pH dependence of neutrophil-endothelial cell adhesion and adhesion molecule expression

Carlos V. Serrano, Aureliano Fraticelli, Rossella Paniccia, Anna Teti, Beth Noble, Stefano Corda, Tullio Faraggiana, Roy C. Ziegelstein, Jay L. Zweier, Maurizio C. Capogrossi

Research output: Contribution to journalArticle

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Abstract

Neutrophil adhesion to the vascular endothelium is enhanced during tissue ischemia and/or inflammation, conditions that are associated with tissue acidosis. This study examined the effects of hypercarbic acidosis (10 or 20% CO2) and of hypocarbic alkalosis (0% CO2) on human neutrophil CD18 and human aortic endothelial cell intercellular adhesion molecule-1 (ICAM-1) vascular cell adhesion molucule-1 (VCAM-1), and E-selectin expression quantified by flow cytometry. Acidosis with 20% CO2 for 4 h decreased ICAM- 1 to 60.6 ± 9.7% of control. In contrast, alkalosis with 0% CO2 for 4 h enhanced ICAM-1 expression to 143.8 ± 10.1% of control. There was no pH dependence of VCAM-1 or E-selectin expression. Tumor necrosis factor-α (TNF- α; 10 ng/ml) increased endothelial ICAM-1, E-selectin, and VCAM-1; under these conditions, acidosis with 20% CO2 blunted both ICAM-1 and E-selectin surface expression compared with 5% CO2-, TNF-α-treated cells. Hypercarbic acidosis with 20% CO2 increased neutrophil CD18 expression and enhanced neutrophil adhesion. This latter effect was inhibited by neutrophil pretreatment with an anti-CD18 monoclonal antibody. In contrast, when only endothelial cells were preincubated with the hypercarbic buffer, neutrophil adhesion diminished to 55.6 ± 7.84% of control. The results suggest that acidosis generated during tissue ischemia/inflammation may induce CDl8- mediated neutrophil adhesion despite a decrease in ICAM-1 expression.

Original languageEnglish
JournalAmerican Journal of Physiology - Cell Physiology
Volume271
Issue number3 40-3
Publication statusPublished - Sep 1996

Fingerprint

Cell adhesion
Endothelial cells
Intercellular Adhesion Molecule-1
Cell Adhesion
Acidosis
Neutrophils
E-Selectin
Adhesion
Endothelial Cells
Molecules
Blood Vessels
Alkalosis
Tissue
Ischemia
Flow cytometry
Inflammation
Vascular Endothelium
Cell Adhesion Molecules
Buffers
Tumor Necrosis Factor-alpha

Keywords

  • acidosis
  • alkalosis
  • hydrogen ion
  • inflammation
  • ischemia

ASJC Scopus subject areas

  • Clinical Biochemistry
  • Cell Biology
  • Physiology
  • Physiology (medical)

Cite this

Serrano, C. V., Fraticelli, A., Paniccia, R., Teti, A., Noble, B., Corda, S., ... Capogrossi, M. C. (1996). pH dependence of neutrophil-endothelial cell adhesion and adhesion molecule expression. American Journal of Physiology - Cell Physiology, 271(3 40-3).

pH dependence of neutrophil-endothelial cell adhesion and adhesion molecule expression. / Serrano, Carlos V.; Fraticelli, Aureliano; Paniccia, Rossella; Teti, Anna; Noble, Beth; Corda, Stefano; Faraggiana, Tullio; Ziegelstein, Roy C.; Zweier, Jay L.; Capogrossi, Maurizio C.

In: American Journal of Physiology - Cell Physiology, Vol. 271, No. 3 40-3, 09.1996.

Research output: Contribution to journalArticle

Serrano, CV, Fraticelli, A, Paniccia, R, Teti, A, Noble, B, Corda, S, Faraggiana, T, Ziegelstein, RC, Zweier, JL & Capogrossi, MC 1996, 'pH dependence of neutrophil-endothelial cell adhesion and adhesion molecule expression', American Journal of Physiology - Cell Physiology, vol. 271, no. 3 40-3.
Serrano CV, Fraticelli A, Paniccia R, Teti A, Noble B, Corda S et al. pH dependence of neutrophil-endothelial cell adhesion and adhesion molecule expression. American Journal of Physiology - Cell Physiology. 1996 Sep;271(3 40-3).
Serrano, Carlos V. ; Fraticelli, Aureliano ; Paniccia, Rossella ; Teti, Anna ; Noble, Beth ; Corda, Stefano ; Faraggiana, Tullio ; Ziegelstein, Roy C. ; Zweier, Jay L. ; Capogrossi, Maurizio C. / pH dependence of neutrophil-endothelial cell adhesion and adhesion molecule expression. In: American Journal of Physiology - Cell Physiology. 1996 ; Vol. 271, No. 3 40-3.
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abstract = "Neutrophil adhesion to the vascular endothelium is enhanced during tissue ischemia and/or inflammation, conditions that are associated with tissue acidosis. This study examined the effects of hypercarbic acidosis (10 or 20{\%} CO2) and of hypocarbic alkalosis (0{\%} CO2) on human neutrophil CD18 and human aortic endothelial cell intercellular adhesion molecule-1 (ICAM-1) vascular cell adhesion molucule-1 (VCAM-1), and E-selectin expression quantified by flow cytometry. Acidosis with 20{\%} CO2 for 4 h decreased ICAM- 1 to 60.6 ± 9.7{\%} of control. In contrast, alkalosis with 0{\%} CO2 for 4 h enhanced ICAM-1 expression to 143.8 ± 10.1{\%} of control. There was no pH dependence of VCAM-1 or E-selectin expression. Tumor necrosis factor-α (TNF- α; 10 ng/ml) increased endothelial ICAM-1, E-selectin, and VCAM-1; under these conditions, acidosis with 20{\%} CO2 blunted both ICAM-1 and E-selectin surface expression compared with 5{\%} CO2-, TNF-α-treated cells. Hypercarbic acidosis with 20{\%} CO2 increased neutrophil CD18 expression and enhanced neutrophil adhesion. This latter effect was inhibited by neutrophil pretreatment with an anti-CD18 monoclonal antibody. In contrast, when only endothelial cells were preincubated with the hypercarbic buffer, neutrophil adhesion diminished to 55.6 ± 7.84{\%} of control. The results suggest that acidosis generated during tissue ischemia/inflammation may induce CDl8- mediated neutrophil adhesion despite a decrease in ICAM-1 expression.",
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AU - Noble, Beth

AU - Corda, Stefano

AU - Faraggiana, Tullio

AU - Ziegelstein, Roy C.

AU - Zweier, Jay L.

AU - Capogrossi, Maurizio C.

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N2 - Neutrophil adhesion to the vascular endothelium is enhanced during tissue ischemia and/or inflammation, conditions that are associated with tissue acidosis. This study examined the effects of hypercarbic acidosis (10 or 20% CO2) and of hypocarbic alkalosis (0% CO2) on human neutrophil CD18 and human aortic endothelial cell intercellular adhesion molecule-1 (ICAM-1) vascular cell adhesion molucule-1 (VCAM-1), and E-selectin expression quantified by flow cytometry. Acidosis with 20% CO2 for 4 h decreased ICAM- 1 to 60.6 ± 9.7% of control. In contrast, alkalosis with 0% CO2 for 4 h enhanced ICAM-1 expression to 143.8 ± 10.1% of control. There was no pH dependence of VCAM-1 or E-selectin expression. Tumor necrosis factor-α (TNF- α; 10 ng/ml) increased endothelial ICAM-1, E-selectin, and VCAM-1; under these conditions, acidosis with 20% CO2 blunted both ICAM-1 and E-selectin surface expression compared with 5% CO2-, TNF-α-treated cells. Hypercarbic acidosis with 20% CO2 increased neutrophil CD18 expression and enhanced neutrophil adhesion. This latter effect was inhibited by neutrophil pretreatment with an anti-CD18 monoclonal antibody. In contrast, when only endothelial cells were preincubated with the hypercarbic buffer, neutrophil adhesion diminished to 55.6 ± 7.84% of control. The results suggest that acidosis generated during tissue ischemia/inflammation may induce CDl8- mediated neutrophil adhesion despite a decrease in ICAM-1 expression.

AB - Neutrophil adhesion to the vascular endothelium is enhanced during tissue ischemia and/or inflammation, conditions that are associated with tissue acidosis. This study examined the effects of hypercarbic acidosis (10 or 20% CO2) and of hypocarbic alkalosis (0% CO2) on human neutrophil CD18 and human aortic endothelial cell intercellular adhesion molecule-1 (ICAM-1) vascular cell adhesion molucule-1 (VCAM-1), and E-selectin expression quantified by flow cytometry. Acidosis with 20% CO2 for 4 h decreased ICAM- 1 to 60.6 ± 9.7% of control. In contrast, alkalosis with 0% CO2 for 4 h enhanced ICAM-1 expression to 143.8 ± 10.1% of control. There was no pH dependence of VCAM-1 or E-selectin expression. Tumor necrosis factor-α (TNF- α; 10 ng/ml) increased endothelial ICAM-1, E-selectin, and VCAM-1; under these conditions, acidosis with 20% CO2 blunted both ICAM-1 and E-selectin surface expression compared with 5% CO2-, TNF-α-treated cells. Hypercarbic acidosis with 20% CO2 increased neutrophil CD18 expression and enhanced neutrophil adhesion. This latter effect was inhibited by neutrophil pretreatment with an anti-CD18 monoclonal antibody. In contrast, when only endothelial cells were preincubated with the hypercarbic buffer, neutrophil adhesion diminished to 55.6 ± 7.84% of control. The results suggest that acidosis generated during tissue ischemia/inflammation may induce CDl8- mediated neutrophil adhesion despite a decrease in ICAM-1 expression.

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