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Effects of macrophage‐CSF on pulmonary‐macrophage repopulation after bone marrow transplantation
Author(s) -
Bernier Tanja,
Tschernig Thomas,
Pabst Reinhard,
Macke Olaf,
Steinmueller Christiane,
Emmendörffer Andreas
Publication year - 2001
Publication title -
journal of leukocyte biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.819
H-Index - 191
eISSN - 1938-3673
pISSN - 0741-5400
DOI - 10.1189/jlb.70.1.39
Subject(s) - macrophage , biology , immunosuppression , lung , alveolar macrophage , immunology , inflammation , macrophage colony stimulating factor , transplantation , bone marrow , immune system , cytokine , chemokine , medicine , biochemistry , in vitro
Pulmonary infections are important causes of morbidity and mortality in immunosuppressed patients after transplantation. After experimental irradiation and syngeneic bone marrow transplantation in mice, macrophages show reduced repopulation in the lung compared with that in other tissues. Macrophages are major microbicidal immune effector cells in host pulmonary defense. Therefore, we examined the role of locally applied cytokines for macrophage repopulation in the lung. An accelerated repopulation of macrophages in the lung was observed after intranasal application of macrophage‐colony stimulating factor (M‐CSF), but this effect was not enhanced by a combination of M‐CSF with interleukin (IL)‐3. Local proliferation contributed to this effect. Macrophages in the lung tissue of M‐CSF‐treated mice displayed greater secretion of IL‐6, whereas M‐CSF treatment did not enhance the gene expression of other macrophage‐specific chemokines. The role of M‐CSF treatment was determined in pulmonary murine cytomegalovirus infection using an irradiation/reconstitution model. The M‐CSF treatment had no effect on virus load in the lung tissue. However, phosphate‐buffered saline‐treated mice seemed to develop stronger inflammation after viral infection than M‐CSF‐treated mice. We conclude that local M‐CSF treatment modulates cellular inflammation in the lung during immunosuppression.