Current In Vitro Models of Leukocyte Migration

Methods and Interpretation
  • Jennifer R. Allport
  • Guillermo García-Cardeña
  • Yaw-Chyn Lim
  • Francis W. Luscinskas
Part of the Methods in Molecular Medicine book series (MIMM, volume 56)

Abstract

A large component of airway inflammatory disease is the recruitment of activated leukocytes (primarily eosinophils and T lymphocytes) from the lung vasculature into the bronchial walls resulting in lung edema. Ultimately, many of the infiltrating leukocytes progress across the airway epithelium into respiratory bronchioles, compromising lung capacity (1,2). In the case of an infection, such as pneumonia, leukocytes (primarily neutrophils and monocyte/macrophages) are recruited to alveolar air spaces reducing the capacity for gaseous exchange. In both cases, resident leukocytes then release further factors that promote additional leukocyte recruitment. During an inflammatory response in the peripheral microvasculature leukocyte recruitment takes place predominantly in the postcapillary venules via the multistep adhesion cascade (reviewed in 3,4,5). In the lung, however, leukocyte extravasation takes place via capillaries. This may be due to the specialized architecture of the lung vasculature (e.g., large numbers of branch points), or because of the differing expression of surface adhesion molecules that are required for leukocyte recruitment (1,6). In addition, local concentrations of cytokines, chemokines or other chemoattractant factors will play a role in the site and degree of leukocyte infiltration (7,8) through acute local activation of endothelial cells.

Keywords

Cellulose Migration Albumin EDTA Pneumonia 

References

  1. 1.
    Martin, T.R. (1997) Eur.Respir.J. 10Leukocyte migration and activation in the lungs,770-771. Eur.Respir.J. 10, 770–771.PubMedGoogle Scholar
  2. 2.
    Liu, L., Mul, F.P., Kuijpers, T.W., Lutter, R., Roos, D., and Knol, E.F. (1996) Neutrophil transmigration across monolayers of endothelial cells and airway epithelial cells is regulated by different mechanisms. Ann. N.Y. Acad. Set 796, 21–29.CrossRefGoogle Scholar
  3. 3.
    Butcher, E.C. (1991) Leukocyte-endothelial cell recognition; three (or more) steps to specificity and diversity. Cell 67, 1033–1036.CrossRefPubMedGoogle Scholar
  4. 4.
    Luscinskas, F.W. and Lawler, J. (1994) Integrins as dynamic regulators of vascular function. FASEB J. 8, 929–938.PubMedGoogle Scholar
  5. 5.
    Symon, F.A. and Wardlaw, A.J. (1996) Selectins and their counter receptors; a bitter sweet attraction. Thorax 51, 1155–1157.CrossRefPubMedGoogle Scholar
  6. 6.
    Cotran, R.S. and Mayadas-Norton, T. (1998) Endothelial adhesion molecules in health and disease. Pathol. Biol. (Paris) 46, 164–170.Google Scholar
  7. 7.
    Rothenburg, M.E., Zimmermann, N., Mishra, A., Brandt, E., Birkenberger, L.A., Hogan, S.P. and Foster, P.S. (1999) Chemokines and chemokine receptors: their role in allergic airway disease. J. Clin. Immunol. 19, 250–265.CrossRefGoogle Scholar
  8. 8.
    Strieter, R.M., Kunkel, S.L., Keane, M.P., and Standiford, T.J. (1999) Chemokines in lung injury: Thomas A. Neff lecture. Chest 116, 103S–110S.CrossRefPubMedGoogle Scholar
  9. 9.
    Zimmerman, G.A., Albertine, K.H., Carveth, H.J., Gill, E.A., Grissom, C.K., Hoidal, J.R., et al. (1999) Endothelial Activation in ARDS. Chest 116, 18S–24S.CrossRefPubMedGoogle Scholar
  10. 10.
    Sheetz, M.P., Felsenfeld, D.P., Galbraith, C.G. (1998) Cell migration: regulation of force on extracellular matrix-integrin complexes. Trends Cell Biol. 8, 51–54.CrossRefPubMedGoogle Scholar
  11. 11.
    Parent, C.A. & Devreotes, P.N. (1999) A cell’s sense of direction. Science 284, 765–770.CrossRefPubMedGoogle Scholar
  12. 12.
    Wilkinson, P.C. (1988) Micropore methods for leukocyte chemotaxis. Methods Enzymol. 162, 38–50.CrossRefPubMedGoogle Scholar
  13. 13.
    Muir, D., Sukhu, L., Johnson, J., Lahorra, M. A., and Maria, B. L. (1993) Quantitative methods for scoring cell migration and invasion in filter-based assays. Anal. Biochem. 215, 104–109.CrossRefPubMedGoogle Scholar
  14. 14.
    Kundra, V., Escobedo, J.A., Kazlauskas, A, Kim, H.K., Rhee, S.G., Williams, L.T., and Zetter, B.R. (1994) Regulation of chemotaxis by the platelet-derived growth factor receptor-beta. Nature 367, 474–476CrossRefPubMedGoogle Scholar
  15. 15.
    Allport, J.R., Donnelly, L.E., Hayes, B.P., Murray, S., Rendell, N.B., Ray, K.P., and MacDermot, J. (1996) Reduction by inhibitors of mono(ADP-ribosyl)trans-ferase of chemotaxis in human neutrophil leucocytes by inhibition of the assembly of filamentous actin. Br. J. Pharmacol. 118, 1111–1118.PubMedGoogle Scholar
  16. 16.
    Sierra-Honigmann, M.R., Nath, A.K., Murakami, C., Garcia-Cardena, G., Papapetropoulos, A., Sessa, W.C., et al. (1998) Biological action of leptin as an angiogenic factor. Science 281, 1683–1686.CrossRefPubMedGoogle Scholar
  17. 17.
    Papapetropoulos, A., Garcia-Cardena, G., Dengler, T.J., Maisonpierre, P.C., Yancopoulos, G.D., and Sessa, W.C. (1999) Direct actions of angiopoietin-1 on human endothelium: evidence for network stabilization, cell survival, and interaction with other angiogenic growth factors. Lab. Invest. 9, 213–223.Google Scholar

Copyright information

© Humana Press Inc., Totowa, NJ 2001

Authors and Affiliations

  • Jennifer R. Allport
    • 1
  • Guillermo García-Cardeña
    • 1
  • Yaw-Chyn Lim
    • 1
  • Francis W. Luscinskas
    • 1
  1. 1.Vascular Research Division, Department of Pathology, BrighamWomen’s HospitalBoston

Personalised recommendations