Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0032285 (pneumonia)
 54,520 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Immunohistochemical analysis was performed in a case of pulmonary cryptococcosis that showed granulomatous pneumonia. The patient had no immunologic defects or other diseases. To cryostat sections, the immunocytes in granulomatous lesion were examined by application of monoclonal antibodies for T-lymphocytes, B-lymphocyte, macrophage series cells, lymphokines containing gamma interferon (gamma IFN), interleukin 1 (IL-1) and interleukin 2 (IL-2), and interleukin 2 receptor (IL-2R). CD2+ cells, CD3+ cells and CD4+ cells were in and around the granulomas. On the other hand, CD8+ cells were around the granulomas. In granulomatous lesions, the CD4/CD8 ratio was 2.0. Some T-lymphocytes were considered as activated lymphocytes showing OKDR+, IL-2+, gamma IFN+ or IL-2R+. The lymphoid cells that aggregated near the granulomas were B-lymphocytes showing CD21+, CD24+, s-IgD+, s-IgM+, OKDR+. According to these results they were mature B lymphocytes. Alveolar macrophages (AMs) were CD11+, CD36+, IL-1+, OKDR+. Epithelioid cells were CD4+, CD11+, CD36+, OKDR+, IL-1+, IL-2R+. CD1+ cells showing dendritic forms were scattered in granulomas. They were recognized to be Langerhans giant cells. These results suggest that in pulmonary cryptococcosis the formation of epithelioid cell granulomas is mainly induced by CD4+ cells (helper/inducer T-lymphocytes). Additionally, Langerhans giant cells and mature B lymphocytes may be related to humoral immunity in pulmonary cryptococcosis.
 ...
PMID:[Immunohistochemical analysis of granulomatous lung lesion in primary pulmonary cryptococcosis]. 190 96

A fifty-one-year-old male patient visited the Department of Dermatology of Toho University Ohashi Hospital with a complaint of generalized exanthema, which was diagnosed assyringoma; at that time his leukocytosis was recognized. He was admitted to our department on August 8, 1988. Physical examination on admission revealed slight hepatosplenomegaly. WBC count was elevated (50,700/microliters). He was diagnosed as having Ph1-positive CML in the chronic phase and was treated with IFN-alpha (HLBI, Sumitomo, 3 x 10(6) units/day, daily, I. M.) from August 12, but an elevated lesion was detected at the lower part of his esophagus by endoscopy, and it was diagnosed by biopsy as squamous cell carcinoma. Radical operation for esophageal cancer was performed on September 26; at that time his WBC count was 17,400/microliters. After discharge, his WBC level was maintained within normal range by IFN-alpha. On August 2, 1989, he was readmitted to our hospital because of lymphoblastic crisis. Although he attained transient complete remission, he died of pneumonia after the relapse on January 10, 1990. IFN-alpha therapy is suggested to be useful for the treatment of CML associated with gastrointestinal cancer because of its possible parenteral administration and mild toxicity.
 ...
PMID:[Chronic myelocytic leukemia induced into remission by interferon-alpha associated with early esophageal cancer]. 192 Aug 43

Patients with chronic granulomatous disease (CGD), an uncommon inherited disorder of phagocytes resulting in the defective production of reactive oxygen intermediates, are prone to bacterial and fungal infections. In the case presented, therapeutic efforts including white cell transfusions, and amphotericin B and IFN gamma administration were undertaken to treat pneumonia caused by Aspergillus fumigatus. During a phase of artificial respiration, transfused white cells in peripheral blood and bronchoalveolar lavage fluid were monitored in order to examine their kinetics and functional activity. Using flowcytometrical methods, host-derived and transfused neutrophils could be distinguished by cytochrome b558 expression using the monoclonal antibody 7D5 for immunofluorescent staining as well as by production of reactive oxygen intermediates. Transfused PMN could be detected in both compartments and their kinetics could be followed up to 24 hours after transfusion. Using flowcytometry, even small numbers of transfused PMN could be measured during episodes of extreme leukocytosis. Since functionally intact transfused PMN were found in the bronchioalveolar lavage fluid, white cell transfusions in combination with antibiotic and immunomodulating therapy should be considered a part of the therapeutic regimens for life-threatening infections in CGD patients.
 ...
PMID:Kinetics of transfused neutrophils in peripheral blood and BAL fluid of a patient with variant X-linked chronic granulomatous disease. 195 82

We examined the efficacy and toxicity of recombinant interferon-alpha 2b (rIFN-alpha 2b) in 10 previously untreated patients with advanced myelodysplastic syndromes. Morphological subtypes were refractory anaemia with excess of blasts (RAEB) in 4, RAEB in transformation (RAEB/T) in 3 and chronic myelomonocytic leukaemia (CMML) in 3 cases. IFN was administered subcutaneously at increasing doses of 1 to 3 x 10(6) IU per day. The median duration of therapy was 6 months (range, 3 to 14). 2 patients, both with a diagnosis of CMML, achieved a complete and partial remission, respectively. In the complete responder, remission could be maintained for 9.5 months by daily administration of 1 x 10(6) IU IFN. The other patients were classified as failures, although in 4 cases a decrease of bone marrow blasts was noted and none of the patients progressed to overt leukaemia while being treated with IFN. During the study, all patients with RAEB and RAEB/T showed a moderate to severe reduction in peripheral leukocyte and platelet counts, requiring premature termination of IFN therapy in 5 cases. Despite adequate supportive measures, 2 patients died of pneumococcal pneumonia and gastrointestinal bleeding, respectively. In 1 patient, IFN therapy had to be stopped because of neurologic toxicity (polyneuropathy). From these data we conclude that rIFN-alpha 2b at the doses and schedule tried is not a useful treatment for advanced myelodysplastic syndromes. Patients with CMML, however, may be an exception and should further be considered as candidates for therapeutic trials with rIFN-alpha 2b.
 ...
PMID:Treatment of advanced myelodysplastic syndromes with recombinant interferon-alpha 2b. 198 3

The mechanisms that allow circulating basement membrane antibodies (Ab) to interact with the alveolar basement membrane (ABM) inducing Goodpasture's hemorrhagic pneumonitis are unknown. In laboratory animals the ABM is inaccessible to phlogogenic amounts of ABM Ab unless the permeability of the unfenestrated alveolar endothelium is increased. This study was designed to test the hypothesis that in the mouse polypeptide mediators, generated by activated lymphoid cells or cells infected by viruses, contribute to the pathogenesis of passive Goodpasture's hemorrhagic pneumonitis. In naive mice that received rabbit ABM Ab, these bound to the glomerular basement membrane but not to the ABM and their lungs were normal. In the lungs of mice injected with human recombinant IL-2 and IFN-alpha specific binding of ABM IgG, C3, and fibrinogen to the ABM, diffuse and severe erythrocyte extravasation, and accumulation of mononuclear and polymorphonuclear leukocytes were constantly observed. ABM Ab and IL-2 or ABM Ab and IFN-alpha did not produce comparable effects. Mice injected only with IL-2 and IFN-alpha had enlarged, edematous lungs without pulmonary hemorrhages. The results show that the synergism of IL-2 and IFN-alpha convert the lung into a preferential target for AMB Ab, suggesting that cytokines may have a role in the pathogenesis of human Goodpasture's pneumonitis.
 ...
PMID:Pathogenesis of an experimental model of Goodpasture's hemorrhagic pneumonitis. 218 75

Interleukin-1 (IL-1), a modulatory protein with immune and inflammatory functions, is spontaneously released by tissue macrophages in lower concentrations compared with peripheral blood monocytes. Conversely, in idiopathic pulmonary fibrosis, sarcoidosis, and certain inflammatory diseases, increased amounts of IL-1 are released by alveolar macrophages (AM). We examined IL-1 production by AM from patients with adult respiratory distress syndrome (ARDS) and compared it with that in patients with severe pneumonia requiring assisted ventilation, patients with pneumonia requiring parenteral antibiotics, and healthy control subjects. In vitro, ARDS AM released significantly more total IL-1 and IL-1 beta than did ARDS AM in patients with pneumonia and in control subjects. Moreover, after stimulation of these cells with 10 micrograms/ml of lipopolysaccharide (LPS), ARDS AM significantly increased release of IL-1 and IL-1 beta. AM from patients with severe pneumonia also released greater amounts of both IL-1 and IL-1 beta as fresh explants and after LPS stimulation when compared with control subjects. Incubation of AM with 250 U/ml human interferon-gamma (gamma IFN) was associated with less IL-1 beta release. However, stimulating AM from patients with ARDS and severe pneumonia with gamma IFN plus LPS enhanced the release of IL-1 beta compared with that in patients with pneumonia and in control subjects. ARDS AM released significantly more IL-1 beta than did all of the other groups. These results demonstrate that AM from patients with ARDS are capable of releasing significantly greater amounts of IL-1, which may be related to the progression of acute lung injury.
 ...
PMID:Elevated interleukin-1 release by human alveolar macrophages during the adult respiratory distress syndrome. 260 96

We have previously reported pulmonary eosinophils in eosinophilic pneumonia (PIE syndrome) showed two characteristics: hypodensity and nuclear hypersegmentation. Our present working hypothesis is that the eosinophil chemotactic factor and certain lymphokines may be involved in the induction of these characteristic features. Therefore, we examined whether these stimuli can induce two characteristics in vitro. Results were as follows. 1) Chemoattracts (ECF-A, histamine and PAF) can induce both nuclear hypersegmentation and hypodense eosinophils. 2) Hypodense eosinophils can be induced earlier than induction of hypersegmented nuclei (hypodense eosinophils within three hours, hypersegmented nuclei: 12 hrs). 3) Furthermore, lymphokines can not induce hypodense eosinophil. 4) However, PHA-lymphocyte culture medium (PHALCM), gamma-IFN and IL-3 + GM-CSF can induce hypersegmented nuclei but IL-2 has no effect on nuclear segmentation of eosinophils.
 ...
PMID:Induction of hypodense eosinophils and nuclear hypersegmentation of eosinophils by various chemotactic factors and lymphokines in vitro. 264 81

Interferon-alpha (IFN-a) or 2'-deoxycoformycin (pentostatin; DCF) have each been shown to be highly active in hairy-cell leukemia (HCL). In this phase II study of the Leukemia Cooperative Group of the European Organization for Research and Treatment of Cancer (EORTC), the efficacy and toxicity of DCF were investigated in patients who were resistant to IFN-a treatment. Resistance was defined as: (1) progressive disease (PD) under IFN-a therapy for more than 2 months; (2) stable disease (SD) after more than 6 months of IFN-a treatment; (3) relapse within 3 months of discontinuing IFN-a; and (4) intolerance to IFN-a because of World Health Organization (WHO) grade 3 or 4 toxicity. DCF was applied at a dosage of 4 mg/m2 weekly x 3, then 4 mg/m2 every other week x 3. Responders were given a maintenance therapy once per month for a maximum of 6 months. At the time of report, 33 patients with resistant disease were evaluable for response and toxicity. Median duration of IFN-a therapy before DCF administration was 14.7 months (range, 1 to 41 months). Complete remissions (CRs) were achieved in 11 patients and partial remissions (PRs) in 15, resulting in a total response rate of 78.8%. Median interval between beginning of DCF therapy to best response was 3.9 months with a range from 2.0 to 7.0 months. Two patients who achieved PR have relapsed 7 and 14 months after cessation of DCF therapy. The median duration of response was over 11.5 months (range, over 3.0 to over 24.0 months). Three patients died within the first 6 weeks of DCF treatment: one of drug-unrelated cardiomyopathy and two of fungal pneumonia. The patients with early death (n = 3) and nonresponsive disease (n = 4) received IFN-a treatment for a longer period (median, 18.0 months) than did the 26 responsive patients (median, 10.0 months). Major side effects included nausea, skin rash, and infections and were otherwise mild. Thus, DCF is highly active in patients with HCL resistant to IFN-a.
 ...
PMID:Response to pentostatin in hairy-cell leukemia refractory to interferon-alpha. The European Organization for Research and Treatment of Cancer Leukemia Cooperative Group. 278 73

Human leukocyte interferon, HuIFN-alpha (LE), has been tested in combination with radiotherapy and chemotherapy for previously untreated small cell lung cancer. Nine patients with limited disease received high-dose IFN followed by a low-dose regimen; and six patients had a low-dose regimen from the beginning. The high dosage of IFN consisted of 800 X 10(6) IU given as a continuous intravenous infusion for 5 days, followed by 6 X 10(6) IU i.m. three times weekly. If the first site of disease progression was local or in a central nervous system location, radiotherapy (55 Gy/20 F/7 weeks locally and/or 30 Gy/10 F/2 weeks whole brain) was applied and IFN was continued. Chemotherapy was administered only if there was disease dissemination outside the chest. Three patients achieved minor response for as long as 20, 25, and 42 weeks, respectively, with IFN alone. Three of five complete responders to IFN-radiotherapy died 18, 33, and 41 weeks from the start of IFN treatment without chemotherapy. Autopsy did not reveal macroscopic or microscopic tumor at any site, but there was severe radiation pneumonitis. Four of nine patients were administered chemotherapy subsequent to IFN-radiotherapy because of disease dissemination. The median length of survival of the entire group was 41 weeks. On the low-dose regimen, one patient achieved partial response with IFN alone (duration, 12 weeks); of five evaluable patients three achieved complete remission and two partial remission to IFN-radiotherapy, and one of the three complete responders to IFN-radiotherapy died of severe radiation pneumonitis at 21 weeks from the start of IFN treatment. No tumor was detected at autopsy. The study is in progress. Average survival at present is 33 weeks. The results derived from both our studies suggest a growth-delaying effect of HuIFN-alpha (Le) on small cell lung cancer. They also suggest potentiation of radiation by HuIFN-alpha (Le). Memory and psychomotor dysfunction, fatigue, and anorexia were dose limiting with both short-duration, high-dose and long-duration, low-dose IFN therapy. We feel that IFN, as part of a combined multimodality treatment of small cell lung cancer, may play a role by delaying metastatic dissemination.
 ...
PMID:Human leukocyte interferon as part of a combined treatment for previously untreated small cell lung cancer. 298 40

We investigated the effect of human recombinant DNA-derived IFN-alpha-2 given in a dose of 1-2 X 10(6) units daily by subcutaneous injection to five patients with advanced idiopathic myelofibrosis (IM). Transfusion dependent anemia and symptomatic splenomegaly were taken as inclusion criteria for this pilot study. Two patients succumbed, one and three months after starting interferon-treatment because of pneumonia and traumatic cranial injury, respectively. While on IFN-treatment no improvement of cytopenia or reduction of splenomegaly was seen in four of the patients. In one patient, however, the requirement for erythrocyte transfusions decreased from 5 to 1.7 monthly upon IFN-treatment. After two, four and six months respectively IFN-treatment had to be stopped in these cases because of progressive thrombocytopenia and/or neutropenia. These observations suggest, that IFN-alpha might be of only marginal value in the treatment of advanced idiopathic myelofibrosis.
 ...
PMID:Interferon-alpha-2 in the treatment of idiopathic myelofibrosis. 335 3


1 2 3 4 5 6 7 8 9 10 Next >>