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)

Despite the advent of highly active antiretroviral therapy, pulmonary complications in AIDS are a common clinical problem. Pneumocystis jiroveci infection causes a life-threatening pneumonia, especially in individuals with CD4 T cell deficiencies as occurs in AIDS. Although Pneumocystis sp. is an extracellular fungal pathogen, CD8 T cells are the predominant lymphocyte recruited to the lung in CD4-deficient humans and mice during Pneumocystis pneumonia, and we have found that these CD8 T cells are responsible for subsequent lung damage in CD4 T cell-depleted mice. Comparing CD4 T cell-depleted IFN-alpha receptor knockout (KO) mice to wild-type mice, we found that this CD8 T cell recruitment and lung damage is type I IFN (IFN-alphabeta) dependent. However, in both CD4 competent, wild-type and IFN-alpha receptor (IFNAR) KO mice, Pneumocystis infection leads to an eosinophilic granulocyte influx with bronchial epithelial changes as seen in asthma. This response is delayed in IFNAR KO mice, as is pathogen clearance. Although the inflammation is transient in wild-type animals and resolves upon Pneumocystis clearance, it is more severe and persists through day 35 postinfection in IFNAR KO mice, leading to fibrosis. In addition, IFNAR KO, but not wild-type, mice mount a Pneumocystis-specific IgE response, an indicator of allergic sensitization. Thus, in the absence of IFNAR signaling and CD4 T cells, Pneumocystis-mediated lung damage does not occur, whereas in CD4-competent animals, the absence of IFNAR signaling results in an exacerbated Th2 response, asthma-like symptoms, and fibrosis. Therefore, both CD4 T cell- and type I IFN-mediated mechanisms can determine pulmonary complications from Pneumocystis infection.
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PMID:Role of type I IFNs in pulmonary complications of Pneumocystis murina infection. 1584 44

The hyper-IgM syndrome (HIM) is a rare primary immunodeficiency disorder caused by defects in the CD40 ligand (CD40L)/CD40-signaling pathway. It is characterized by recurrent infections with markedly decreased IgG, IgA and IgE levels but normal or elevated serum IgM levels. A 5-month-old boy presented with rapidly progressive pneumonia which responded poorly to antibiotics. High levels of IgM and very low levels of IgG, IgE and IgA were noted in his plasma specimen (IgM, 128 mg/dl; IgG, 18 mg/dl; IgE, 1 IU/ml; IgA, 4 mg/dl). The relative proportions of immune cells were CD3 24.6%, CD4 10.3%, CD8 2.2%, CD19 30.2%, CD57 1.0% and active T cells 1.1%. After IVIG treatment, the pneumonia improved. Repeat assessment at the age of 15 months showed IgM decreased to the normal range (32 mg/dl). Whole blood flow cytometry assay for CD40L expression confirmed the diagnosis of hyper-lgM syndrome when he was 21 months old. Only a small percentage (0.48%) of the patient's in vitro activated CD4+ T cells expressed CD40L, compared with 33.54% from a healthy control. The patient's father, mother and sister all had a normal CD40L expression activation patterns (43.52%, 40.78%, 34.11%, respectively). On a regimen of monthly IVIG infusion and oral trimethoprim-sulfamethoxazole for Pneumocystis carinii pneumonia (PCP) prophylaxis, the patient has had no recurrent infections.
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PMID:Hyper-IgM syndrome: report of one case. 1586 49

A total of 45 children aged 4-16 years with atopic bronchial asthma of different severity level-resulted from a past case of outhospital pneumonia, received vaccine "Pneumo 23" ("Aventis Pasteur", France). The vaccine was found to be well tolerated, no cases of the exacerbation of the atopic process were registered. A reliable Increased level of specific antibodies to the mixture of polysaccharides, contained in the vaccine "Pneumo 23", was found to occur. The tendency towards decreased level of serum IgE was established.
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PMID:[Clinical and immunological effect produced by vaccination with "Pneumo 23" of children with atopic bronchial asthma]. 1588 49

X-linked hyper-IgM syndrome (XHIM) is a rare primary immunodeficiency disorder caused by mutations of the gene encoding the CD40 ligand (CD40L). It is characterized by recurrent infections with markedly decreased serum IgG, IgA and IgE levels but normal or elevated IgM levels. We report the clinical manifestations and complete immune studies in the first family with molecularly proven XHIM in Taiwan. A 5-month-old boy presented with rapidly progressive pneumonia which responded poorly to antibiotics. High levels of IgM and very low levels of IgG, IgA, and IgE were noted in his plasma specimen: IgM, 128 mg/dl; IgG, 18 mg/dl; IgA, 4 mg/dl); IgE, 1 IU/ml. Whole blood flow cytometry when he was 21 months old showed that only a small percentage (0.48%) of his in vitro-activated CD4+ T cells expressed CD40L. When he was 3 years old, repeated flow cytometry showed essentially the same result (0.4%), compared with his father's CD40L expression of over 85%. The patient's mother had moderately decreased CD40L expression (74.4%). Hyper-IgM syndrome was confirmed by CD40L mutation analysis in the boy, which revealed a Lys 96 stop (nucleotide A307T) in exon 2 of CD40L, with a truncated protein resulting in the loss of the entire TNF domain. His mother was a carrier and apparently the individual in whom the mutation originated. Eleven other family members, including the patient's father, sister, and grandmother, and the mother's sisters and their children, all had normal results on CD40L mutation analysis. The patient has remained without significant bacterial infection on a regimen of monthly IVIG infusion and oral trimethoprim-sulfamethoxazole for Pneumocystis carinii pneumonia (PCP) prophylaxis, although he has had recurrent oral ulcers and neutropenia. Bone marrow transplantation is planned.
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PMID:De novo mutation causing X-linked hyper-IgM syndrome: a family study in Taiwan. 1599 75

We used two approaches to examine the role of NK T cells (NKT) in an intracellular bacterial (Chlamydia trachomatis mouse pneumonitis (C. muridarum)) infection. One is to use CD1 gene knockout (KO) mice, which lack NKT, and the other is to activate NKT using alpha-galactosylceramide (alpha-GalCer), a natural ligand of these cells. The data showed a promoting effect of NKT activation on Chlamydia lung infection. Specifically, CD1 KO mice exhibited significantly lower levels of body weight loss, less severe pathological change and lower chlamydial in vivo growth than wild-type mice. Immunological analysis showed that CD1 KO mice exhibited significantly lower C. muridarum-specific IL-4 and serum IgE Ab responses as well as more pronounced delayed-type hypersensitivity response compared with wild-type controls. In line with the finding in KO mice, the in vivo stimulation of NKT using alpha-GalCer enhanced chlamydial growth in vivo, which were correlated with reduced delayed-type hypersensitivity response and increased C. muridarum-driven IL-4/IgE production. Moreover, neutralization of IL-4 activity in the alpha-GalCer-treated BALB/c mice significantly reduced the promoting effect of alpha-GalCer treatment on chlamydial growth in vivo. These data provide in vivo evidence for the involvement of NKT in a bacterial pathogenesis and its role in promoting Th2 responses during infection.
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PMID:NK T cell activation promotes Chlamydia trachomatis infection in vivo. 1611 10

We describe the case of a 50-year-old male with a history of asthma and seizure disorder who presented with a 5-month history of dyspnea. The patient had been treated with multiple courses of antibiotics for presumed community-acquired pneumonia before being determined to have allergic bronchopulmonary aspergillosis (ABPA) by serologic and radiographic criteria. Inflammation resulting from this disease had potentiated a postobstructive pneumonia caused by Nocardia asteroides and Stenotrophomonas maltophilia. Therapy with corticosteroids, trimethoprim sulfa, and voriconazole failed to prevent subsequent destruction of the right upper lobe and the patient required surgical intervention. The discussion emphasizes the diagnostic criteria for ABPA including historic, serologic, and radiographic findings; staging, and treatment. Other possible diagnoses, such as invasive pulmonary aspergillosis, chronic necrotizing aspergillosis, and hyper-IgE syndrome are also briefly reviewed.
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PMID:A case of allergic bronchopulmonary aspergillosis leading to pneumonia with unusual organisms. 1635 Oct 36

Hyperimmunoglobulin E syndrome (HIES) is a rare immunodeficiency associated with elevated serum IgE levels, eczematous skin, recurrent cutaneous infections, and distinctive musculoskeletal features. We report two cases seen at our institution and review the current literature. Patient 1 was an 18-month-old African American boy with recurrent staphylococcal cold abscesses, pneumonia, and bacteremia. He had severely eczematous skin, ultimately complicated by eczema herpeticum. After treatment of systemic infections with culture-directed antibiotics, a brief course of cyclosporine, 5 mg/kg, improved the dermatitis and allowed transition to long-term therapy with oral trimethoprim-sulfamethoxazole. Patient 2 was a 15-year-old Caucasian boy with long-standing HIES. He has been maintained on a regimen of interferon gamma injections given 3 times weekly and monthly intravenous immunoglobulin since the age of 3 years, prophylactic antibiotics, and low-dose fluconazole. He has occasional episodes of cold abscesses and sinusitis, but has had excellent control since institution of this regimen and has not experienced any adverse effects.
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PMID:Hyperimmunoglobulin E syndrome: two cases and a review of the literature. 1663 66

Although Mycoplasma pneumoniae infection is known to be associated with acute wheezing and the exacerbation of asthma, the mechanism by which this pathogen contributes to the development of wheeze-related symptoms is not fully understood. The aim of our study was to examine serum endothelin (ET)-1 and other cytokines in acute M. pneumoniae pneumonia and investigate if there is any relation between these inflammatory mediators and the occurrence of wheezing. We studied 53 patients, aged 3-13 yr, who admitted with pneumonia. These patients were divided into three groups: M. pneumoniae pneumonia with wheeze (n=23) and without wheeze (n=19), and the patients without the evidence of M. pneumoniae infection (n=11). Age-matched controls (n=10) were also studied. The serum concentrations of ET-1, interleukin (IL)-5 and IL-18 were measured using ELISA kits in patient groups and controls. The patients with M. pneumoniae pneumonia had significantly higher serum ET-1 than those without evidence of M. pneumoniae infection. In the presence of M. pneumoniae pneumonia, ET-1 concentrations were significantly higher in the patients with wheeze than those without wheeze. IL-5 and IL-18 in each patient group were higher compared to controls. However, no significant between-group difference was observed. Total serum IgE levels were significantly higher in the patients with M. pneumoniae pneumonia and wheeze than in those without wheeze. A positive correlation was observed between serum ET-1 and total IgE in the patients with M. pneumoniae pneumonia and wheeze. Our results may suggest a role of ET-1 in the occurrence of acute wheezing or exacerbation of asthma associated with M. pneumoniae pneumonia.
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PMID:The relationship between serum endothelin (ET)-1 and wheezing status in the children with Mycoplasma pneumoniae pneumonia. 1677 82

We report about a 35-year-old man with a cavitary legionella pneumonia who had a history of chronic eczematoid lesions since infancy, recurrent skin and lung infections and a very high total IgE level. We carried out further investigations and made a diagnosis of a primary immunodeficiency classified in the Hyper-IgE syndromes. Cavitation of legionella pneumonia may become fairly common in immunocompromised patients, while is found rarely among immunocompetent hosts.
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PMID:Cavitary Legionella pneumonia in a patient with immunodeficiency due to Hyper-IgE syndrome. 1694 72

In order to determine the clinical and laboratory findings of Iranian patients with presumed hyper-immunoglobulin E syndrome (HIES), the medical records of 22 patients from 21 unrelated families, who had been registered in the Iranian Primary Immunodeficiency Registry, were observed. The median age of patients at the time of first symptom and at the time of diagnosis was 1 month and 52.5 months, respectively, with a median diagnosis delay of 70 months. 13 families had consanguineous marriages. IgE level was higher than 2000 IU/ml in all patients, ranging from >2000 to 80,000 IU/ml. The most commonly occurring manifestations were: eczema and dermatitis, pneumonia, upper respiratory tract infections, cutaneous abscesses, diarrhoea, deep abscesses, and otitis media. Other less frequent manifestations were: mucocutaneous candidiasis, sinusitis, cutaneous ulcers, Molluscum contagiosum, herpetic keratitis, onychomycosis, conjunctivitis, septic arthritis, and meningitis. Five patients were complicated by bronchiectasis due to recurrent pneumonia and 5 patients died because of severe infections and malignancy. The HIES is a multisystem disorder that affects especially cutaneous, respiratory, skeletal and the immune system. Although HIES is a rare condition, the recurrent infections should always raise a suspicion, which deserves further evaluation for detecting the syndrome.
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PMID:The clinical and laboratory survey of Iranian patients with hyper-IgE syndrome. 1700 35


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