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)

In order to explore the allelic polymorphism of HLA-DR and TNF B loci and susceptibility to systemic lupus erythematosus (SLE) in the Han nationality of northern China with the aid of methods of polymerase chain reaction/sequence specific primers (PCR/SSP) and polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) respectively. The findings from a case-control study on 151 blood samples (45 from the cases and 106 from the controls) indicated that there were significantly higher frequency of DR2 (P < 0.05, RR = 1.56) and DR3 (P < 0.01, RR = 2.69), which represent candidate susceptible genes or useful markers for SLE. The DR5 allele in the samples (P < 0.05, RR = 0.43) might be an antagonistic or protective allele, or a marker for such allele. The frequency of TNF B * 1 and TNF B * 2 alleles was investigated in 45 SLE patients and 80 healthy controls and it was found that the frequency of TNF B * 2 allele was significantly higher in the patient group (P < 0.05, RR = 1.84). It might also be a suspicious susceptible allele or a marker for such allele. The frequency of HLA polymorphisms in various clinical/immunological subsets of our patient population was also determined. Clinical findings used include plasma SC5b-9 level, SSA, SSB, Sm, RNP, ANA antibodies, and SLE complications (SLE nephritis, pneumonia & encephalopathy). It turned out that there was a positive association between HLA-DR2 allele and SLE nephritis (P < 0.05, RR = 1.32).
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PMID:[Study on some susceptible genes of systemic lupus erythematosus in Han nationality of China]. 927 40

With the aid of methods of polymerase chain reaction/sequence specific primers (PCR/SSP) and polymerase chain reaction-restriction fragment length polymorphism (PCR/RFLP), the allelic polymorphism of HLA-DR and TNFB loci and susceptibility to systemic lupus erythematosus (SLE) in northern Chinese Han nationality were studied. The genetic analysis of 51 patients with SLE and 106 healthy controls indicated that frequencies of DR2 and DR3 alleles were significantly increased in SLE patients (P < 0.05 and < 0.005, relative risks of 1.77 and 4.01 respectively), which represent candidate susceptible genes or useful marker for SLE. The frequency of DR5 was found to decrease in SLE patients compared with control population (P < 0.025, relative risk = 0.38). It might be an antagonistic or protective allele or a marker for such allele. Analysis of 51 patients with SLE and 80 healthy control also revealed that the frequency of TNFB*2 allele was significantly increased (P < 0.05, RR = 1.70). Therefore TNFB*2 gene may also be a susceptibility gene or a marker gene for SLE in northern Chinese Han nationality. It was also investigated the association between HLA-DR, TNF B alleles and Patient plasmic SC5b-9 levels, auto-antibodies (anti-SSA, SSB, Sm, RNP, ds DNA and ANA) and SLE complications (SLE nephritis, SLE pneumonitis and SLE encephalopathy), no relationship was found.
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PMID:The polymorphisms of HLA-DR and TNF B loci in northern Chinese Han nationality and susceptibility to systemic lupus erythematosus. 1132 94

Allergic bronchopulmonary aspergillosis (ABPA) occurs in patients with asthma or cystic fibrosis resulting in pulmonary infiltrates, tenacious mucus plugs that harbor hyphae of Aspergillus fumigatus, elevations of total serum IgE concentration and peripheral blood, and sputum eosinophilia. Bronchiectasis is an irreversible complication of ABPA. The key to early diagnosis is considering ABPA in anyone with asthma or cystic fibrosis and a positive skin test to Aspergillus and /or recurrent infiltrates on radiographs. The differential diagnosis for ABPA in patients with asthma includes diseases in which there is an overlap of asthma, peripheral blood eosinophilia, and radiographic infiltrates. Examples include chronic eosinophilic pneumonia, Churg-Strauss syndrome, drug-induced pulmonary infiltrates, infection with a parasite, asthma with atelectasis, and lymphoma. Mucus plugging causing a "tree in bud" pattern on CT examination of the lungs may be from ABPA or other conditions such as nontuberculous (atypical) mycobacteria (Mycobacteria avium-intracellulare complex). Prednisone is indicated to clear pulmonary infiltrates, and a usual course is for 3 months. Itraconazole and voriconazole are adjunctive and drug-drug interactions must be considered as azoles decrease elimination of various medications. Although not familial in most patients, presentation of Asp f1 antigen is restricted to specific major histocompatability complex class II molecules, HLA-DR2 and HLA-DR5. There is an increased number of CD4(+) Th2 lymphocytes in bronchoalveolar lavage, and Aspergillus fumigatus can serve as a growth factor of eosinophils potentiating the effects of IL-3, IL-5, and granulocyte colony-stimulating factor.
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PMID:Chapter 18: Allergic bronchopulmonary aspergillosis. 2279 91

Apoptotic death of alveolar macrophages observed during lung infection with Streptococcus pneumoniae is thought to limit overwhelming lung inflammation in response to bacterial challenge. However, the underlying apoptotic death mechanism has not been defined. Here, we examined the role of the TNF superfamily member TNF-related apoptosis-inducing ligand (TRAIL) in S. pneumoniae-induced macrophage apoptosis, and investigated the potential benefit of TRAIL-based therapy during pneumococcal pneumonia in mice. Compared with WT mice, Trail(-/-) mice demonstrated significantly decreased lung bacterial clearance and survival in response to S. pneumoniae, which was accompanied by significantly reduced apoptosis and caspase 3 cleavage but rather increased necrosis in alveolar macrophages. In WT mice, neutrophils were identified as a major source of intraalveolar released TRAIL, and their depletion led to a shift from apoptosis toward necrosis as the dominant mechanism of alveolar macrophage cell death in pneumococcal pneumonia. Therapeutic application of TRAIL or agonistic anti-DR5 mAb (MD5-1) dramatically improved survival of S. pneumoniae-infected WT mice. Most importantly, neutropenic mice lacking neutrophil-derived TRAIL were protected from lethal pneumonia by MD5-1 therapy. We have identified a previously unrecognized mechanism by which neutrophil-derived TRAIL induces apoptosis of DR5-expressing macrophages, thus promoting early bacterial killing in pneumococcal pneumonia. TRAIL-based therapy in neutropenic hosts may represent a novel antibacterial treatment option.
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PMID:TNF-related apoptosis-inducing ligand (TRAIL) exerts therapeutic efficacy for the treatment of pneumococcal pneumonia in mice. 2307 Dec 53

Allergic bronchopulmonary aspergillosis (ABPA) occurs in patients with asthma or cystic fibrosis, and results in pulmonary infiltrates, tenacious mucus plugs that harbor hyphae of Aspergillus fumigatus, elevations of total serum immunoglobulin E concentration and peripheral blood and sputum eosinophilia. Bronchiectasis is an irreversible complication of ABPA. The key to early diagnosis is to consider ABPA in anyone with asthma or cystic fibrosis and with a positive skin test result for Aspergillus, and/or recurrent infiltrates on radiographs. The differential diagnosis for ABPA in patients with asthma includes diseases in which there is an overlap of asthma, peripheral blood eosinophilia, and radiographic infiltrates. Examples include chronic eosinophilic pneumonia, Churg-Strauss syndrome, drug-induced pulmonary infiltrates, infection with a parasite, asthma with atelectasis, and lymphoma. Mucus plugging that causes a "tree in bud" pattern on computerized tomography examination of the lungs may be from ABPA or other conditions, such as nontuberculous (atypical) mycobacteria (Mycobacteria avium-Mycobacteria intracellulare complex). Prednisone is indicated to clear pulmonary infiltrates, and a usual course is for 3 months. Itraconazole and voriconazole are adjunctive, and drug-drug interactions must be considered because azoles decrease elimination of various medications. Although not familial in most patients, presentation of Aspergillus fumigatus f1 (Asp f1) antigen is restricted to specific major histocompatibility complex (MHC) class II molecules, Human Leukocyte Antigen-DR2 (HLA-DR2), and HLA-DR5. There is an increased number of CD4+ T-helper type 2 lymphocytes in bronchoalveolar lavage, and A. fumigatus can serve as a growth factor of eosinophils potentiating the effects of interleukin (IL) 3, IL-5, and Granulocyte-colony stimulating factor (G-CSF). Eosinophils interact directly with A. fumigatus spores and generate extracellular traps, which can injure the bronchial epithelium.
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PMID:Allergic bronchopulmonary aspergillosis. 3169 Mar 85