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Query: UNIPROT:P04141 (granulocyte-macrophage colony-stimulating factor)
 6,790 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Granulocyte-macrophage colony-stimulating factor (GM-CSF) is a cytokine that affects the various developmental steps of hematopoietic cells and enhances the phagocytic activity of these cells. The effect of GM-CSF on acute osteomyelitis, developed in rats, was investigated. For this purpose, osteomyelitis was firstly developed through the direct inoculation of Staphylococcus aureus into rat tibial metaphysis. Twenty-four rats in which diagnosis of osteomyelitis was histopathologically established were divided into two groups. Antibiotic only was given to the first group, and antibiotic as well as GM-CSF to the second group. Rats were followed up for 3 months with plain radiographs and scintigraphic methods using 67Ga-citrate. Material obtained from the rats that had been killed at the end of the 3rd month were histopathologically investigated. One rat in the first group died. In another rat, chronic osteomyelitis developed and fracture was observed. In 12 rats of the second group, physical examination, plain radiographs, and histopathologic findings were normal. In scintigraphic studies with 67Ga-citrate, when the pre- and posttreatment value of the same groups were evaluated by the Mann-Whitney U-test, the mean values at 48 h after treatment were found to be significant (P < 0.05), indicating a decrease in the 2nd group (experimental group). In conclusion, the antibiotics were effective in the elimination of infection only together with neutrophils. In this manner, infections may be eliminated by strengthening the host's defense mechanism as well as by administering antibiotics. We believe that an adequate number of long-term studies will shed light on this issue. Besides we consider that this factor will be more important in the study of chronic osteomyelitis.
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PMID:Effect of granulocyte-macrophage colony-stimulating factor on treatment of acute osteomyelitis. An experimental investigation in rats. 1126 85

Bacterially induced bone infections often result in significant local inflammatory responses which are coupled with loss of bone. However, the mechanisms necessary for the protective host response, or those responsible for pathogen-induced bone loss, are not clear. Recent evidence demonstrates that bacterially infected osteoblasts secrete chemokines and cytokines, suggesting that these cells may have an unappreciated role in supporting localized inflammation. In this study, mouse and human osteoblasts were investigated for their ability to express functional CD40 upon exposure to two important pathogens of bone, Staphylococcus aureus and Salmonella enterica serovar Dublin. Bacterial infection of cultured mouse or human osteoblasts resulted in increased CD40 mRNA and CD40 protein expression induced by either pathogen. Importantly, CD40 expression by osteoblasts was functional, as assessed by ligation of this molecule with recombinant, soluble CD154. CD40 activity was assessed by induction of interleukin-6 and granulocyte-macrophage colony-stimulating factor in osteoblasts following ligation. Cocultures of activated CD4(+) T lymphocytes and osteoblasts could interact via CD40 and CD154, since an antibody against CD40 could block macrophage inflammatory protein-1alpha secretion. Taken together, these studies conclusively demonstrate that infected osteoblasts can upregulate expression of functional CD40 molecules which mediate cytokine secretion. This surprising result further supports the notion that bone-forming osteoblasts can directly interact with CD154-expressing cells (i.e., T lymphocytes) and can contribute to the host response during bone infection.
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PMID:Functional CD40 expression induced following bacterial infection of mouse and human osteoblasts. 1259 34