Isolation of Mycobacteria in Patients with Pulmonary Alveolar Proteinosis

Witty, Lynn A.; Tapson, Victor F.; Piantadosi, Claude A.

doi:10.1097/00005792-199403000-00003

Cited by 115 publications

(56 citation statements)

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“…Some investigators have postulated that increased levels of SP-A are associated with increased susceptibility to TB. This hypothesis is based on studies which showed that there were increased SP-A levels in subjects with silicosis, pulmonary alveolar proteinosis, and HIV, three diseases in which there is increased susceptibility to mycobacterial infection (8,16,35,36). Recent data have extended these observations, and polymorphisms in the SP-A gene are associated with susceptibility to TB in certain populations (9).…”

Section: Discussionmentioning

confidence: 99%

“…Interestingly, patients with three diseases in which there is increased susceptibility to pulmonary mycobacterial infections, HIV, silicosis, and alveolar proteinosis, all have increased levels of SP-A in the bronchoalveolar lavage (BAL) fluid (BALF) (8,16,35,36). However, there is little data on the status of SP-A levels in patients with TB and how these levels change in response to therapy.…”

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confidence: 99%

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Surfactant Protein A Modulates the Inflammatory Response in Macrophages during Tuberculosis

et al. 2004

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Tuberculosis leads to immune activation and increased human immunodeficiency virus type 1 (HIV-1) replication in the lung. However, in vitro models of mycobacterial infection of human macrophages do not fully reproduce these in vivo observations, suggesting that there are additional host factors. Surfactant protein A (SP-A) is an important mediator of innate immunity in the lung. SP-A levels were assayed in the human lung by using bronchoalveolar lavage (BAL). There was a threefold reduction in SP-A levels during tuberculosis only in the radiographically involved lung segments, and the levels returned to normal after 1 month of treatment. The SP-A levels were inversely correlated with the percentage of neutrophils in BAL fluid, suggesting that low SP-A levels were associated with increased inflammation in the lung. Differentiated THP-1 macrophages were used to test the effect of decreasing SP-A levels on immune function. In the absence of infection with Mycobacterium tuberculosis, SP-A at doses ranging from 5 to 0.01 g/ml inhibited both interleukin-6 (IL-6) production and HIV-1 long terminal repeat (LTR) activity. In macrophages infected with M. tuberculosis, SP-A augmented both IL-6 production and HIV-1 LTR activity. To better understand the effect of SP-A, we measured expression of CAAT/enhancer binding protein beta (C/EBP␤), a transcription factor central to the regulation of IL-6 and the HIV-1 LTR. In macrophages infected with M. tuberculosis, SP-A reduced expression of a dominant negative isoform of C/EBP␤. These data suggest that SP-A has pleiotropic effects even at the low concentrations found in tuberculosis patients. This protein augments inflammation in the presence of infection and inhibits inflammation in uninfected macrophages, protecting uninvolved lung segments from the deleterious effects of inflammation.

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Section: Discussionmentioning

confidence: 99%

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confidence: 99%

Surfactant Protein A Modulates the Inflammatory Response in Macrophages during Tuberculosis

et al. 2004

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“…103,104 The crazy-paving pattern is not pathognomonic of pulmonary alveolar proteinosis, and occurs in other infectious or non-infectious conditions. [104][105][106][107][108][109][110][111][112][113][114] The subacute or chronic clinical course, absence of architectural distortion, smooth 78 Cryptococcus neoformans 79,80 Mycobacterium tuberculosis [81][82][83][84] Mycobacterium avium-intracellulare 85,86 inter-lobular septal thickening, geographical distribution, and discordance between the clinical and radiological features help differentiate pulmonary alveolar proteinosis from other causes of crazy paving. In a study of 42 patients, Ishii et al 115 reported differences in the pattern and distribution of ground-glass opacity on high-resolution CT, which help to differentiate secondary from autoimmune pulmonary alveolar proteinosis.…”

Section: High-resolution Computed Tomographymentioning

confidence: 99%

Pulmonary Alveolar Proteinosis

Khan

Agarwal

2011

Respir Care

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“…M. avium complex pulmonary infections are found in patients with predisposing lung conditions, such as silicosis and black lung (5,43), and in patients with pulmonary alveolar proteinosis (42) and cystic fibrosis (23). Infections in elderly women without any of the known risk factors for M. avium complex infection have also been described (30).…”

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confidence: 99%

Factors Influencing Numbers of Mycobacterium avium , Mycobacterium intracellulare , and Other Mycobacteria in Drinking Water Distribution Systems

Falkinham

Norton

LeChevallier

2001

Appl Environ Microbiol

469

451

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Eight water distribution systems were sampled over an 18-month period (528 water and 55 biofilm samples) to measure the frequency of recovery and number of mycobacteria, particularly Mycobacterium avium and Mycobacterium intracellulare, in raw source waters before and after treatment and within the distribution system. The systems were chosen to assess the influence of source water, treatment, and assimilable organic carbon levels on mycobacterial numbers. Overall, mycobacterial recovery from the systems was low (15% of samples). Numbers of mycobacteria ranged from 10 to 700,000 CFU liter ؊1 . The number of M. avium in raw waters was correlated with turbidity. Water treatment substantially reduced the number of mycobacteria in raw waters by 2 to 4 log units. Mycobacterial numbers were substantially higher in the distribution system samples (average, 25,000-fold) than in those collected immediately downstream from the treatment facilities, indicating that mycobacteria grow in the distribution system. The increase in mycobacterial numbers was correlated with assimilable organic carbon and biodegradable organic carbon levels (r 2 ‫؍‬ 0.65, P ‫؍‬ 0.03). Although M. intracellulare was seldom recovered from water samples, it was frequently recovered (six of eight systems) in high numbers from biofilms (average, 600 CFU/cm 2 ). Evidently, the ecological niches of M. avium and M. intracellulare are distinct.Members of the Mycobacterium avium complex (i.e., M. avium and Mycobacterium intracellulare) are environmental opportunistic human and animal pathogens (11,21,43). M. avium complex pulmonary infections are found in patients with predisposing lung conditions, such as silicosis and black lung (5, 43), and in patients with pulmonary alveolar proteinosis (42) and cystic fibrosis (23). Infections in elderly women without any of the known risk factors for M. avium complex infection have also been described (30). M. avium, but not M. intracellulare, infections are found in (and are limited to) the cervical lymph nodes of young children with erupting teeth (44). Immune deficiency resulting in AIDS (18) or due to interleukin-12 deficiency (1), malignancy (41), or immunosuppression associated with transplantation (33) is also a risk factor for M. avium complex infection. Infections in AIDS patients are disseminated (e.g., bacteremia [19]) and are almost entirely (i.e., 95%) due to M. avium, whereas both mycobacterial infections occur at equal frequencies in nonimmunodeficient patients with pulmonary disease (8, 17).One source of M. avium infection in AIDS patients is water. DNA fingerprints of M. avium isolates from water to which AIDS patients were exposed were identical to those of the patients (38). Further, the high incidence of M. avium infections in AIDS patients in Finland correlated with high numbers of M. avium in drinking and environmental waters (31). Water also appears to be the source of M. avium infections in simian immunodeficiency virus-infected macaques, based on the identity of DNA fingerprints of M. avium re...

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Isolation of Mycobacteria in Patients with Pulmonary Alveolar Proteinosis

Cited by 115 publications

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Surfactant Protein A Modulates the Inflammatory Response in Macrophages during Tuberculosis

Surfactant Protein A Modulates the Inflammatory Response in Macrophages during Tuberculosis

Pulmonary Alveolar Proteinosis

Factors Influencing Numbers of Mycobacterium avium , Mycobacterium intracellulare , and Other Mycobacteria in Drinking Water Distribution Systems

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