IL-13 induces eosinophil recruitment into the lung by an IL-5- and eotaxin-dependent mechanism

J Allergy Clin Immunol. 2001 Oct;108(4):594-601. doi: 10.1067/mai.2001.118600.


Background: IL-13 induces several characteristic features of asthma, including airway eosinophilia, airway hyperresponsiveness, and mucus overproduction; however, the mechanisms involved are largely unknown.

Objective: We hypothesized that IL-13-induced inflammatory changes in the lung were dependent in part on IL-5 and eotaxin, two eosinophil-selective cytokines.

Methods: Recombinant murine IL-13 was repeatedly administered to the lung by intranasal delivery until the characteristic features of asthma developed. To analyze the role of IL-5 and eotaxin, we subjected eotaxin gene-targeted, IL-5 gene-targeted, eotaxin/IL-5-double-deficient, IL-5 transgenic, and wild-type mice of the Balb/C background to the experimental regime.

Results: The induction of IL-13-mediated airway eosinophilia was found to occur independently of eosinophilia in the blood or bone marrow, indicating that IL-13-induced airway inflammation is primarily mediated by local effects of IL-13 in the lung. Eosinophil recruitment into both the lung tissue and bronchoalveolar lavage fluid was markedly attenuated in IL-5-deficient mice in comparison with wild-type controls. Accordingly, IL-13 delivery to IL-5 transgenic mice resulted in a large increase in airway eosinophils in comparison with wild-type mice. Interestingly, IL-13-induced eosinophilia in the bronchoalveolar lavage fluid of eotaxin-deficient mice was not impaired; however, these same mice failed to mount a significant tissue eosinophilia in response to IL-13. Finally, IL-13-induced mucus production was not affected by the presence of IL-5 or eotaxin, suggesting that IL-13-induced mucus secretion is mechanistically dissociated from airway eosinophilia.

Conclusion: Selective components of the IL-13-induced asthma phenotype--airway eosinophilia but not mucus secretion--are differentially regulated by IL-5 and eotaxin. IL-5 is required for IL-13 to induce eosinophilia throughout the lung, whereas eotaxin regulates the distribution of airway eosinophils.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Animals
  • Chemokine CCL11
  • Chemokines, CC*
  • Chemotaxis, Leukocyte
  • Cytokines / genetics
  • Cytokines / metabolism*
  • Female
  • Interleukin-13 / pharmacology*
  • Interleukin-5 / genetics
  • Interleukin-5 / metabolism*
  • Lung / pathology
  • Male
  • Mice
  • Mice, Transgenic
  • Mucus / metabolism
  • Pulmonary Eosinophilia / chemically induced*


  • Ccl11 protein, mouse
  • Chemokine CCL11
  • Chemokines, CC
  • Cytokines
  • Interleukin-13
  • Interleukin-5