Surfactant protein-A levels increase during Pneumocystis carinii pneumonia in the rat

Phelps, DS; Umstead, TM; Rose, R. M.; Ja, Fishman

doi:10.1183/09031936.96.09030565

Cited by 34 publications

(17 citation statements)

References 27 publications

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“…We observed a marked increase in SP-A and SP-D (up to three-fold) in PCP patients, which was paralleled by virtually unchanged SP-B and SP-C concentrations in both the large surfactant aggregate fraction and cell-depleted but further unprocessed BALF (data not given in detail). In the context of SP-A and SP-D, these findings are in accordance with previous clinical (33,34) and animal (31,32,35) studies of PCP. They conflict, however, with other reports concerning SP-B and SP-C, where previous studies in animal models of PCP suggested a significant suppression of SP-B and SP-C Our study is limited in that only HIVpositive patients with signs of parenchymal lung disease were subjected to bronchoscopy and BAL; thus, HIV-positive patients without any sign of parenchymal lung disease were not included.…”

Section: Discussionsupporting

confidence: 92%

Pulmonary surfactant in patients with Pneumocystis pneumonia and acquired immunodeficiency syndrome

Schmidt

Markart

Ruppert

et al. 2006

Critical Care Medicine

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Section: Discussionsupporting

confidence: 92%

Pulmonary surfactant in patients with Pneumocystis pneumonia and acquired immunodeficiency syndrome

Schmidt

Markart

Ruppert

et al. 2006

Critical Care Medicine

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“…Low levels of SP-A have also been found in other inflammatory disorders of the lung, including pulmonary fibrosis and cystic fibrosis (17,31). Conversely, patients with AIDS-related pneumonia and specifically Pneumocystis carinii pneumonia have elevated levels of SP-A (22,23). We concluded that the reductions in SP-A levels in TB patients are regional in nature and occur only in the radiographically involved lung segments.…”

Section: Discussionmentioning

confidence: 79%

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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“…Immunohistochemistry of lung sections from Pneumocystis-infected mice demonstrates that upregulation of SP-A was localized to regions of atelectasis and cellular infiltrates containing organisms (3). In a corticosteroid-treated rat model of PCP the SP-A levels are also reported to be increased (50,58) and, similarly, BAL samples from HIV-infected patients with PCP have an elevated SP-A content (49). SP-A has been shown to bind to isolated Pneumocystis organisms in a calcium-and mannosedependent manner via its carbohydrate recognition domain to gpA (gp-120), the major glycoprotein found on cell surfaces of trophozoites and cysts (69).…”

mentioning

confidence: 99%

Enhanced Lung Injury and Delayed Clearance ofPneumocystis cariniiin Surfactant Protein A-Deficient Mice: Attenuation of Cytokine Responses and Reactive Oxygen-Nitrogen Species

et al. 2004

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Surfactant protein A (SP-A Increases in SP-D content, gamma interferon, interleukin-4, interleukin-5, and tumor necrosis factor alpha in BAL fluid occurred but were attenuated in PCP-infected SP-A؊/؊ mice compared to WT mice. There were increases in total BAL NO levels in both infected groups, but nitrite levels were higher in SP-A ؊/؊ mice, indicating a reduction in production of higher oxides of nitrogen that was also reflected in lower levels of 3-nitrotyrosine staining in the SP-A ؊/؊ group. We conclude that despite increases in inflammatory cells, SP-A-deficient mice infected with P. carinii exhibit an enhanced susceptibility to the organism and attenuated production of proinflammatory cytokines and reactive oxygen-nitrogen species. These data support the concept that SP-A is a local effector molecule in the lung host defense against P. carinii in vivo.

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Surfactant protein-A levels increase during Pneumocystis carinii pneumonia in the rat

Cited by 34 publications

References 27 publications

Pulmonary surfactant in patients with Pneumocystis pneumonia and acquired immunodeficiency syndrome

Pulmonary surfactant in patients with Pneumocystis pneumonia and acquired immunodeficiency syndrome

Surfactant Protein A Modulates the Inflammatory Response in Macrophages during Tuberculosis

Enhanced Lung Injury and Delayed Clearance ofPneumocystis cariniiin Surfactant Protein A-Deficient Mice: Attenuation of Cytokine Responses and Reactive Oxygen-Nitrogen Species

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