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

Cutaneous T-cell lymphomas (CTCL) are diseases characterized by cutaneous infiltrates of malignant clonally expanded T cells. CTCL cells exhibit a cytokine profile consistent with T helper-2 type (TH2) cells. Eosinophilic pneumonias are individual syndromes characterized by eosinophilic pulmonary infiltrates and commonly peripheral blood eosinophilia. CTCL and chronic eosinophilic pneumonia are rare clinical entities. We report a patient with the association of CTCL and chronic eosinophilic pneumonia. To understand the mechanism leading to the eosinophilia, we examined the patient's cytokine profile. This was consistent with a high TH2 activity. Her interleukin (IL) 5, 6, and 10 levels were extremely high, while her IL-2 and interferon-gamma (IFN-gamma) levels (TH1 profile) were low. We believe that eosinophilic pneumonia in this patient is probably secondary to high TH2 cytokine levels induced by tumor cells. We suggest that eosinophilic pneumonia should be considered as a possible diagnosis in patients with CTCL who have respiratory complaints.
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PMID:Chronic eosinophilic pneumonia associated with cutaneous T-cell lymphoma. 992 8

Respiratory infections remain common and may be more difficult to treat because new microbes have been identified; commensal flora can become pathogens; and antibiotic resistance is developing, especially to Streptococcus pneumoniae. Contributing to the severity of pneumonia is the increasing number of more susceptible hosts--immunodeficient patients, created as a by-product of modern medical therapy or from infection with HIV, and elderly patients who have associated illnesses. Better strategies to replete immunocompromised hosts are required. Vaccination to modify infection with S. pneumoniae must be given higher priority by health care providers. New means to immunize the respiratory mucosal surface are needed. Research approaches to consider involve 1) targeting (carrying) relevant antigens to appropriate antigen-processing cells in the airways, eg, dendritic cells; and 2) coupling the immunomodulatory effects of cytokines, eg, interleukin-12. Interleukin-12, for example, can stimulate mucosal antibody responses producing S-IgA and IgG and cause T lymphocytes to produce interferon-gamma that can enhance microbial killing by macrophages.
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PMID:Defense mechanisms against infections. 1022 37

Rhodococcus equi is a facultative intracellular bacterial pathogen that causes pneumonia in foals and immunosuppressed humans. There are at least three virulence levels of R. equi and these pathogenicities are associated, in mice, with the presence of virulence plasmids. This study focused on cytokine secretion, in mice, in the course of a primary infection with sublethal doses of R. equi strains of different virulence levels (virulent, intermediately virulent and avirulent). Tumour necrosis factor (TNF) and interferon-gamma (IFN-gamma), but not interleukin-4 (IL-4) and interleukin-10 (IL-10), were induced endogenously in mice in relation to the multiplication and clearance of virulent and intermediately virulent strains of R. equi. These cytokines were not detected in mice infected with avirulent R. equi. Deaths occurred among mice treated with monoclonal antibodies (mAbs) against either TNF or IFN-gamma prior to sublethal dose infection with virulent and intermediately virulent strains of R. equi, but not with avirulent R. equi. These results suggested that cytokine production depended largely on the virulence levels of R. equi: TNF and IFN-gamma were required early during infection with virulent R. equi to limit replication and clearance of bacteria within the organs, but they were not necessary for limiting infection with avirulent R. equi.
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PMID:Tumour necrosis factor and interferon-gamma are required in host resistance against virulent Rhodococcus equi infection in mice: cytokine production depends on the virulence levels of R. equi. 1023 86

Studies were carried out to characterize the cellular and humoral immune responses evoked by intramuscular DNA vaccination with the major outer membrane protein (MOMP) gene of Chlamydia trachomatis mouse pneumonitis strain. The data demonstrate that DNA vaccinated mice develop antigen-specific delayed-type hypersensitivity, lymphocyte proliferation and interferon-gamma (IFN-gamma) production. Serum antibody responses (mainly immunoglobulin G2a; IgG2a) were evoked in two-thirds of the mice. We conclude that intramuscular DNA immunization with the MOMP gene evokes cellular and humoral immune responses suggestive of a T helper 1 (Th1) bias.
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PMID:Characterization of immune responses following intramuscular DNA immunization with the MOMP gene of Chlamydia trachomatis mouse pneumonitis strain. 1023 11

Strains of the Burkholderia cepacia complex have emerged as a serious threat to patients with cystic fibrosis due to their ability to infect the lung and cause, in some patients, a necrotizing pneumonia that is often lethal. It has recently been shown that several strains of the B. cepacia complex can escape intracellular killing by free-living amoebae following phagocytosis. In this work, the ability of two B. cepacia complex strains to resist killing by macrophages was explored. Using fluorescence microscopy, electron microscopy and a modified version of the gentamicin-protection assay, we demonstrate that B. cepacia CEP021 (genomovar VI), and Burkholderia vietnamiensis (previously B. cepacia genomovar V) CEP040 can survive in PU5-1.8 murine macrophages for a period of at least 5 d without significant bacterial replication. Furthermore, bacterial entry into macrophages stimulated production of tumour necrosis factor and primed them to release toxic oxygen radicals following treatment with phorbol myristoyl acetate. These effects were probably caused by bacterial LPS, as they were blocked by polymyxin B. Infected macrophages primed with interferon gamma produced less nitric oxide than interferon-gamma-primed uninfected cells. We propose that the ability of B. cepacia to resist intracellular killing by phagocytic cells may play a role in the pathogenesis of cystic fibrosis lung infection. Our data are consistent with a model where repeated cycles of phagocytosis and cellular activation without bacterial killing may promote a deleterious inflammatory response causing tissue destruction and decay of lung function.
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PMID:Intracellular survival of Burkholderia cepacia complex isolates in the presence of macrophage cell activation. 1062 44

Vitamin A supplementation during acute pneumonia has not improved recovery in most human clinical trials. We hypothesize that high vitamin A intake may decrease the production of T-helper type-1 (Th1) cytokines and thereby inhibit antiviral responses. Such decreases might impair recovery from viral respiratory infections. We thus examined the effect of three interventions on viral pneumonia: 1) a high level vitamin A [250,000 IU/kg diet or 75,000 retinol equivalents (RE)/kg], or 2) control diet (4000 IU/kg diet or 1200 RE/kg) given before and during infection, and 3) initiating the high level diet upon infection to simulate the adjuvant therapy used in clinical trials. No difference was seen among the interventions in severity of disease (weight loss, lung virus titers and survival). However, both the high level diet group and the group in which vitamin A was increased at the time of infection had greater salivary immunoglobulin (Ig)A responses (geometric means, 166 and 105 microg/L, respectively) than did the control group (59 microg/L) (P = 0.0019). In contrast, the serum IgG response was higher in the control group (324+/-158 mg/L) than in the high level group (225+/-95 mg/L) (P = 0.028), although it did not differ from the group in which the diet was changed upon infection (230+/-163 mg/L) (P = 0.084). The production of interferon-gamma (IFN-gamma), a Th1 cytokine, was lower in the high level diet group (median, 0.153 microg/L) compared with the control group (median, 0.839 microg/L) (P = 0.014), whereas the production of interleukin-10 (IL-10), a Th2 cytokine, was higher with the high level diet (median, 0.304 microg/L) than with the control (median, 0.126 microg/L) (P = 0.022). This change in the Th1/Th2 pattern was not sufficient to affect recovery from viral pneumonia but may account for the increased IgA and decreased IgG responses seen with high level dietary vitamin A in this study. These data reinforce the lack of utility of vitamin A in treating acute pneumonia in children and suggest that high dose vitamin A supplements may enhance Th2-mediated immune responses, which are particularly beneficial in the case of extracellular bacterial and parasitic infections and IgA-mediated responses to mucosal infections.
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PMID:High-level dietary vitamin A enhances T-helper type 2 cytokine production and secretory immunoglobulin A response to influenza A virus infection in BALB/c mice. 1080 9

A 62-year-old white woman with chronic hepatitis C virus infection was diagnosed with systemic sarcoidosis during treatment with interferon-alpha. Seventeen cases of sarcoidosis associated with interferon treatment have been reported, with only 8 inpatients with chronic hepatitis C virus infection. Our patient, with no past history of sarcoidosis, developed subcutaneous sarcoid nodules, arthritis, uveitis, pneumonitis and heart involvement two months after she was started on treatment with interferon-alpha. Her symptoms resolved when she began corticosteroid therapy and interferon-alpha was stopped. This case report suggests that exogenous interferon-alpha may trigger or contribute to the development of this multisystem granulomatous disorder in which interferon-gamma and CD4 + T-lymphocyte are mainly involved. Patients should be monitored during and following interferon-alpha therapy, since the autoimmune diseases induced by interferon therapy do not always improve after cessation of treatment.
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PMID:[Systemic sarcoidosis during interferon-alpha therapy for chronic hepatitis C virus infection]. 1080 48

Bacterial empyema is a frequent complication of pneumonia in patients with acquired immunodeficiency syndrome (AIDS). A model of Staphylococcus aureus empyema was developed that closely resembles bacterial empyema in patients infected with human immunodeficiency virus (HIV). Results show a compartmentalized chemokine response in bacterial empyema. The chemokine levels were higher in the pleural compartment than in the peripheral circulation. Polymorphonuclear leukocyte counts, murine GRO-alpha (KC), and macrophage inflammatory protein-2 levels were significantly (P<.001) lower in CD4+ knockout (CD4 KO) mice pleural fluid than in CD4+ wild-type (CD4 WT) mice. The CD4 KO mice had poorer bacterial clearance than CD4 WT mice. During S. aureus infection, interleukin-10 levels increased in the CD4 KO mice, whereas interferon-gamma levels were increased in CD4 WT mice. CD4+ T cell depletion results in a decreased pleural chemokine response, decreased neutrophil influx into pleural space, and impaired bacterial clearance in empyema.
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PMID:Induction of acute pleural inflammation by Staphylococcus aureus. I. CD4+ T cells play a critical role in experimental empyema. 1082 70

Several studies have been carried out to clarify the relationship between CD30 expression and Th2 lymphocytes, although the results have been controversial. To investigate whether CD30 is a useful marker for Th2 lymphocytes in bronchoalveolar lavage (BAL) in interstitial lung diseases (ILD), we studied six control subjects and 31 patients with ILD (12 with idiopathic pulmonary fibrosis, seven with hypersensitivity pneumonitis, three with chronic eosinophilic pneumonia and nine with sarcoidosis). The levels of interleukin-5 (IL-5) (secreted by Th2 cells), interferon-gamma (IFNgamma) (secreted by Th1 cells) and the expression of CD30 on lymphocytes were determined in BAL fluid. There were no differences in the percentage of CD30+ lymphocytes between controls and patients with ILD (0.8+0.4% vs. 2+/-0.4%). In order to determine the relationship between Th2 cells and CD30 expression, we divided the patients into two groups according to BAL IL-5 levels. Group I consisted of eight patients (three chronic eosinophilic pneumonia, three hypersensitivity pneumonitis, two idiopathic pulmonary fibrosis) with high IL-5 levels (298+/-138 pg ml(-1)). Group II consisted of the remaining 23 ILD patients with normal IL-5 levels (0.9+/-0.6 pg ml(-1)). The percentage of eosinophils in BAL fluid was significantly higher in group I compared with group 11 (34+/-16% vs. 3+/-1%, P < 0.05). A correlation between CD30+ lymphocytes and IL-5 in group 1 was not shown. There were no differences in the number of CD30+ I we found a significant correlation between IL-5 levels and the percentage of eosinophils (r = 0.95, P < 0.0001). Our results suggest that CD30 does not appear to be a useful marker for Th2 lymphocytes in BAL from patients with ILD.
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PMID:Evaluation of CD30 as a marker for th2 lymphocytes in bronchoalveolar lavage in interstitial lung diseases. 1084 32

We report a rare case of a male patient without known immunodeficiency consecutively diagnosed with visceral leishmaniasis, brain abscess and cavitating pneumonia in the 3rd decade of life. Chronic granulomatous disease (CGD) was diagnosed by a nitroblue tetrazolium test. A p47-phox mutation of the NADPH oxidase of the leukocytes was suspected by immunoblotting and confirmed by DNA analysis. The patient was homozygous for this mutation while his mother and sister were heterozygous asymptomatic carriers. After the CGD diagnosis the patient started a chronic prophylactic regimen with subcutaneous interferon-gamma (0.05 mg/m2 of body surface/three times a week), and oral trimethoprim-sulfamethoxazole and itraconazole (both at 5 mg/kg/day) with no subsequent infections after 12 months of follow-up.
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PMID:Visceral leishmaniasis and other severe infections in an adult patient with p47-phox-deficient chronic granulomatous disease. 1087 44


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