UMLS:C0032285 - FACTA Search

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Query: UMLS:C0032285 (pneumonia)
54,520 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Pneumonia due to Pneumocystis carinii (PCP) is regularly encountered in organ allograft recipients who are immunosuppressed to prevent rejection. Recipients of lung/heart allografts may be particularly prone to pulmonary infection due to systemic immunosuppression and the fact that defense mechanisms in the transplanted lung may be further impaired through tissue incompatibility and the effects of surgery. In this study, we monitored 16 lung transplant recipients for infection with Pneumocystis carinii using serial bronchoalveolar lavage (BAL) and found the prevalence of Pneumocystis infection of the lung to be 88%. Six episodes were associated with the usual symptoms of pneumonia, whereas 10 episodes were associated with minimal or no symptoms. In 3 of the 6 symptomatic episodes, a concurrent bacterial infection was also found. The total number of cells recovered from the lung by BAL, the proportion of T-lymphocytes, and the number of cytotoxic/suppressor and helper/inducer cells were elevated during infection with Pneumocystis compared to before and after. Spontaneous and interleukin-2-induced proliferation of BAL cells in vitro was also higher during infection, suggesting that there was an increased number of activated T-lymphocytes in the airspaces of the infected allograft. BAL cells cultured with irradiated spleen cells from the donor proliferated at higher levels when obtained after Pneumocystis infection than when obtained before or during infection even for subclinical infections. These results indicate that in the absence of prophylaxis, the prevalence of Pneumocystis infestation is very high after lung/heart transplantation. Impaired defense of the transplanted lung does not seem to stem from the inability of activated T-lymphocytes to accumulate in the allograft.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Unexpectedly high incidence of Pneumocystis carinii infection after lung-heart transplantation. Implications for lung defense and allograft survival. 314 96

Interleukin-2 (IL-2) production by cells from children with various forms of arthritis, systemic lupus erythematosus, and cystic fibrosis was compared. In all cases more IL-2 was detectable at 24 than at 48 h and production was increased by addition of indomethacin. Cultures from children with either active lupus or the pneumonia of cystic fibrosis produced very little IL-2, but cultures from children with arthritis produced apparently normal amounts. We conclude that depressed production of IL-2 in juvenile arthritis may be a secondary epiphenomenon and not a primary immunologic deficit.
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PMID:Interleukin-2 production by lymphocytes from blood of children with arthritis is less suppressed than in systemic lupus or cystic fibrosis. 349 11

Interleukin-2 (IL-2), a T cell derived lymphokine, acts in nonspecific hormone-like fashion to maintain proliferation of activated lymphocytes in vitro and is believed to play a key role in cell-mediated immune function in vivo. The parameters of induction and assay of factors with IL-2 activity were examined in a group of clinically normal sheep seronegative for antibodies to ovine progressive pneumonia virus (OPPV-). Supernatants from cultures of Concanavalin A (Con A) stimulated mononuclear leukocytes (ML) derived from peripheral blood and lymph nodes contained factors with the capacity to maintain continued proliferation in Con A stimulated lymphoblasts. This activity was localized by gel chromatography to fractions containing proteins of 17,000-20,000 daltons. In a group of sheep seropositive for antibodies to OPPV (OPPV+), decreased levels of IL-2 activity were found in ML culture supernatants derived from the posterior mediastinal lymph nodes of sheep with clinical and pathological evidence of OPP, when compared to OPPV+ sheep with no lesions and sheep with visceral caseous lymphadenitis. This decrease in IL-2 activity appeared not to be associated directly with levels of prostaglandin E2 in these supernatants. These findings may correlate with virus induced alterations in cell mediated immune function in lymphoproliferative lesions of OPP.
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PMID:Ovine interleukin-2: partial purification and assay in normal sheep and sheep with ovine progressive pneumonia. 387 87

We investigated a T-cell activation deficiency in a 3-month-old boy with protracted diarrhea, serious cytomegalovirus pneumonia, and a family history (in a brother) of cytomegalovirus infection and toxoplasmosis. In spite of detection of normal number of peripheral lymphocytes, T cells did not proliferate after activation by anti-CD3 and anti-CD2 antibodies, although proliferation induced by antigens was detectable. We sought to determine the origin of this defect as it potentially represented a valuable tool to analyze T-cell physiology. T-cell activation by anti-CD3 antibody or phytohemagglutinin (PHA) led to reduced interleukin-2 (IL-2) production and abnormal nuclear factor-activated T cell (NF-AT; a complex regulating the IL-2 gene transcription) binding activity to a specific oligonucleotide. T-cell proliferation was restored by IL-2. Early events of T-cell activation, such as anti-CD3 antibody-induced cellular protein tyrosine phosphorylation, p59fyn and p56lck kinase activities, and phosphoinositide turnover, were found to be normal. In contrast, anti-CD3 antibody-induced Ca2+ flux was grossly abnormal. Release from endoplasmic reticulum stores was detectable as tested in the presence of anti-CD3 antibody or thapsigargin after cell membrane depolarization in a K+ rich medium, whereas extracellular entry of Ca2+ was defective. The latter abnormality was not secondary to defective K+ channel function, which was found to be normal. A similar defect was found in other hematopoietic cell lineages and in fibroblasts as evaluated by both cytometry and digital video imaging experiments at a single-cell level. This primary T-cell immunodeficiency appears, thus, to be due to defective Ca2+ entry through the plasma membrane. The same abnormality did not alter B-cell proliferation, platelet function, and polymorphonuclear neutrophil (PMN) function. Elucidation of the mechanism underlying this defect would help to understand the physiology of Ca2+ mobilization in T cells.
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PMID:A primary T-cell immunodeficiency associated with defective transmembrane calcium influx. 753 12

The goal of any treatment strategy for cancer is to improve not only patient survival but also quality of that survival. Between March 1990 and February 1993, we treated 10 patients with advanced RCC (9 men and 1 woman) by combined immunotherapy using natural interferon-alpha (IFN-alpha), recombinant interleukin-2 (rIL-2) and lymphokine-activated killer (LAK) cells, and resulting the quality of life (QOL) issues examined. The ages of the patients ranged from 36 to 78 years (mean: 60.2) and the performance status (PS) ranged from 30 to 100% (mean: 77%). There were 8 lung, 3 bone, 2 brain and 1 neck and para-aortic lymph node metastases. We could evaluate 8 patients, 2 patients dropped out because of bone fracture and acute pneumonia. The protocol was as follows; 1 x 10(6) IU of rIL-2 as an intravenous infusion and 6 x 10(6) IU of IFN-alpha intramuscularly on days 1-7 and 15-21. In additions LAK cells obtained from the patients were given on days 14, 21, 28, and 35 intravenously. This protocol was repeated for more than three cycles (mean: 4.13 cycles) in each patient. The maintenance therapy on outpatient basis were performed in 4 patients after confirmation of the safety of the combined immunotherapy. This outpatient regimen was composed of 1 x 10(6) IU of rIL-2 intravenously, 6 x 10(6) IU of IFN-alpha intramuscularly on days, 1, 8, 15, 22, and 29, plus LAK cells on days 15 and 29. We repeated this protocol for 3-5 cycles (mean: 4.25 cycles).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Combined immunotherapy using interferon-alpha, interleukin-2 and lymphokine-activated killer cells--improvement of quality of life in patients with advanced renal cell carcinoma]. 760 59

The activation of autologous cytotoxic cells by interleukin-2 (IL-2) may be a promising tool for elimination of minimal residual blast populations in patients with acute myelocytic leukemia (AML) to prolong disease-free survival. Here, we report the results of a phase II study using IL-2 for consolidation therapy in patients with second remission of de novo AML. All patients in 1st relapse of AML received a uniform induction therapy consisting of intermediate high-dose AraC (iHDAraC) 2 x 600 mg/m2 d1-4 and VP-16 100 mg/m2 d1-7. Patients achieving 2nd remission were treated with 4 cycles recombinant IL-2 (rIL-2) 9 x 10(6) IU/m2 administered on d1-5 and 8-12/cycle as 1h infusion every six weeks. In 37/66 (56%) evaluable patients, complete remission (CR) was achieved. So far, 21/37 patients (4 after additional autologous bone marrow transplantation (ABMT) received rIL-2 consolidation. Three patients are too early for evaluation, 4 received allogeneic BMT, 6 relapsed before IL-2 was scheduled and 4 refused treatment with rIL-2. The median disease-free survival (DFS) was 11 (4-49+) months. Up to now, in 5/21 (24%) patients the duration of 2nd remission exceeded that of 1st remission 7/21 (33%) are in ongoing 2nd remission (7+ to 49+ months). The side effects of rIL-2 were generally moderate and manageable. Only in two patients, previously treated with ABMT, severe side effects occurred; septicaemia and pneumonia in one patient and desquamative erythrodermia in the second one. In accordance with other studies rebound lymphocytosis with a marked increase of CD56(+)-cells and release of secondary cytokines such as TNF-alpha, IFN-gamma and IL-6 was observed. The schedule is feasible and the data suggest a possible benefit for DFS, which, however has to be confirmed by randomized trials.
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PMID:Interleukin-2 bolus infusion as late consolidation therapy in 2nd remission of acute myeloblastic leukemia. 771 35

The use of alpha interferon (alpha IFN) and, more recently, of the purine analogues deoxycoformycin (dCF) and 2-chlorodeoxyadenosine (2-CdA) has dramatically improved the prognosis of patients affected by hairy cell leukemia (HCL). DCF has been shown to induce an higher and more durable response rate than IFN, with only moderate myelosuppression and relatively few side effects. In this paper, we report our experience with dCF in a series of 38 HCL patients who had progression of their disease after IFN therapy. Serum interleukin-1 beta (IL-1 beta), soluble interleukin-2 receptors (sIl-2R) and Tumor Necrosis Factor alpha (TNF alpha) levels were also evaluated before, both during and after treatment in order to monitor clinical response. Two schedules of treatment were employed: 23 patients were treated with the EORTC protocol and the following 15 with the NCI regimen. The overall response rate was 94.7%; no significant differences in response rates were observed between the two schedules. In respect to toxicity, we recorded nausea and in two cases a cutaneous rash. Four patients experienced localized herpes zoster and one had a fungal pneumonia. Median overall survival after therapy is 38.5 months, 55 percent of patients enrolled in the EORTC schedule and 77% of those who received the NCI program are currently in CCR at 3 years. Serum IL-1 beta and sIL-2R levels significantly decreased after treatment, while no significant changes in serum TNF alpha levels were observed. In our study, dCF was confirmed as an effective agent in HCL, inducing an high response rate with only moderate side effects.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Deoxycoformycin induces long-lasting remissions in hairy cell leukemia: clinical and biological results of two different regimens. 782 42

In order to better understand the immunopathology of acute complications of lung transplantation we have analysed the different parameters of cytotoxic cell and macrophage activation during the course of pulmonary allograft rejection and cytomegalovirus pneumonia. In transplanted patients presenting with an acute pulmonary allograft rejection, a cytomegalovirus pneumonia or no complication (control group), we have studied, first serum markers of immune activation: interleukin-2 soluble receptor (IL-2sR), neopterin, IL-6, TNF soluble receptors (TNF-sR55 and TNF-sR75). Secondly the intrapulmonary compartmentalisation of allogenic and antiviral responses were evaluated by studying bronchoalveolar lavage fluid (BAL). The level of IL-6 was measured in BAL supernatants and the gene expression of two cytokines (IL-1 beta and IL-6) and two markers of activated cytotoxic cells (granzyme B and perforin) were studied by in situ hybridisation on the alveolar cells. Acute pulmonary allograft rejection was characterised by the paucity of systemic stigmata of immune activation and by the intrapulmonary compartmentalisation of the inflammatory response principally expressed by an increase in alveolar concentration of IL-6, TNF-sR55 and TNF-sR75, and an increased expression of the IL-1 beta gene. Cytomegalovirus pneumonia is accompanied by an intense local and systemic inflammatory activity as evidenced by the serum level of IL-2sR, neopterin, TNF-sR55 and TNF-sR75, the alveolar concentration of IL-6, TNF-sR55 and TNF-sR75, and the expression of monokine (IL-1 beta, IL-6) and of cytotoxic mediator (granzyme b, perforin) genes by BAL cells. These mediators could participate in the elaboration of an acute or chronic inflammatory response which would be potentially deleterious for the graft.
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PMID:[Immunopathology of cytomegalovirus pneumonia and allograft rejection in lung transplantation. Group of Pulmonary Transplantation of the University Paris-Sud]. 783 5

Intercellular adhesion molecule-1 (ICAM-1) is a membrane-bound molecule that is primarily involved in cell to cell adhesive interactions of the immune system. Concentrations of soluble ICAM-1 (s-ICAM-1) shed into the circulation were measured by a quantitative ELISA in HIV-infected persons without AIDS, patients with AIDS with or without evidence of acute opportunistic infection at the time of sampling, and HIV-seronegative patients with toxoplasmosis, community-acquired pneumonia, leishmaniasis and rickettsial infections. Patients were classified on the basis of clinical condition and CD4+ T-cell counts according to the 1993 revised HIV classification of the USA Centers for Disease Control. Concentrations of s-ICAM-1 in the serum of HIV-infected persons without AIDS-indicator conditions (categories A1, A2, B1 and B2) as well as in the serum of patients with AIDS (categories A3, B3, C1, C2 and C3) were significantly higher than normal (mean +/- S.E.M. 469 +/- 23, n = 60 and 780 +/- 73, n = 56, respectively, versus 329 +/- 15 ng/ml, P < 0.0001 and < 0.0001 respectively) and differed also significantly from each other (P < 0.0001). Raised concentrations of s-ICAM-1 in the serum of afebrile patients with AIDS but without acute opportunistic infection at the time of sampling (mean +/- S.E.M. 672 +/- 76, n = 29) did not differ from those of the remaining patients with AIDS or from those of HIV-seronegative patients with the infections studied. A steady and significant increase of serum concentrations of s-ICAM-1 with progress of disease according to clinical category (categories A-->B-->C, p = 0.0007) as well as with the loss of circulating CD4+ T-cells (categories 1-->2-->3, p = 0.009) was observed. Individual serum concentrations of s-ICAM-1 showed negative correlations with individual total lymphocyte (P = 0.004), CD4+ T-cell (P = 0.05), CD8+ T-cell counts (P = 0.03) as well as positive correlation with serum concentrations of soluble interleukin-2 receptors (P < 0.0001), an indirect marker of progress of HIV-related disease. Serum concentrations of s-ICAM-1 did not differ between patients with AIDS who were receiving or not receiving zidovudine at the time of sampling. A longitudinal survey is needed in order to determine whether measuring serum concentrations of s-ICAM-1, although not specific, has any predictive or prognostic value in these patients as well as whether this bioactive molecule has any pathogenetic role in the progress of disease in HIV infection.
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PMID:Serum concentrations of soluble intercellular adhesion molecule-1 and progress towards disease in patients infected with HIV. 788 20

We evaluated soluble interleukin-2 receptors (sIL-2R), neopterin and adenosine deaminase (ADA) in pleural effusions from 93 patients with tuberculosis, malignancies, uremia, pneumonia and other kinds of pleurisy. There were significantly elevated ADA (102.7 +/- 47 U/l) and sIL-2R (8,238 +/- 4,117 U/ml) values in tuberculous (TB) pleural fluids as compared with other non-TB pleural fluids (p < 0.005). The neopterin levels in pleural fluid were significantly lower in the cancer group (17.3 +/- 7.8 nmol/l; p < 0.005) and most strikingly elevated (309.4 +/- 112.2 nmol/l; p < 0.0001) in patients with uremic pleural effusions. Using cut-off values of 60 U/l in ADA and 5,000 U/l in sIL-2R, 92.0 and 86.9% of pleural effusions were TB in origin. Eighty-four percent of patients with malignant pleural effusions had neopterin levels less than 25 nmol/l.
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PMID:Neopterin, soluble interleukin-2 receptor and adenosine deaminase levels in pleural effusions. 804 18

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