Differential mechanisms of neutrophil and monocyte adhesion on neuroblastoma cells: CD18 and VLA-4 integrins mediate adhesion to SK-N-SH, but not to SK-N-MC cell line.
We examined the adhesion of monocytes and polymorphonuclear leukocytes (PMNLs) to the neuroblastoma (NB) cell lines SK-N-SH and SK-N-MC, which have some distinct differentiation characteristics. Monocytes adhered to SK-N-SH and SK-N-MC to the same extent (20 +/- 1.4% and 24 +/- 0.8% of monocytes added). Monocyte adhesion to SK-N-SH but not SK-N-MC was partially inhibited by treating monocytes with a mAb to the CD18 (beta2) integrin chain. The adhesion was further inhibited when monocytes were treated with a combination of mAb to CD18 and VLA-4. Treatment of both NB cell lines with interleukin-1alpha (0.5 ng/ml), tumor necrosis factor alpha (100 U/ml), interferon gamma (200 U/ml), or their combinations increased monocyte adhesion to SK-N-SH and SK-N-MC. With each condition, monocyte adhesion to SK-N-SH was partially blocked by mAb to CD18. The inhibition of adhesion to IL-1alpha- or TNFalpha-treated SK-N-SH cells was greater when the monocytes were treated with mAb to both CD18 and VLA-4. In contrast, monocyte adhesion to IL-1alpha or IFNgamma treated SK-N-MC was only slightly inhibited with a combination of mAb to CD18 + VLA-4 and there was no inhibition at all to TNFalpha-treated SK-N-MC. Spontaneous PMNL adhesion to SK-N-SH was almost negligible but increased by treating the cell line with IL-1alpha, TNFalpha, IFNgamma or their combinations. A mAb to CD18 blocked this increase in each case. The pattern of adhesion of PMNLs to SK-N-MC was totally different. PMNL adhesion to unstimulated SK-N-MC was very high (24 +/- 1.3%), was not inhibited by mAb to CD18, and did not increase by stimulating the cell line with IL-1alpha, TNFalpha, IFNgamma or their combinations. Overall, these results suggest two distinct patterns of monocyte and PMNL interaction with neural cells, such as the SK-N-SH and MC cell lines. While monocyte and PMNL adhesion to SK-N-SH is mainly via CD18/VLA-4 or the CD18 mechanisms, respectively, leukocyte adhesion to SK-N-MC is CD18- and VLA-4-independent. Thus, leukocyte-neural cell interactions share some mechanisms common also to leukocyte-endothelium interaction, but there are also unique mechanisms which may be neural cell and differentiation specific.
Chuluyan
H E
HE
Department of Pediatrics, Pathology and Microbiology and Immunology, Dalhousie University, Halifax, Nova Scotia, Canada.
Lang
B J
BJ
Issekutz
A C
AC
D018821:CD18 Antigens / Q000276:immunology* / Q000378:metabolism; D002448:Cell Adhesion / Q000502:physiology*; D015815:Cell Adhesion Molecules / Q000276:immunology* / Q000378:metabolism*; D002465:Cell Movement / Q000502:physiology; D016207:Cytokines / Q000494:pharmacology; D039041:Integrin alpha4beta1; D016023:Integrins / Q000276:immunology* / Q000378:metabolism; D009000:Monocytes / Q000166:cytology / Q000276:immunology* / Q000378:metabolism*; D009447:Neuroblastoma; D009504:Neutrophils / Q000166:cytology / Q000276:immunology* / Q000378:metabolism*; D016201:Receptors, Lymphocyte Homing / Q000276:immunology* / Q000378:metabolism; D014407:Tumor Cells, Cultured
D018821:CD18 Antigens; D015815:Cell Adhesion Molecules; D016207:Cytokines; D039041:Integrin alpha4beta1; D016023:Integrins; D016201:Receptors, Lymphocyte Homing