Claus Munck Petersen

Pneumocystis carinii-induced activation of the respiratory burst in human monocytes and macrophages

Research output: Contribution to journal/Conference contribution in journal/Contribution to newspaperJournal articleResearchpeer-review

Standard

Pneumocystis carinii-induced activation of the respiratory burst in human monocytes and macrophages. / Laursen, A L; Møller, B; Rungby, J; Petersen, C M; Andersen, P L.

In: Clinical and Experimental Immunology, Vol. 98, No. 2, 1994, p. 196-202.

Research output: Contribution to journal/Conference contribution in journal/Contribution to newspaperJournal articleResearchpeer-review

Harvard

Laursen, AL, Møller, B, Rungby, J, Petersen, CM & Andersen, PL 1994, 'Pneumocystis carinii-induced activation of the respiratory burst in human monocytes and macrophages', Clinical and Experimental Immunology, vol. 98, no. 2, pp. 196-202.

APA

Laursen, A. L., Møller, B., Rungby, J., Petersen, C. M., & Andersen, P. L. (1994). Pneumocystis carinii-induced activation of the respiratory burst in human monocytes and macrophages. Clinical and Experimental Immunology, 98(2), 196-202.

CBE

Laursen AL, Møller B, Rungby J, Petersen CM, Andersen PL. 1994. Pneumocystis carinii-induced activation of the respiratory burst in human monocytes and macrophages. Clinical and Experimental Immunology. 98(2):196-202.

MLA

Laursen, A L et al. "Pneumocystis carinii-induced activation of the respiratory burst in human monocytes and macrophages". Clinical and Experimental Immunology. 1994, 98(2). 196-202.

Vancouver

Laursen AL, Møller B, Rungby J, Petersen CM, Andersen PL. Pneumocystis carinii-induced activation of the respiratory burst in human monocytes and macrophages. Clinical and Experimental Immunology. 1994;98(2):196-202.

Author

Laursen, A L ; Møller, B ; Rungby, J ; Petersen, C M ; Andersen, P L. / Pneumocystis carinii-induced activation of the respiratory burst in human monocytes and macrophages. In: Clinical and Experimental Immunology. 1994 ; Vol. 98, No. 2. pp. 196-202.

Bibtex

@article{ae81c1fda1424abea3bb0f4d183f72d1,
title = "Pneumocystis carinii-induced activation of the respiratory burst in human monocytes and macrophages",
abstract = "Human monocytes and monocyte-derived macrophages were studied for their ability to phagocytose Pneumocystis carinii and produce superoxide (O2-) during the process. One x 10(6) freshly isolated monocytes, incubated with 0.1-3.75 x 10(6) P. carinii cysts, increased O2- production in a dose-related way. Antibodies were essential for the process since opsonized, but not unopsonized, pneumocysts induced O2- production significantly above the response obtained by lung tissue from rats (10.7 and 4.9 versus 3.0 fmol/cell per 90 min). The difference between pneumocysts opsonized in untreated versus complement-depleted serum was not significant (10.7 versus 12.6 fmol/cell per 90 min). Monocyte-derived macrophages also activated the respiratory burst when stimulated with pneumocysts, and this effect could be significantly increased, from 4.2 to 8.8 fmol/cell per 90 min, when cells were primed with interferon-gamma (IFN-gamma). Cells primed with IL-3 also increased O2- production, though to a lesser extent. In contrast, granulocyte-macrophage colony-stimulating factor (GM-CSF) had only a small effect on the respiratory burst in cells stimulated with P. carinii. Priming with IFN-gamma increased the rate of phagocytosis in macrophages. After incubation for 90 min or more, however, the percentage of cells with phagocytic vacuoles was only slightly higher in IFN-gamma-primed cells. When examined by electron microscopy (EM), most vacuoles contained partially or totally degraded pneumocysts. In conclusion, we have demonstrated the ability of monocytes and monocyte-derived macrophages to ingest and degrade pneumocysts, activating the respiratory burst during the process.",
keywords = "Animals, Cells, Cultured, Humans, Macrophages, Male, Monocytes, Opsonin Proteins, Pneumocystis, Pneumocystis Infections, Rats, Rats, Wistar, Respiratory Burst, Superoxides",
author = "Laursen, {A L} and B M{\o}ller and J Rungby and Petersen, {C M} and Andersen, {P L}",
year = "1994",
language = "English",
volume = "98",
pages = "196--202",
journal = "Clinical and Experimental Immunology",
issn = "0009-9104",
publisher = "Wiley-Blackwell Publishing Ltd",
number = "2",

}

RIS

TY - JOUR

T1 - Pneumocystis carinii-induced activation of the respiratory burst in human monocytes and macrophages

AU - Laursen, A L

AU - Møller, B

AU - Rungby, J

AU - Petersen, C M

AU - Andersen, P L

PY - 1994

Y1 - 1994

N2 - Human monocytes and monocyte-derived macrophages were studied for their ability to phagocytose Pneumocystis carinii and produce superoxide (O2-) during the process. One x 10(6) freshly isolated monocytes, incubated with 0.1-3.75 x 10(6) P. carinii cysts, increased O2- production in a dose-related way. Antibodies were essential for the process since opsonized, but not unopsonized, pneumocysts induced O2- production significantly above the response obtained by lung tissue from rats (10.7 and 4.9 versus 3.0 fmol/cell per 90 min). The difference between pneumocysts opsonized in untreated versus complement-depleted serum was not significant (10.7 versus 12.6 fmol/cell per 90 min). Monocyte-derived macrophages also activated the respiratory burst when stimulated with pneumocysts, and this effect could be significantly increased, from 4.2 to 8.8 fmol/cell per 90 min, when cells were primed with interferon-gamma (IFN-gamma). Cells primed with IL-3 also increased O2- production, though to a lesser extent. In contrast, granulocyte-macrophage colony-stimulating factor (GM-CSF) had only a small effect on the respiratory burst in cells stimulated with P. carinii. Priming with IFN-gamma increased the rate of phagocytosis in macrophages. After incubation for 90 min or more, however, the percentage of cells with phagocytic vacuoles was only slightly higher in IFN-gamma-primed cells. When examined by electron microscopy (EM), most vacuoles contained partially or totally degraded pneumocysts. In conclusion, we have demonstrated the ability of monocytes and monocyte-derived macrophages to ingest and degrade pneumocysts, activating the respiratory burst during the process.

AB - Human monocytes and monocyte-derived macrophages were studied for their ability to phagocytose Pneumocystis carinii and produce superoxide (O2-) during the process. One x 10(6) freshly isolated monocytes, incubated with 0.1-3.75 x 10(6) P. carinii cysts, increased O2- production in a dose-related way. Antibodies were essential for the process since opsonized, but not unopsonized, pneumocysts induced O2- production significantly above the response obtained by lung tissue from rats (10.7 and 4.9 versus 3.0 fmol/cell per 90 min). The difference between pneumocysts opsonized in untreated versus complement-depleted serum was not significant (10.7 versus 12.6 fmol/cell per 90 min). Monocyte-derived macrophages also activated the respiratory burst when stimulated with pneumocysts, and this effect could be significantly increased, from 4.2 to 8.8 fmol/cell per 90 min, when cells were primed with interferon-gamma (IFN-gamma). Cells primed with IL-3 also increased O2- production, though to a lesser extent. In contrast, granulocyte-macrophage colony-stimulating factor (GM-CSF) had only a small effect on the respiratory burst in cells stimulated with P. carinii. Priming with IFN-gamma increased the rate of phagocytosis in macrophages. After incubation for 90 min or more, however, the percentage of cells with phagocytic vacuoles was only slightly higher in IFN-gamma-primed cells. When examined by electron microscopy (EM), most vacuoles contained partially or totally degraded pneumocysts. In conclusion, we have demonstrated the ability of monocytes and monocyte-derived macrophages to ingest and degrade pneumocysts, activating the respiratory burst during the process.

KW - Animals

KW - Cells, Cultured

KW - Humans

KW - Macrophages

KW - Male

KW - Monocytes

KW - Opsonin Proteins

KW - Pneumocystis

KW - Pneumocystis Infections

KW - Rats

KW - Rats, Wistar

KW - Respiratory Burst

KW - Superoxides

M3 - Journal article

C2 - 7955522

VL - 98

SP - 196

EP - 202

JO - Clinical and Experimental Immunology

JF - Clinical and Experimental Immunology

SN - 0009-9104

IS - 2

ER -