limited skin and joint disease, or a more progressive, systemic vasculitis. Both forms can usually be treated with splenectomy or corticosteroids, but alkylating agents can also be used successfully. Bone disease is usually localized and responds well to radiotherapy. Other problems such as amyloidosis, multiple myeloma, and paraproteinemia are uncommon in HCL.
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PMID:Clinical problems in hairy cell leukemia: diagnosis and management. 639 Jun 85

Malaria and filariasis surveys were carried out as part of a broader general health survey between December, 1982 and May, 1983 in the Ok Tedi region of the Star Mountains, Western Province. Malaria, tropical splenomegaly syndrome (TSS) and anaemia were identified as significant health problems. Malaria slide positivity rates of 64.9% in children 2 to 9 years of age and 19.5% in adults 15 years and older indicate high levels of stable malaria transmission. Infections with Plasmodium falciparum were the most common (75.2%), but P. vivax (17.4%) and P. malariae (7.4%) were also encountered. Palpable splenomegaly occurred in 79.2% of adults and children over two years of age with more than 50% of the enlarged spleens grade III or greater (Hackett). Microfilariae (Wuchereria bancrofti) were present in 34.3% of night blood films, and estimated haemoglobin values were considerably below WHO standards. Data from the surveys provide a baseline against which to monitor changes in health status which might be expected to occur in conjunction with the development of a major mining project in the area.
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PMID:Malaria and filariasis in the Ok Tedi Region of the Star Mountains, Papua New Guinea. 659 55

The authors reviewed the clinical course of 31 consecutive patients with hairy cell leukemia seen at the University of California Los Angeles. The clinical presentation included varying degrees of pancytopenia, splenomegaly, and bone marrow infiltration with hairy cells. Ten patients were identified as having an "atypical" disease, which is defined as absence of palpable splenomegaly and/or marrow cellularity of less than 45%. These atypical patients had clinically milder disease and significantly less anemia than the usual patient (mean hemoglobin, 12.1 g/dl versus 9.4 g/dl; P = 0.016), although neutropenia and thrombocytopenia were comparable. Mortality and infection rates were similar in both groups. Infections were common in all patients, but opportunistic infections and septicemia were rare in patients prior to initiation of therapy. Two thirds of the patients who received corticosteroids and/or cytotoxic agents had serious infections, with a 50% mortality rate. Nearly 70% of the neutropenic patients (leukocyte count less than 1000) who received any form of treatment had a serious infection. The most important factors predicting mortality were chemotherapy and an age older than 50 years. Patients who survived 2 years with their disease had an excellent prognosis, and four patients in this series are alive and well with their disease for more than 10 years.
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PMID:Hairy cell leukemia. Disease pattern and prognosis. 673 79

Infection of (C57BL/6 X DBA/2)F1 (BDF1) mice with 2,500 FFU of Friend virus complex (FV) resulted in erythroleukemia followed by recovery, at which time virus could not be detected in the spleens of mice, and with splenomegaly (progressor mice) or without splenomegaly (regressor mice). Progressor and regressor mice developed equally high amounts of FV-neutralizing activity in their sera. Progressor mice contained cells capable of producing virus, despite the lack of viral envelope antigen(s) in their spleens. The tropism of FV recoverable from the spleens of secondary recipients, injected with spleen cells from progressor mice, did not show any change, although the viral genome was present in Fv-I-restrictive host for at least 7 weeks. When the number of spleen colony-generating cells was enumerated, by the spleen colony assay, the frequency in normal syngeneic and in allogeneic hosts was approximately the same at the early stage of erythroleukemia but was about 1,000 times higher in the syngeneic recipients during leukemia progression. These spleen colony-generating cells were considered to be FV-transformed cells capable of self-renewal and capable of generating infectious centers (IC), respectively. Most of these transformed cells might be non-producer leukemia cells.
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PMID:Shut-down of virus synthesis during progression of erythroleukemia induced by Friend virus in mice. 695 90


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