Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:6.2.1.7 (BAL)
1,977 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Previous studies have shown that exposure of pathogen-free C57BL/6N mice to 5 or 10 ppm NO2 increases the severity of murine respiratory mycoplasmosis and that this effect is associated with decreased intrapulmonary killing of Mycoplasma pulmonis. The purposes of the present studies were to determine the effects of doses of NO2 lower than 5 ppm on pulmonary clearance and to provide experimental links between NO2 exposure, defects in intrapulmonary killing, and alterations in alveolar macrophages. Exposure to less than 5 ppm NO2 had no effect on intrapulmonary killing of M. pulmonis. Bronchoalveolar lavage cells killed M. pulmonis in vitro only if they were allowed to associate with mycoplasmas in vivo. Prior exposure to NO2 abrogated killing in this in vivo-in vitro model. More than 95% of the BAL cells were macrophages, and more than 98% of the cell-associated mycoplasmas were on or in alveolar macrophages. Immediately after exposure, the viability of alveolar macrophages was 89 +/- 4% in the control group, 56 +/- 19% in the group receiving M. pulmonis alone, 23 +/- 7% in the group receiving 10 ppm NO2, and 16 +/- 6% in the group receiving both M. pulmonis and NO2 exposures. Viability was significantly decreased following exposure to 10 and 5 ppm NO2 but not following exposure to 2 ppm. Both viability and intrapulmonary killing were depressed at 3 days after exposure to NO2 but were normal by 7 days after exposure. The cellular target of NO2 exposure in relation to intrapulmonary killing of M. pulmonis appears to be the alveolar macrophages.
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PMID:Decreased intrapulmonary killing of Mycoplasma pulmonis after short-term exposure to NO2 is associated with damaged alveolar macrophages. 173 50

A young man undergoing chemotherapy for Ewing's sarcoma presented with fever, neutropenia, anemia, thrombocytopenia, and a new infiltrate on the chest roentgenogram. Routine cultures and cytopathologic examination of bronchoalveolar lavage fluid provided no evidence for an etiology; however, special cultures of the BAL fluid demonstrated heavy growth of Mycoplasma pneumoniae. We recommend that evaluation of pneumonia in the immuno-compromised host include appropriate cultures of BAL fluid for M pneumoniae, particularly when the patient is 5 to 25 years old, the age of high incidence of mycoplasmal pneumonia.
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PMID:Mycoplasma pneumoniae as the causative agent for pneumonia in the immunocompromised host. 139 98

A case of pneumonia caused by C. pneumoniae, strain TWAR is described in this paper. A 65 year-old male with a persistent dry cough was admitted to our division for left lower lobe infiltrates of the chest X-ray. The serum antibody titers against mycoplasma and some viruses were not elevated, but the serum antibody titers against TWAR reached the maximum level (IgG X 1024, IgA X 256) using microplate immunofluorescence antibody technique (MFA). Isolation of TWAR was tried by BAL and nasophalingial swabs, but were not successful. TBLB from Lt. S10 revealed TWAR inclusion bodies within alveolar epithelial cells using TWAR specific monoclonal antibody (Washington Research Foundation).
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PMID:[A case of pneumonia caused by Chlamydia pneumoniae, strain TWAR]. 216 5

A dose-defined nose-only inhalation system for pigs was used to study the immunogenic and protective potentials of a single aerosol application of viable or killed Actinobacillus pleuropneumoniae serotype 9. Respiratory volumes were measured for each pig to calculate inhaled individual doses. Eight pigs inhaled 107 CFU A. pleuropneumoniae CVI 13261 reference strain for serotype 9. Another eight pigs received an identical dose of killed actinobacilli. After three weeks the pigs and nonexposed controls were challenged with 108 CFU of the homologous strain by aerosol. Bronchoalveolar lavage (BALF) in pigs was performed during the experiment to obtain lavage samples for assessment of local antibodies. Isotype-specific antibody responses in serum and BAL fluids were measured by ELISAs based on whole-cell antigens. The protective efficacy of aerosol immunization was evaluated by clinical and post-mortem examinations. The controls developed fever and severe pleuropneumonia, whereas previously exposed pigs had less fever and less extensive gross pulmonary lesions. After the first aerosol exposure pulmonary IgM, and IgG antibodies reactive with A. pleuropneumoniae increased significantly in both aerosol exposed groups. IgA in BALF and serum concentrations of each Ig class were significantly increased in the group exposed to viable bacteria when compared to the non-exposed controls. After aerosol challenge a pronounced increase of systemic and pulmonary IgA, IgM, and IgG antibodies was detected in both exposure groups. Aerosol application of whole-cell A. pleuropneumoniae bacterins induced similar protective effects against aerosol challenge infection as administration of an identical dose of viable bacteria. Inhalation of A. pleuropneumoniae may lead to asymptomatic carriers in some pigs that could spread the disease under field conditions.
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PMID:Aerosol exposure of pigs to viable or inactivated Actinobacillus pleuropneumoniae serotype 9 induces antibodies in bronchoalveolar lining fluids and serum, and protects against homologous challenge. 860 53

The local B-cell response in the respiratory tract to infectious challenge has been analyzed in pigs and calves using two techniques: flow cytometry and antibody secreting cell (ASC) probes. Pneumonia in pigs caused by experimental infection with Mycoplasma hyopneumoniae resulted in a 25-fold increase in the B-cell population in BAL and lung parenchyma 28 days post infection. ASC probes revealed that the B-cell response of immune pigs to a large challenge infection was localized to lung parenchyma and tracheobronchal lymph nodes. Naive calves infected with Pasteurella multocida had a 5-fold increase in the B-cell blast population in lung parenchyma and BAL, and a greater than 60-fold increase in the draining lymph node at 9 days post infection. The ASC probes prepared post challenge from immune calves showed the response to be localized to the draining lymph nodes, with little response in lung parenchyma. A major finding was that ASC probes prepared from lung parenchyma and from pulmonary lymph nodes of both calves and pigs recognized a restricted range of bacterial antigens, particularly compared to the range of antigens recognized by concurrently circulating sera. The use of ASC probes demonstrates that there is a restricted B-cell repertoire in the respiratory tract.
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PMID:Restricted B-cell responses to microbial challenge of the respiratory tract. 898 66

Pathogenic mechanisms of mycoplasmal pneumonia is not fully understood at present though some kind of cell-mediated hypersensitivity is closely related to its mechanisms. Though eosinophilia in peripheral blood are sometimes revealed in patient with mycoplasmal pneumonia, it is not unclear whether eosinophils related to its pathogenesis, or not. We evaluated the clinical significance of ECP in serum and BAL fluid in patients with mycoplasmal pneumonia. The diagnosis of mycoplasmal pneumonia was confirmed both by serological diagnosis from paired serum and by the polymerase chain reaction (PCR) methods using specific primers of the Mycoplasma pneumoniae for detecting specific DNA from bronchial washing fluids. ECP level in serum were measured in 27 patients (11 male, 16 female, average age 31.7 yo) with mycoplasmal pneumonia by ELISA methods. ECP level in BALF were also measured in ten of all patients. The level of ECP in serum was high in 17 cases (63%) of the total cases. In addition the level of ECP in BALF was also high in all tested patients (10 cases). There was a correlation between serum ECP level and days from onset. There was also a correlation between serum ECP level and WBC counts, the degree of PaO2. These results suggested that ECP derived from activated eosinophils in the lung might in part play a role in the pathogenesis of mycoplasmal pneumonia.
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PMID:[Clinical significance of eosinophilic cationic protein in serum and bronchoalveolar lavage fluid of adult patients with mycoplasmal pneumonia]. 1121 84

Respiratory Mycoplasma pneumoniae (Mp) infection is involved in several acute and chronic lung diseases including community-acquired pneumonia, asthma and chronic obstructive pulmonary disease. In the chronic disease process, recurrent respiratory bacterial infections could occur, which may result in varying degrees of symptoms and lung inflammation among patients. However, the lung immunologic differences of host responses to repeated bacterial (i.e., Mp) infections remain to be determined. In the present study, we examined cellular and humoral responses to multiple (up to 3) Mp infections in two genetically different strains of mice (BALB/c and C57BL/6). Mice were intranasally inoculated with one Mp infection, two or three Mp infections (4 weeks apart), and sacrificed on days 3, 7 and 14 after the last Mp infection. Overall, compared to C57BL/6 mice, BALB/c mice demonstrated a significantly higher degree of lung tissue inflammatory cell infiltrate, BAL cellularity, and release of pro-inflammatory cytokines (TNF-alpha, keratinocyte-derived chemokine (KC, a mouse homolog of human chemokine Gro-alpha [CXCL1], and IFN-gamma). In addition, BALB/c mice presented higher levels of serum Mp-specific IgG and IgM, but not IgA. Consistently with lung and serum data, Mp load in BAL and lung specimens was significantly higher in BALB/c mice than C57BL/6 mice. Moreover, repeated Mp infections in BALB/c, but not C57BL/6 mice, produced a greater inflammatory response than did a single Mp infection. Our results suggest that hosts with different genetic background may have different susceptibility to repeated respiratory Mp infections along with inflammatory responses.
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PMID:Repeated respiratory Mycoplasma pneumoniae infections in mice: effect of host genetic background. 1671 27

Mycoplasma hyopneumoniae is the etiological agent of swine enzootic pneumonia, a chronic nonfatal disease affecting pigs of all ages. To obtain better insight in the mechanisms responsible for differences in virulence between highly and low virulent M. hyopneumoniae isolates, 23 caesarean-derived, colostrum-deprived piglets were randomly assigned to three groups. Groups 1 and 2 consisted of nine animals each, which were intratracheally inoculated at 1 week of age with a highly or a low virulent isolate of M. hyopneumoniae, respectively. The remaining five animals were inoculated with sterile culture medium. Animals were euthanized at 5, 10, 15 and 28 days post-inoculation (DPI). Animals inoculated with the highly virulent isolate had more neutrophils in BAL fluid at 10, 15 and 28DPI compared to the other groups. At 10 and 15DPI, animals in the highly virulent group had significantly higher concentrations of TNF-alpha in BAL fluid. IL-1beta concentration in this group was higher at 5 and 28DPI compared to the other groups. From 10DPI onwards, significantly higher titres of M. hyopneumoniae were detected in the BAL fluid of animals inoculated with the highly virulent isolate compared to animals inoculated with the low virulent isolate. Additionally, the in vitro generation time of the highly virulent M. hyopneumoniae isolate was significantly shorter than that of the low virulent isolate. The present study indicates that the difference in pathogenicity between the highly and low virulent isolates is associated with a faster in vitro growth, a higher capacity to multiply in the lungs and the induction of a more severe inflammation process by the highly virulent isolate.
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PMID:Interactions of highly and low virulent Mycoplasma hyopneumoniae isolates with the respiratory tract of pigs. 1712 52

Mycoplasma pneumoniae has rarely been reported in renal transplant recipients. We present the case of a 10-yr-old boy with a six-month history of chronic cough, recurrent pyrexia, and weight loss three yr after RTx. The patient's post-transplant course was complicated by recurrence of NS that resolved with plasmapheresis and PTLD, which was successfully treated with an anti-CD20 monoclonal antibody. Chest X-ray showed a round mass-like lesion in the left upper lobe; MRT, PET, and bronchoscopy ruled out a PTLD. BAL fluid revealed M. pneumoniae-DNA. A three-wk course of macrolide therapy induced rapid recovery. We conclude that M. pneumoniae infection should be considered in immunosuppressed patients with long-lasting respiratory complaints and fever of unknown origin. Antibiotic treatment should be given for a minimum of three wk.
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PMID:Chronic Mycoplasma pneumoniae infection in a child after renal transplantation. 1949 Apr 90

In 2008, 50 samples (BAL), coming from hospital patients, with acute respiratory symptoms have been investigated using two real-time PCR methods: one assay for the single detection of Chlamydophila pneumoniae and Mycoplasma pneumoniae DNA and one commercially available real-time duplex PCR assay for the detection of C. pneumoniae and M. pneumoniae DNA. Both techniques used here showed compliant results, with 100% concordance for detection of C. pneumoniae and 98% for detection of M. pneumoniae. The positive results obtained agreed with the clinical suspicion of such infections in some cases and with the presence of IgM specific for C. pneumoniae and M. pneumoniae in all cases of acute infection.
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PMID:Simultaneous use of direct and indirect diagnostic techniques in atypical respiratory infections from Chlamydophila pneumoniae and Mycoplasma pneumoniae. 1962 57


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