PMID- 7657294 OWN - NLM STAT- MEDLINE DCOM- 19951004 LR - 20071114 IS - 0270-9139 (Print) IS - 0270-9139 (Linking) VI - 22 IP - 3 DP - 1995 Sep TI - Differential expression and release of CD54 induced by cytokines. PG - 866-75 AB - Intercellular adhesion molecule-1 (ICAM-1, CD54) is upregulated in many cell types stimulated by cytokines. A human hepatoblastoma cell line (C3A, a subclone of HepG2/C3 that is currently being used as a surrogate liver) and human lung adenocarcinoma cells (A549) were stimulated with interleukin-1 beta (IL-1 beta), tumor necrosis factor-alpha (TNF alpha), interferon-gamma (IFN gamma), or IL-6 to determine any differences in cell type responsiveness to individual cytokines for ICAM-1 upregulation. Time courses were performed with each cytokine evaluating ICAM-1 mRNA, surface expression, and cICAM-1 in the cell culture media. Between 3 and 6 hours, IL-1 beta (30 U/mL) stimulated the greatest increase in hepatocyte ICAM-1 mRNA, followed by IFN gamma (100 U/ mL), and IL-6 (100 U/mL) in order of potency. Except for IL-6, cytokine-induced hepatocyte surface levels of ICAM-1 (immunofluorescence flow cytometry, mAb R6.5) were dose dependent, with inhibition at higher concentration. Highest levels followed stimulation with INF gamma (P < .05). Significantly less was found after both IL-1 beta and TNF alpha; none was detected after IL-6 (P < .05). In contrast, IL-1 beta stimulated significantly more cICAM-1 release from hepatocytes than the other cytokines (P < .001), and IL-6 stimulated modest cICAM-1. Between 3 and 6 hours in the A549 cells, IL-1 beta stimulated the greatest increase in ICAM-1 mRNA, followed by TNF alpha. Both responses were greater than that observed in the hepatocytes. IFN gamma- and IL-6-induced ICAM-1 mRNA synthesis was not different from unstimulated A549 cells. Cytokine-induced A549 surface levels of ICAM-1 (immunofluorescence flow cytometry, mAb R6.5) was highest for IL-1 beta (peak levels similar to hepatocyte response), modest with TNF alpha (peak levels less than hepatocytes), detectable with IFN gamma (much less than hepatocytes), and nondetectable after IL-6. No ICAM-1 release from A549 cells was induced under any condition. In hepatocytes the amount of ICAM-1 mRNA was best accounted for by considering both cell surface levels of ICAM-1 and cICAM-1 levels. In human lung adenocarcinoma cells, the cytokine induction of ICAM-1 mRNA could potentially be accounted for by observing cell surface levels of ICAM-1 because no cICAM-1 was produced. These results suggest that surface ICAM-1 and cICAM-1 may be differentially controlled by each cytokine and by each parenchymal cell type. FAU - Mickelson, J K AU - Mickelson JK AD - Section of Cardiology, Methodist Hospital, Houston TX, USA. FAU - Kukielka, G AU - Kukielka G FAU - Bravenec, J S AU - Bravenec JS FAU - Mainolfi, E AU - Mainolfi E FAU - Rothlein, R AU - Rothlein R FAU - Hawkins, H K AU - Hawkins HK FAU - Kelly, J H AU - Kelly JH FAU - Smith, C W AU - Smith CW LA - eng GR - ES06091/ES/NIEHS NIH HHS/United States PT - Journal Article PT - Research Support, Non-U.S. Gov't PT - Research Support, U.S. Gov't, P.H.S. PL - United States TA - Hepatology JT - Hepatology (Baltimore, Md.) JID - 8302946 RN - 0 (Culture Media) RN - 0 (Cytokines) RN - 0 (RNA, Messenger) RN - 126547-89-5 (Intercellular Adhesion Molecule-1) SB - IM MH - Adenocarcinoma/metabolism/pathology MH - Culture Media/metabolism MH - Cytokines/*pharmacology MH - Dose-Response Relationship, Drug MH - Hepatoblastoma/metabolism/pathology MH - Humans MH - Immunohistochemistry MH - Intercellular Adhesion Molecule-1/genetics/*metabolism MH - Liver Neoplasms/metabolism/pathology MH - Lung Neoplasms/metabolism/pathology MH - RNA, Messenger/metabolism MH - Time Factors MH - Tumor Cells, Cultured EDAT- 1995/09/01 00:00 MHDA- 1995/09/01 00:01 CRDT- 1995/09/01 00:00 PHST- 1995/09/01 00:00 [pubmed] PHST- 1995/09/01 00:01 [medline] PHST- 1995/09/01 00:00 [entrez] AID - 0270-9139(95)90309-7 [pii] PST - ppublish SO - Hepatology. 1995 Sep;22(3):866-75.