Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0024312 (lymphopenia)
 4,859 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Treatment with human recombinant tumour necrosis factor-alpha (rTNF alpha) significantly enhanced resistance to Listeria monocytogenes infection in mice. The level of protection (which was dose-dependent and maximal at approximately 1.0 microgram per mouse) was similar to that previously reported for the monokine rIL-1 alpha, although somewhat greater amounts of rTNF alpha than rIL-1 alpha were required. Combined administration of suboptimal concentrations of rTNF alpha and rIL-1 alpha resulted in significant enhancement of resistance beyond that obtained with either monokine alone, whereas further increases in anti-listeria resistance were not observed at doses of rTNF alpha or IL-1 alpha that were themselves capable of inducing substantial protection. Combined administration of rTNF alpha and rIL-1 alpha was associated with a delay in onset and lessening in severity of the lymphopenia that accompanied L. monocytogenes infection. The reduced bacterial burden in the spleens and livers of mice treated with rTNF alpha and rIL-1 alpha was associated with a more rapid decline in serum colony-stimulating activity. Peritoneal macrophages from rTNF alpha- and rIL-1 alpha-treated listeria-infected mice did not demonstrate enhanced anti-listeria activity in vitro. These results provide further evidence for the potential benefits of rTNF alpha and other cytokines in promoting anti-bacterial resistance. They further suggest that use of combinations of cytokines is a strategy worthy of further consideration.
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PMID:Human rTNF alpha augments anti-bacterial resistance in mice: potentiation of its effects by recombinant human rIL-1 alpha. 230 86

The effect of T-2 toxin on cell-mediated resistance to bacterial infection was evaluated in mice exposed to Listeria monocytogenes. Mice were inoculated with 4.0 X 10(5) (LD50) or 4.0 X 10(4) (nonlethal) L. monocytogenes on day 0 and treated orally on days 0, 1, 2, and 3 with 2.0, 1.0, or 0 mg/kg T-2 toxin. Toxin induced suppression of resistance was indicated by the rapid growth of Listeria in the spleen and by significant (P less than 0.005) increases in mortality due to listeriosis. Necrosis and depletion of lymphoid tissue, lymphopenia, and a marked decrease in the influx of lymphocytes and macrophages into Listeria elicited peritoneal exudates and at sites of infection in the liver and spleen occurred in the toxin treated mice. The immunotoxic effect of T-2 toxin on cell-mediated resistance to listeriosis was dosage dependent and attributed to toxin induced lymphoid depletion and the failure of surviving lymphocytes and mononuclear cells to clear the host of infection.
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PMID:Immunotoxic effects of T-2 mycotoxin on cell-mediated resistance to Listeria monocytogenes infection. 310 15

Immunotoxic effects of T-2 toxin and cyclophosphamide on cell-mediated resistance were evaluated in mice exposed to Listeria monocytogenes infection. Mice were inoculated intraperitoneally with 4.0 X 10(5) (LD50) or 4.0 X 10(4) (nonlethal) L monocytogenes and were treated with 4.0 mg of T-2 toxin/kg of body weight or 180 mg of cyclophosphamide/kg. The immunosuppressive effect of the toxin and cyclophosphamide was indicated by the rapid growth of Listeria and significant (P less than 0.005) increases in mortality because of listeriosis. Necrosis and depletion of lymphoid tissue, lymphopenia, and significant (P less than 0.005) decreases in the influx and number of lymphocytes and macrophages occurred in Listeria-elicited peritoneal exudates and at sites of infection in the liver and spleen of the toxin- and cyclophosphamide-treated mice. Immunotoxic effects of T-2 toxin and cyclophosphamide were comparable and attributed primarily to the depletion of T lymphocytes and the subsequent failure of surviving immunologically committed T cells and T-cell dependent immune-activated macrophages to clear the host of bacteria.
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PMID:Immunotoxic effects of T-2 toxin on cell-mediated immunity to listeriosis in mice: comparison with cyclophosphamide. 376 3

A case of maternal death due to Listeria monocytogenes bacteremia, with survival of the prematurely delivered infant, is presented. Lymphopenia and a Haitian origin suggest that the fatal outcome was related to the acquired immunodeficiency syndrome (AIDS). To our knowledge, this is the first recorded instance of a maternal death due to listeriosis.
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PMID:Listeriosis as a cause of maternal death: an obstetric complication of the acquired immunodeficiency syndrome (AIDS). 661 87

Prolactin (PRL) is the primary lactogenic pituitary hormone that plays an essential role in many aspects of reproduction, from fertilization to mammary gland development and maternal behavior. PRL has also been reported to play a role in immunoregulation. Because initial observations indicated that hypophysectomized rats present abnormalities of the immune system, including increased thymic atrophy and lymphopenia, a number of studies have focused on the potential immunomodulatory roles of PRL. This hormone exerts its biological activities following binding to specific cell surface PRL receptors (PRLRs). In this report, we have characterized the development and function of the immune system in PRLR-deficient mice. Compared with wild-type control mice, PRLR-/- mice demonstrate no alterations in thymic or splenic cellularity or in the composition of the lymphocyte subsets present in primary (bone marrow and thymus) or secondary (spleen and lymph nodes) lymphoid organs. Lymphocytes from PRLR-/- mice are functional in vitro, as they can proliferate normally to mitogens, cytokines, and allogeneic cells. PRLR-/- splenocytes display normal NK-mediated cytotoxicity to YAC-1 target cells. In vivo studies have revealed that PRLR-/- mice are able to 1) generate normal steady-state Ig levels, 2) mount a normal specific Ig response following immunization with a T-dependent Ag, 3) eliminate injected allogeneic tumor cells, and 4) effectively control Listeria monocytogenes infection. Taken together, these results show that immune system development and function proceed normally in the absence of PRL-mediated signaling and suggest that PRLR pathways are not essential for immunomodulation in vivo.
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PMID:Immune system development and function in prolactin receptor-deficient mice. 1039 43

Listeriosis (LT) is an important infection in immunocompromised patients, but no large series of LT in cancer patients have been recently described. We reviewed the records of 34 cancer patients with LT at our institution (1990-2001). Twenty patients (59%) had an underlying hematologic malignancy. In 11 patients, LT complicated bone marrow transplantation. Lymphocytopenia was observed in 62% of the patients. Twenty-six patients (76%) received prior corticosteroids. Bacteremia was the most common presentation of LT (74%) followed by meningoencephalitis (21%). The most common treatment of LT was ampicillin with or without gentamicin (68%). The median duration of treatment was 26 days (range, 8-74 days). The rate of response to antimicrobial therapy was 79%. No relapses were identified. LT contributed to death in 9 (75%) of the 12 patients who died. Meningoencephalitis had the worst prognosis (3 of 6 cases were fatal). Treatment of central nervous system LT continues to have a high failure rate.
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PMID:Listeria monocytogenes infection in patients with cancer. 1452 12