Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0432222 (SEM)
 47,337 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The aim of this study was to determine and to evaluate silica induced lung cell reactivity--if any--in bronchoalveolar space, before clinical changes develop. Bronchoalveolar lavage (BAL) was carried out in 15 nonsmoking individuals with chronic professional silica exposure, free of lung signs and symptoms. Controls were healthy nonsmokers. Routine BAL cytology (HE, MGG) was completed by mast cell staining (toluidine blue). BAL lymphocyte subsets were phenotyped by direct two- and three-color immunofluorescence (applied DAKO A/S monoclonal antibodies: anti-CD3, CD4, CD8, CD11b, CD14, CD15, CD16 + 56, CD19, CD25, CD45, HLA-DR). Parallel staining was performed in peripheral blood. In individuals with chronic silica exposure we found: significant increase in alveolar macrophage (362 +/- 45 vs 160 +/- 33 x 10(3) cells/ml, p < 0.05), lymphocyte (61 +/- 9 vs 24 +/- 5 x 10(3) cells/ml, p < 0.05) and BAL total cell (415 +/- 76 vs 187 +/- 34 x 10(3) cells/ml, p < 0.05) numbers; significant increase in mast cell (0.4 +/- 0.1 vs 0.2 +/- 0.1, p < 0.05), NK cell (7.0 +/- 1.8 vs 3.6 +/- 1.0, p < 0.05) and Th early activated lymphocyte percent (CD4 + CD25+ calculated as percentage of CD4+ cells: 15.1 +/- 1.5 vs 7.8 +/- 1.6, p < 0.01). All results were presented as median +/- SEM. Bronchoalveolar space of people with chronic silica exposure usually shows pathological reaction (especially macrophagic alveolitis), although they are free of manifested pulmonary disease. Th early activated lymphocytes, NK cells and mast cells seem to play important role in the early interstitial lung tissue reaction to silica.
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PMID:[Cytoimmunologic changes in material obtained from bronchoalveolar lavage (BAL) in asymptomatic individuals chronically exposed to silica dust]. 1100 45

This study aimed at documenting airway inflammation and subepithelial collagen deposition in patients using only inhaled beta(2)-agonists with either recently diagnosed asthma (RDA: </= 2 yr, n = 16) or long-standing asthma (LSA: >/= 13 yr, n = 16) and at the influence of an intense inhaled corticosteroid (ICS) treatment on these parameters, in relation to changes in airway responsiveness. Patients had a methacholine inhalation test and a bronchoscopy with bronchial biopsies before and after an 8-wk treatment with inhaled fluticasone propionate (FP), 1,000 microgram/day. Baseline FEV(1) (mean +/- SEM) was normal and similar in both groups (RDA: 98.1 +/- 2.7, LSA: 94.5 +/- 4.6%). Geometric mean methacholine PC(20) was lower in LSA than in RDA (0.44 versus 3.37 mg/ml) at baseline and improved similarly by 1.85 and 1.86 double concentrations with FP treatment. PC(20) normalized (>/= 16 mg/ml) in five patients with RDA and two patients with LSA. Baseline mean bronchial cell counts (per mm(2) connective tissue surface) for CD3(+), CD4(+), CD8(+), CD25(+), EG1(+), CD45ro(+), and AA1(+) cells were similar in both groups. With FP, EG1(+) (p < 0.001), EG2(+) (p = 0.018), and AA1(+) counts (p = 0.009) decreased significantly in both groups while CD45ro(+) (p = 0.02) counts decreased only in LSA. Baseline type 1 and type 3 collagen deposition underneath the basement membrane was similar in RDA and LSA and did not change significantly after FP. This study shows that recent compared to long-standing mild asthma is associated with a similar degree of airway inflammation and subepithelial fibrosis, and a similar improvement in airway hyperresponsiveness after 8 wk on high-dose ICS. It also indicates that once asthma becomes symptomatic, airway responsiveness cannot normalize in most subjects over such a time period, even with a high dose of ICS.
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PMID:Airway hyperresponsiveness, inflammation, and subepithelial collagen deposition in recently diagnosed versus long-standing mild asthma. Influence of inhaled corticosteroids. 1102 36

Transplantation of embryonic porcine neurons may restore neurological function in patients with Parkinson's disease, if immunological rejection could be prevented. This study was performed to investigate the role of natural killer cells (NK cells) and NK1.1+ T cells (NK T cells) in the rejection of neural xenografts. A cell suspension was prepared from the ventral mesencephalon of 26-27-day-old pig embryos, and 2 microl was implanted in the right striata of mutant CD1d1 null (CD1.1-/-) mice, NK1.1-depleted mice, and controls. The CD1.1-/- mice are deficient in NK T cells and the antigen-presenting molecule CD1d1. Graft survival and host responses were determined immunohistochemically using markers for dopamine neurons, CD4-, CD8- cells, microglia, and macrophages. At 2 weeks, the grafts were significantly larger in CD1.1-/- mice, 0.09 +/- 0.02 microl (mean +/- SEM), compared with controls, 0.05 +/- 0.01 microl. There was no significant difference between NK1.1-depleted mice, 0.02 +/- 0.01 microl, and controls. At 5 weeks, two grafts were still present in the CD1-/- mice, whereas only scars remained in the controls and in the NK1.1-depleted mice. Immune reactions were strong at 2 weeks and less pronounced at 5 weeks in all groups. Microglial activation was lower in NK-depleted mice than in the controls at 2 weeks. In contrast to organ xenografting, NK1.1+ cells do not seem to be important mediators of the rejection of discordant cellular neural xenografts. However, our results suggest that the antigen-presenting molecule CD1d1 may be involved in the rejection process.
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PMID:Enhanced survival of porcine neural xenografts in mice lacking CD1d1, but no effect of NK1.1 depletion. 1143 75

The relationship between monocyte immune responses and cognitive impairment during progressive human immunodeficiency virus type 1 (HIV-1) infection was investigated in 28 subjects receiving highly active antiretroviral therapy. The mean+/-SEM CD4(+) T lymphocyte count and virus load for all patients were 237+/-41 cells/mm(3) and 77,091+/-195,372 HIV-1 RNA copies/mL, respectively. Levels of soluble tumor necrosis factor-alpha type II receptor (sTNF-RII) and soluble CD14 (sCD14) were measured in plasma by ELISA and were correlated with results from neuropsychological, magnetic resonance imaging, and magnetic resonance spectroscopy tests. Plasma sCD14 and sTNF-RII levels were elevated in subjects with cognitive impairment and in those with brain atrophy. Furthermore, both factors were correlated with spectroscopic choline:creatine ratios. These findings support the idea that peripheral immune responses are linked to cognitive dysfunction during advanced HIV-1 disease.
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PMID:Plasma levels of soluble CD14 and tumor necrosis factor-alpha type II receptor correlate with cognitive dysfunction during human immunodeficiency virus type 1 infection. 1151 30

The insulin-sensitizing drugs thiazolidinediones (TZDs), such as rosiglitazone, improve insulin sensitivity and also promote adipocyte differentiation in vitro. The authors hypothesized that TZDs might be beneficial to patients with HIV disease to improve insulin sensitivity and the distribution of body fat by increasing peripheral fat. The ability of rosiglitazone (8 mg/d) to improve insulin sensitivity (from hyperinsulinemic-euglycemic clamp) and to improve body fat distribution (determined from computed tomography measurements of visceral adipose tissue [VAT] and subcutaneous adipose tissue [SAT]) was determined in 8 HIV-positive patients. Before treatment, the insulin sensitivity of the patients was reduced to approximately 34% of that in control subjects. The rate of glucose disposal during a hyperinsulinemic-euglycemic clamp (Rd) was 3.8 +/-.4 (SEM) mg glucose/kg lean body mass/min compared with 11.08 +/- 1.1 (p<.001) in healthy age- and body mass index (BMI)-matched control subjects. After rosiglitazone treatment of 6 to 12 weeks, Rd increased to 5.99 +/-.9 (p=.02), an improvement of 59 +/- 22%. SAT increased by 23 +/- 10% (p=.05), and, surprisingly, VAT was decreased by 21 +/- 8% (p=.04) with a trend for increased SAT/VAT that failed to reach statistical significance. There were no significant changes in blood counts, viral loads, or CD4 counts with rosiglitazone treatment. The study demonstrates that rosiglitazone therapy improves insulin resistance and body fat distribution in some patients with HIV disease.
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PMID:Improved insulin sensitivity and body fat distribution in HIV-infected patients treated with rosiglitazone: a pilot study. 1239 94

The purpose of this study was to determine the efficacy of a treatment regimen consisting of CD 40 costimulation blockade, T-cell depletion, and megadose donor bone marrow transfusion in the limb allograft model. C57Bl/6 mice underwent limb transplantation from Balb/c mice and received MR1 (anti-CD 40 ligand monoclonal antibody), and CD4(+) and CD8(+) T cell-depleting antibodies with and without 120 x 10(6) donor bone-marrow transfusion. Recipients treated only with antibodies showed rejection at 51.4+/-17 (mean+/-SEM) days, while those who also received donor bone marrow had allograft survival of 67+/-16.4 days, with a range up to 91 days. Treated specimens with rejection had less lymphocytic infiltration than untreated controls. Recipients of donor bone marrow also demonstrated early mixed chimerism, which disappeared after 1 month. While allograft survival was prolonged, tolerance was not achieved, and the mechanism of rejection was more consistent with a chronic process.
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PMID:Prolonged limb allograft survival with CD 40 costimulation blockade, T-cell depletion, and megadose donor bone-marrow transfusion. 1628 Dec 78

Cigarette smoking enhances apoptosis rate of alveolar macrophages. However, little is known about the appearance and extension of apoptosis in bronchoalveolar lavage (BAL) lymphocytes originating from smoker individuals, both in pulmonary sarcoidosis (the disease characterized by lymphocytic alveolitis) and in controls. BAL was carried out in 60 nontreated patients with pulmonary sarcoidosis, subdivided acc. smoking status and in 22 control persons, free of any lung pathology. BAL (alveolar) lymphocytes were a) stained for TUNEL; b) permeabilized and stained with PI for late apoptosis/cell cycle analyses; c) immunophenotyped, including CD95, CD95 Ligand, Bcl-2, Bcl-XL, Bak and insulin-like growth factor-I (IGF-I) expression. BD FACSCalibure flow cytometer, PC Lysys and ModFit software were applied. The low number of AL entered apoptosis, which was confirmed by both techniques. Cigarette smokers were characterized by higher AL apoptosis percentage in respective subgroups (sarcoidosis: 0.6 +/- 0.13 in nonsmokers vs 0.9 +/- 0.23 in smokers; controls: 0.85 +/- 0.23 in nonsmokers vs 1.5 +/- 0.35 smokers, median +/- SEM, p < 0.05); the proliferation rate was lower. Decreased IGF-I expression in AL of sarcoidosis smokers was observed (13.5 +/- 9.2 vs 46.0 +/- 6.0 in nonsmokers, p < 0.05). No differences were found between studied groups in expression of Bcl-2, Fas and FasL molecules (except significantly declined ratio of CD8+FasL+ cells in sarcoidosis nonsmokers). AL apoptosis rate was positively correlated with respective alveolar macrophage results (Rs = +0.59, p < 0.00001) and negatively with CD4/CD8 ratio (Rs = -0.32, p < 0.001); no correlation was found with lung function test results and with Bcl-2, Fas and FasL expression in BAL cells. Apoptosis of alveolar lymphocytes was more frequent in nonsmokers both in pulmonary sarcoidosis and in controls; lower AL percentage proliferates. These phenomena seem to participate in lower AL percentage, observed in smoker subgroup of sarcoidosis. Some mechanisms of local apoptosis alterations in smokers may be common for alveolar lymphocytes and macrophages.
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PMID:[Apoptosis of alveolar lymphocytes in sarcoidosis and in control group is more frequent in smokers than in nonsmoking persons]. 1728 68

The aim of this study was to evaluate peripheral blood lymphocyte subpopulations, neutrophil phagocytic capacity and proteinogram characteristics in mares, during the last trimester of pregnancy and in postpartum. Measurement of phagocytosis and quantification of T-lymphocyte subsets were done by flow cytometry. Quantification of T-lymphocyte subsets was performed with monoclonal antibodies specific for CD2, CD3, CD4 and CD8 cell markers. Natural killer and B-cell counts were estimated mathematically. Serum proteinogram was obtained by electrophoresis. No significant differences were observed between gestation and postpartum on CD4(+), CD8(+) and NK(+) lymphocyte subsets, CD4 : CD8 ratio and phagocytosis. The percentage of cells expressing CD3 (64.2 +/- 1.8) and CD2 (68.4 +/- 1.7) (Mean +/- SEM) was reduced during gestation vs postpartum (69.7 +/- 1.5 and 73.8 +/- 1.4 respectively) (p < 0.05). During pregnancy, CD19(+) (31.6 +/- 1.7) was higher than in postpartum (26.2 +/- 1.4) (p < 0.05). Total T cells (2911 +/- 227 cells/mul), T helper cells (2144 +/- 169 cells/mul) and T-cytotoxic cells (767 +/- 68 cells/mul) were depressed in pregnancy, when compared with postpartum (4093 +/- 337 cells/mul; 3004 +/- 276 cells/mul; 1089 +/- 94 cells/mul respectively) (p < 0.01). Total white blood cell count was reduced during pregnancy (8815 +/- 427 cells/mul) with respect to postpartum (10742 +/- 446 cells/mul) (p < 0.01), while neutrophil count did not change. Total proteins, albumin, alpha(1),alpha(2),beta(1), beta(2), gamma globulins and albumin : globulin did not differ. Our results suggest that the physiological immune depression occurring in mares, during gestation might be due to T-helper and T-cytotoxic lymphocytes reduction.
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PMID:Blood lymphocyte subpopulations, neutrophil phagocytosis and proteinogram during late pregnancy and postpartum in mares. 1798 70

Idiopathic pulmonary fibrosis (IPF) is an interstitial lung disease with unfavourable outcome. Tobacco consumption in IPF exacerbates the clinical manifestations and limits the time of patient survival. The cyto-immunological alterations caused by smoking in IPF patients need particular explanation. BAL was carried out in 21 non-treated patients with IPF, subdivided according to the smoking status (n=7 for smokers). BAL routine cytology was completed by; immunotyping, including T cell major subsets (CD4 and CD8) stained for Fas, Fas ligand (FasL) and TNFR-1, late apoptosis/cell cycle analyses (BAL cells were permeabilized and stained with PI) and TUNEL assay. BAL cytology in IPF, as compared with control group, was characterized by significantly higher total cell and macrophage number, increased lymphocyte, neutrophile and eosinophile percentage and relatively low CD4/CD8 ratio. Cigarette smoking in IPF resulted in enhanced BAL lymphocyte CD8 cell percentage and number, as compared with nonsmoking subgroup and further decline in CD4/CD8 ratio (0.41+/-0.15 vs 1.23+/-0.29 in nonsmokers, median +/- SEM, p<0.05). The percentage of CD8, but not CD4 cells carrying Fas Ligand was significantly increased in IPF smokers (12.0+/-3.1% vs 3.7+/-0.9% in nonsmokers, median +/- SEM, p<0.05). Apoptosis rate of BAL macrophages and lymphocytes was enhanced in IPF, as compared with controls (confirmed by both techniques), but without remarkable changes, if compared one IPF subgroup to another. The number and percentage of CD8+FasL+ was negatively correlated with vital capacity (VC) values in IPF patients, but not with BAL inflammatory cell apoptosis rate. Cigarette smoking enhanced a percentage as well as a total number of both BAL CD8 and BAL CD8+FasL+ cells in IPF patients. BAL cytotoxic cells (CD8+FasL+ lymphocytes) seem to have impact on impaired lung function in smoking IPF patients.
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PMID:[Cigarette smoking results in the number of CD8+Fas Ligand+ T cytotoxic lymphocytes in bronchoalveolar lavage (BAL) fluid of patients with idiopathic pulmonary fibrosis (IPF)]. 1840 87

Antiretroviral therapy in human immunodeficiency virus infection is occasionally associated with poor immunologic responses despite full suppression of viral replication. As some combinations of nucleoside analogues (NA) have been associated with paradoxical depletion of CD4(+) T- cells, we postulated that depleting the antiretroviral regimen of NAs would improve quantitative immunological parameters. In a longitudinal prospective study we quantified CD4(+) T-cells after removing NAs from antiretroviral therapy. The NA for regimen consisted of atazanavir (300 mg qd), saquinavir (1000 mg bid), and ritonavir (100mg qd) in 14 patients with immunologic failure despite undetectable plasma HIV-RNA (CD4(+) T-cells < 250 cells/microL (<17%) HIV RNA, <= 50 copies/mL). Additionally, we assessed the state of immunologic activation markers (CD38(+)HLA-DR(+) on CD4(+) and CD8(+) T-cells) by flow cytometry. The regimen was well tolerated. During the 48 week study CD4(+) T-cell counts improved significantly (mean and +/- SEM [standard error of mean], baseline: 174/microL (12.4%) [15, 5.8%], week 24: 232/microL (14%) [26, 5.3%], week 48: 267/microL (15.4%) [34, 4.3%]) with preservation of full viral suppression (p<0.05). Activation parameters of CD4(+) T-cells, but not of CD8(+) T-cells, decreased significantly. This treatment strategy may represent an option for patients with poor immunologic responses to antiretroviral therapy despite undetectable viremia.
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PMID:Nucleoside-free boosted double PI regimen: significant CD4+ T-cell recovery in patients with poor immunologic response despite virologic suppression. 1899 21


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