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Query: UMLS:C0021051 (immunodeficiency)
 71,517 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The level of human immunodeficiency virus type 1 (HIV-1) in lymphocytes and mononuclear phagocytes (MP) from the blood and pulmonary alveoli from 14 HIV-1-infected subjects during early (asymptomatic) and late (AIDS) stages of disease and the relationship between virus burden in MP and cytokine expression were assessed. Among asymptomatic subjects, HIV-1 was undetectable or low in both blood monocytes and alveolar macrophages (AM). Among subjects with AIDS, there was a significant increase of HIV-1 in AM but not monocytes. The level of HIV-1 in blood lymphocytes was higher than in either monocytes or AM. AM (but not monocytes) expressed increased levels of lipopolysaccharide-stimulated cytokine mRNA (tumor necrosis factor-alpha, interleukin-1 beta, interleukin-6) during both early and late stages of HIV-1 infection regardless of virus load. AM thus may serve as a reservoir for virus in late stages of disease yet contribute to the immunopathogenesis of lung disease in both early and late stages through increased cytokine expression.
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PMID:Relationship between load of virus in alveolar macrophages from human immunodeficiency virus type 1-infected persons, production of cytokines, and clinical status. 827 80

Surfactant lipids are not only important to the physiologic function of the lungs, but may also influence disease processes like Pneumocystis pneumonia, in which the interaction of host-defense cells with pathogen occurs within the confines of the surfactant-rich alveolar hypophase. In the present studies the lipid profile of bronchoalveolar lavage fluid (BALF) was characterized in subjects with AIDS-related lung diseases including Pneumocystis pneumonia. BALF lipid and total protein measurements were made in 43 subjects with acquired immune deficiency syndrome (AIDS)-related lung disease and compared with those made in 50 normal human immunodeficiency virus (HIV)-seronegative controls. The AIDS patient samples contained significantly greater amounts of total cholesterol, phosphatidylglycerol (PG), and protein than the control samples; in contrast to previous observations in rodent P. carinii infection, no differences were seen in total phospholipid (PL) or phosphatidylcholine (PC) in the two groups. The proportions of several of these lipids were deranged in BALF obtained from the patient group: PG/PL and PC/cholesterol differed significantly from normal samples. In the subset of patients with AIDS-related Pneumocystis pneumonia, no correlation was apparent between discrete BALF lipids and clinical indices reflective of disease severity. Using these measurements to approximate the lipid composition of the alveolar microenvironment in AIDS-related lung disease, we performed experiments in which normal human alveolar macrophages were exposed to exogenous liposomal lipids and then challenged with P. carinii. The ingestion but not binding of P. carinii by macrophages was diminished as a result of lipid exposure.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Abnormal lipid composition of bronchoalveolar lavage fluid obtained from individuals with AIDS-related lung disease. 830 26

Tuberculosis continues to be one of the major causes of morbidity and mortality in the developed and developing countries. There are more than 5000 cases of active open tuberculous lung disease in Germany. Worldwide approximately 10 million persons get tuberculous infections each year. Other not yet infected people in the community are endangered by this disease, especially those with immunodeficiency e.g. AIDS-patients or tumor patients. M. tuberculosis with its unique glycolipid cell wall is fairly resistant against the immune system. Only specialized activated macrophages are able to inhibit its growth. The bacteria may persist for years in the living body, probably in granulomas. A positive tuberculin-reaction indicates an infection and persistance of mycobacteria but does not prove a disease. Approximately 1.5 billion people are tuberculin positive worldwide. Any weakening of the immune system can unleash M. tuberculosis to cause reactivation and active tuberculous disease. The main diagnostic tools since the time of Robert Koch are microscopy and culture. Neither immunoserology nor polymerase chain reaction are of significant diagnostic value until now. It is possible to cure each new tuberculosis case by adequate and continuous therapy. Resistance of M. tuberculosis against the "classical" antituberculotic agents mainly arises from non-compliance of treated patients. Multiresistant strains make tuberculosis incurable. In Germany, in contrast to some regions in Africa, Asia or in the United States of America, resistance against one of the antituberculotic drugs is still relatively low (5-10%). BCG-vaccination is recommended for high risk-groups only. Preventive chemotherapy is indicated for persons with conversion of tuberculin-reaction from negative to positive. The main infectious danger results from individuals with undiscovered active tuberculous lung disease via airborne droplet transmission. Therefore the most important task is to discover these persons in time by always considering the disease, when the corresponding symptoms are being observed. Because of the mentioned problems new efforts should be done to investigate the pathogenesis of the disease and its therapy with alternative drugs.
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PMID:[Persistence of mycobacteria in the host: epidemiology, immunopathology and prophylaxis]. 833 93

CD8+ T cells predominate in the lungs in hypersensitivity and human immunodeficiency virus-related lymphocytic pneumonitis, but their role in the immunopathogenesis of lung disease is unknown. We have shown that in immunized mice depleted of CD4+ T cells, CD8+ T cells are recruited into the lungs in response to intratracheal antigen challenge with sheep red blood cells (SRBC) (J. Clin. Invest. 1991; 88:1244-1254) or to pulmonary infection with Pneumocystis carinii (Am. J. Respir. Cell Mol. Biol. 1991; 5:186-197), suggesting that recruitment of CD8+ T cells does not depend on CD4+ T cell-derived signals. Because CD8+ T cells themselves produce a variety of chemotactic and immunoregulatory cytokines, CD8+ T cells may be important participants in, and modulators of, pulmonary immune responses. To test this hypothesis, we examined the effects of CD8+ T cell depletion on the generation of a pulmonary immune response in vivo. We monitored the recruitment of mononuclear cells into lungs in the absence of CD8-dependent signals and measured the duration of pulmonary inflammation in the absence of suppressor CD8+ T cells. Primed mice were treated with anti-CD8 monoclonal antibody to deplete CD8+ T cells and subsequently were challenged intratracheally with 5 x 10(8) SRBC. At various times after challenge, total and differential cell counts and lymphocyte phenotypes were measured in bronchoalveolar lavage fluid by flow cytometry and lungs were scored histologically. We found that depletion of CD8+ T cells neither decreased recruitment of immune and inflammatory cells nor prolonged the pulmonary immune response.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Pulmonary lymphocyte recruitment: depletion of CD8+ T cells does not impair the pulmonary immune response to intratracheal antigen. 833 79

Pulmonary aspergillosis is a relatively common fungal infection in individuals who are immunocompromised or have intrinsic lung disease. Clinical, radiological, and pathologic manifestations are quite varied and depend to a large extent on the type and severity of local or systemic host defense abnormalities. In individuals with only structural lung damage, saprophytic growth alone is the rule. Patients with atopy or other hypersensitivity state typically develop allergic disease, most often allergic bronchopulmonary aspergillosis. Individuals with other immunologic abnormalities, particularly immunodeficiency, and with granulocytopenia characteristically develop invasive disease, which may take several morphological forms. Identification of Aspergillus as the cause of all these disease variants is usually not a problem. However, recognition of the different patterns of disease is useful in understanding the pathogenesis of disease and in interpreting premortem clinical and radiographic abnormalities.
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PMID:Pulmonary aspergillosis: pathologic and pathogenetic features. 841 39

The authors report the radiographic findings in two patients with the human immunodeficiency virus (HIV) who presented with cavitary lung disease caused by Aspergillus. Recognition of the disease in one of the patients led to successful medical therapy. Disease due to Aspergillus must be considered in HIV-positive patients with cystic or cavitary disease appearing in chest radiographs.
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PMID:Cavitary aspergillosis as a complication of AIDS. 842 53

Penicillium marneffei, a dimorphic fungus that is endemic in southeast Asia, causes deep-seated infection in humans and rodents. About 20 cases have been reported among the local populations of China, Thailand, and Hong Kong, and 35 cases have now been described in patients infected with the human immunodeficiency virus (HIV). We present a review of the literature and report two additional cases. Both immunocompromised and apparently immunocompetent hosts tend to develop disseminated, symptomatic infection. HIV-infected patients having travelled to southeast Asia and presenting with fever, skin lesions, hepatomegaly, adenopathies, or lung disease should be investigated for Penicillium marneffei infection. The diagnosis is based on the demonstration of the organism in clinical specimens. Treatment with amphotericin B or itraconazole is generally successful, but maintenance therapy is warranted for patients with an underlying immunodeficiency.
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PMID:Disseminated Penicillium marneffei infection associated with human immunodeficiency virus: a report of two cases and a review of 35 published cases. 848 10

A 5-year-old boy with spastic quadriplegia, T cell immunodeficiency, hypouricemia and immune cytopenias from age 8 months, was found to have purine nucleoside phosphorylase (PNP) deficiency, and developed chronic lung disease. Successful matched sibling BMT for PNP deficiency has not previously been reported. BMT using marrow from an HLA-identical sibling donor was performed after conditioning with busulfan (16 mg/kg), cyclophosphamide (200 mg/kg), melphalan (90 mg/m2) and anti-thymocyte globulin (36 mg/kg). T lymphocyte numbers, PNP activity and uric acid levels rapidly improved and he remains well 12 months after transplant.
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PMID:Late diagnosis and correction of purine nucleoside phosphorylase deficiency with allogeneic bone marrow transplantation. 867 45

The differential diagnosis of cavitary pulmonary lesions in individuals infected with human immunodeficiency virus (HIV) is broad, especially in patients with advanced disease. In patients with Pneumocystis carinii pneumonia, cavitation is an uncommon manifestation of a common disease. It is unusual in patients with pulmonary cryptococcosis, coccidioidomycosis, and histoplasmosis but occurs frequently in patients with invasive pulmonary aspergillosis. In patients with pulmonary tuberculosis, cavities are more common during earlier stages of HIV disease, when cellular immunity is relatively preserved. Mycobacterium avium complex is an uncommon cause of lung disease and infrequently produces cavities. However, Mycobacterium kansasii, is often associated with cavitation. Cavities can complicate any bacterial pneumonia and are especially common with pneumonia due to Pseudomonas aeruginosa, Nocardia asteroides, and Rhodococcus equi. Noninfectious causes of cavitary lesions are rare, but cavitary lesions caused by pulmonary Kaposi's sarcoma and non-Hodgkin's lymphoma have been reported. Because of the broad differential diagnosis and because most cavities are caused by treatable opportunistic infections, a definitive diagnosis is essential.
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PMID:Cavitary pulmonary lesions in patients infected with human immunodeficiency virus. 872 7

Use of methotrexate to treat rheumatoid arthritis is associated with pulmonary adverse effects in 3% to 5% of cases. In addition to immunoallergic lung disease, bronchitis and pneumonia due to pyogenic organisms, opportunistic lower respiratory tract infections have been reported, including, to our knowledge, 18 cases of Pneumocystis carinii pneumonia. We report two new cases of P. carinii pneumonia in methotrexate-treated rheumatoid arthritis patients. One case occurred in a 62-year-old woman with a nine-year history of seropositive rheumatoid arthritis treated for the last seven months with methotrexate, 15 mg per week, and prednisone, 10 mg/d. The other patient was a 58-year-old woman who had been diagnosed with rheumatoid arthritis 18 months earlier and had been receiving 15 mg per week of methotrexate for eight months in combination with 12.5 mg of prednisone per day. Both patients had negative tests for the human immunodeficiency virus. Symptoms consisted of fever, cough and dyspnea, with interstitial infiltrates on chest films, hypoxia, and lymphopenia (700 and 600/mm3, respectively). The diagnosis was confirmed by bronchoalveolar lavage. Both patients recovered under treatment with trimethoprim-sulfamethoxazole. An analysis of the 20 cases of P. carinii pneumonia reported to date in methotrexate-treated rheumatoid arthritis patients demonstrated a number of characteristics: the rheumatoid arthritis was of recent onset in some cases (a few months in one patient); lymphopenia was present in two thirds of cases; one-third of patients were not receiving corticosteroid therapy; the dosage and duration of methotrexate therapy varied widely, from 5 to 30 mg per week and two to 48 months; and four patients died.
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PMID:Pneumocystis carinii pneumonia in rheumatoid arthritis patients treated with methotrexate. A report of two cases. 881 57


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