Regulation of leukocyte binding to endothelial tissues by tumor‐derived GM‐CSF

Abstract

The adherence of leukocytes to endothelial cells is the first step in the migration of these cells into tumor tissues. Specific binding to the endothelial cells by leukocytes is mediated by the development and maintenance of adhesion molecules on the endothelium; however, the mechanisms of leukocyte traffic into tumors and of their interactions with neoplastic tissue are not clearly understood. The infiltration of leukocytes occurs in most spontaneous and transplanted solid tumors and we have previously reported that not only are murine mammary tumors heavily infiltrated by leukocytes but tumor-derived factors alter the development and function of leukocytes in tumor-bearing mice. We now present evidence that a tumor-derived cytokine, namely granulocyte-macrophage-colony-stimulating factor, appears to be of importance in the regulation of leukocyte binding to endothelial cells. The data suggest that tumor-derived factors may influence leukocyte trafficking within tumor tissue.

Cytokine regulation of endothelial cell function

“…The EC responses elicited by these CSFs (but not by IL-6 and M-CSF) included migration and proliferation but not inflammatory activities. GM-CSF was reported to induce expression of adhesion structures weakly, ICAM-i in particular (72,74,75). As expected on the basis of these in vitro actions, G and GM-CSF were found to have angiogenic activity in vivo (71, 77).…”

Cytokine regulation of endothelial cell function

“…The EC responses elicited by these CSFs (but not by IL-6 and M-CSF) included migration and proliferation but not inflammatory activities. GM-CSF was reported to induce expression of adhesion structures weakly, ICAM-i in particular (72,74,75). As expected on the basis of these in vitro actions, G and GM-CSF were found to have angiogenic activity in vivo (71, 77).…”

CCL26 Participates in the PRL-3–Induced Promotion of Colorectal Cancer Invasion by Stimulating Tumor-Associated Macrophage Infiltration

“…CCL26 is a small cytokine belonging to the CC chemokine family and is also known as eotaxin-3 (27). Many cytokines have been found to induce TAM infiltration, including CCL2, CCL5, VEGF, GM-CSF, and TGFb (28)(29)(30). Interestingly, CCL26 mobilizes intracellular Ca 2þ by binding to the CCR3 receptor on the cell surface to promote migration (18).…”

Granulocyte-Macrophage Colony-Stimulating Factor Enhances Leptomeningeal Collateral Growth Induced by Common Carotid Artery Occlusion

“…17 GM-CSF is produced and released by monocytes, macrophages, and endothelial cells, and its receptor has been detected on the surface of endothelial cells. 18 GM-CSF produced by endothelial cells act in an autocrine or paracrine manner to affect the adhesion of leukocytes to endothelial cells by modulating adhesion molecule expression on the surface of endothelial cells, 19 and the GM-CSF production is enhanced by FSS. 20 The results of the present study showed that monocyte/macrophage lineage was associated with leptomeningeal collateral growth and showed that GM-CSF enhanced the enlargement of leptomeningeal collateral vessels.…”

Cytokine regulation of endothelial cell function

“…The EC responses elicited by these CSFs (but not by IL-6 and M-CSF) included migration and proliferation but not inflammatory activities. GM-CSF was reported to induce expression of adhesion structures weakly, ICAM-i in particular (72,74,75). As expected on the basis of these in vitro actions, G and GM-CSF were found to have angiogenic activity in vivo (71, 77).…”

CCL26 Participates in the PRL-3–Induced Promotion of Colorectal Cancer Invasion by Stimulating Tumor-Associated Macrophage Infiltration

“…CCL26 is a small cytokine belonging to the CC chemokine family and is also known as eotaxin-3 (27). Many cytokines have been found to induce TAM infiltration, including CCL2, CCL5, VEGF, GM-CSF, and TGFb (28)(29)(30). Interestingly, CCL26 mobilizes intracellular Ca 2þ by binding to the CCR3 receptor on the cell surface to promote migration (18).…”

Granulocyte-Macrophage Colony-Stimulating Factor Enhances Leptomeningeal Collateral Growth Induced by Common Carotid Artery Occlusion

“…17 GM-CSF is produced and released by monocytes, macrophages, and endothelial cells, and its receptor has been detected on the surface of endothelial cells. 18 GM-CSF produced by endothelial cells act in an autocrine or paracrine manner to affect the adhesion of leukocytes to endothelial cells by modulating adhesion molecule expression on the surface of endothelial cells, 19 and the GM-CSF production is enhanced by FSS. 20 The results of the present study showed that monocyte/macrophage lineage was associated with leptomeningeal collateral growth and showed that GM-CSF enhanced the enlargement of leptomeningeal collateral vessels.…”

Cytokine regulation of endothelial cell function

“…The EC responses elicited by these CSFs (but not by IL-6 and M-CSF) included migration and proliferation but not inflammatory activities. GM-CSF was reported to induce expression of adhesion structures weakly, ICAM-i in particular (72,74,75). As expected on the basis of these in vitro actions, G and GM-CSF were found to have angiogenic activity in vivo (71, 77).…”

CCL26 Participates in the PRL-3–Induced Promotion of Colorectal Cancer Invasion by Stimulating Tumor-Associated Macrophage Infiltration

“…CCL26 is a small cytokine belonging to the CC chemokine family and is also known as eotaxin-3 (27). Many cytokines have been found to induce TAM infiltration, including CCL2, CCL5, VEGF, GM-CSF, and TGFb (28)(29)(30). Interestingly, CCL26 mobilizes intracellular Ca 2þ by binding to the CCR3 receptor on the cell surface to promote migration (18).…”

Granulocyte-Macrophage Colony-Stimulating Factor Enhances Leptomeningeal Collateral Growth Induced by Common Carotid Artery Occlusion

“…17 GM-CSF is produced and released by monocytes, macrophages, and endothelial cells, and its receptor has been detected on the surface of endothelial cells. 18 GM-CSF produced by endothelial cells act in an autocrine or paracrine manner to affect the adhesion of leukocytes to endothelial cells by modulating adhesion molecule expression on the surface of endothelial cells, 19 and the GM-CSF production is enhanced by FSS. 20 The results of the present study showed that monocyte/macrophage lineage was associated with leptomeningeal collateral growth and showed that GM-CSF enhanced the enlargement of leptomeningeal collateral vessels.…”