Leukocyte-borne α(1,3)-fucose is a negative regulator of β2-integrin-dependent recruitment in lung inflammation

Alexander Buffone, Mehrab Nasirikenari, Charles T. Manhardt, Amit Lugade, Paul N. Bogner, Robert Sackstein, Yasmin Thanavala, Sriram Neelamegham, Joseph T.Y. Lau

Research output: Contribution to journalArticlepeer-review

11 Scopus citations


Leukocyte recruitment in inflammation is a multistep, sequential cascade where the initial step is the selectindependent tethering, followed by the formation of firmer integrin-mediated adhesive forces leading to extravasation. The α(1,3)-fucose-containing sialyl-Lewis X (sLeX) is the archetypical ligand on leukocyte surfaces mediating selectin interactions. Canonically, disruption of α(1,3)- fucose formation ablates selectin-mediated adhesion, dramatically reducing trafficking. We report a paradoxical response to α(1,3)-fucose deficiency in which the loss exacerbated rather than attenuated leukocyte recruitment in a murine model of acute airway inflammation. The architecture of the capillary-dominated vasculature in the lung minimized the importance of the selectin dependent step, and we observed that α(1,3)-fucose deficiency augmented CXCR2-mediated Rap1-GTP signaling to enhance the β2-integrin-ICAM-1-binding axis. The data disclose a previously unknown function for α(1,3)-fucose, in which this structure negatively regulates the integrin activation step in leukocyte recruitment.

Original languageEnglish (US)
Pages (from-to)459-470
Number of pages12
JournalJournal of Leukocyte Biology
Issue number2
StatePublished - Feb 2017
Externally publishedYes

All Science Journal Classification (ASJC) codes

  • Immunology and Allergy
  • Immunology
  • Cell Biology


  • CXCR2
  • Fucosyltransferase
  • ICAM-1
  • NTHI
  • Neutrophil


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