Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
10
pubmed:dateCreated
2007-5-3
pubmed:abstractText
To assess the combined role of G-CSF, GM-CSF, and M-CSF in myeloid cell production, mice deficient in all three myeloid CSFs were generated (G-/-GM-/-M-/- mice). G-/-GM-/-M-/- mice share characteristics found in mice lacking individual cytokines: they are toothless and osteopetrotic and furthermore acquire alveolar proteinosis that is more severe than that found in either GM-/- or G-/-GM-/- mice. G-/-GM-/-M-/- mice have a significantly reduced lifespan, which is prolonged by antibiotic administration, suggesting compromised ability to control bacterial infection. G-/-GM-/-M-/- mice have circulating neutrophils and monocytes, albeit at significantly reduced numbers compared with wild-type mice, but surprisingly, have more circulating monocytes than M-/- mice and more circulating neutrophils than G-/-GM-/- mice. Due to severe osteopetrosis, G-/-GM-/-M-/- mice show diminished numbers of myeloid cells, myeloid progenitors, and B lymphocytes in the bone marrow, but have significantly enhanced compensatory splenic hemopoiesis. Although G-/-GM-/-M-/- mice have a profound deficiency of myeloid cells in the resting peritoneal cavity, the animals mount a moderate cellular response in a model of sterile peritonitis. These data establish that in the absence of G-CSF, GM-CSF, and M-CSF, additional growth factor(s) can stimulate myelopoiesis and acute inflammatory responses.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
May
pubmed:issn
0022-1767
pubmed:author
pubmed:issnType
Print
pubmed:day
15
pubmed:volume
178
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
6435-43
pubmed:meshHeading
pubmed-meshheading:17475873-Animals, pubmed-meshheading:17475873-Cell Differentiation, pubmed-meshheading:17475873-Colony-Stimulating Factors, pubmed-meshheading:17475873-Disease Models, Animal, pubmed-meshheading:17475873-Granulocyte Colony-Stimulating Factor, pubmed-meshheading:17475873-Granulocyte-Macrophage Colony-Stimulating Factor, pubmed-meshheading:17475873-Granulocytes, pubmed-meshheading:17475873-Inflammation Mediators, pubmed-meshheading:17475873-Leukopenia, pubmed-meshheading:17475873-Macrophage Colony-Stimulating Factor, pubmed-meshheading:17475873-Macrophages, Peritoneal, pubmed-meshheading:17475873-Mice, pubmed-meshheading:17475873-Mice, Inbred C57BL, pubmed-meshheading:17475873-Mice, Knockout, pubmed-meshheading:17475873-Mice, Mutant Strains, pubmed-meshheading:17475873-Myeloid Cells, pubmed-meshheading:17475873-Myelopoiesis, pubmed-meshheading:17475873-Peritonitis
pubmed:year
2007
pubmed:articleTitle
Mice lacking three myeloid colony-stimulating factors (G-CSF, GM-CSF, and M-CSF) still produce macrophages and granulocytes and mount an inflammatory response in a sterile model of peritonitis.
pubmed:affiliation
Signal Transduction Laboratory, Ludwig Institute for Cancer Research, Melbourne Tumour Biology Branch, Royal Melbourne Hospital, Victoria, and Department of Medicine, University of Melbourne, Parkville, Australia. Margaret.Hibbs@ludwig.edu.au
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't