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Gene Review

Ccl11  -  chemokine (C-C motif) ligand 11

Mus musculus

Synonyms: C-C motif chemokine 11, Eosinophil chemotactic protein, Eotaxin, Scya11, Small-inducible cytokine A11, ...
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Disease relevance of Ccl11

  • The identification of constitutive eotaxin mRNA expression in multiple tissues suggests that in addition to regulating airway eosinophilia, eotaxin is likely to be involved in eosinophil recruitment into other tissues as well as in baseline tissue homing [1].
  • Pulmonary expression of interleukin-13 causes inflammation, mucus hypersecretion, subepithelial fibrosis, physiologic abnormalities, and eotaxin production [2].
  • Treatment of cpdm/cpdm mice with CCL11-neutralizing polyclonal antibodies did not affect the number of eosinophils in the skin or the severity of the dermatitis [3].
  • Such mice demonstrate that eotaxin enhances the magnitude of the early (but not late) eosinophil recruitment after antigen challenge in models of asthma and stromal keratitis [4].
  • Expression and participation of eotaxin during mycobacterial (type 1) and schistosomal (type 2) antigen-elicited granuloma formation [5].

High impact information on Ccl11

  • Mouse Eotaxin expression parallels eosinophil accumulation during lung allergic inflammation but it is not restricted to a Th2-type response [6].
  • We describe the identification and cloning of a cDNA that encodes a mouse C-C chemokine with 68% amino acid identity to guinea pig Eotaxin [6].
  • The mRNA expression of mouse Eotaxin is not restricted to Th2 T cells in vitro and is independent of the development of a Th2-type response during N. brasiliensis infection, in vivo [6].
  • Notably, in mice deficient in IL-5/eotaxin the ability of CD4(+) T helper cell (Th)2 lymphocytes to produce IL-13, a critical regulator of airways smooth muscle constriction and obstruction, was significantly impaired [7].
  • Neutralization of RANTES (regulated upon activation, normal T cell expressed and secreted) receptor(s) with a receptor antagonist decreases significantly lymphocyte and eosinophil infiltration as well as mRNA expression of eotaxin and RANTES [8].

Chemical compound and disease context of Ccl11


Biological context of Ccl11

  • Using a guinea pig lung cDNA library, we have cloned full-length eotaxin cDNA [1].
  • Taken together, these results suggest that CD8(+) cells from sensitized SD rats exhibit the functional capacity to suppress the LAR, possibly through downregulation of eotaxin expression and increased expression of IFN-gamma mRNA [14].
  • CONCLUSIONS: Acute rejection of corneal xenografts in mice is mediated by T cells that display a mixed T-helper (Th) type 2/Th1 phenotype and secrete eotaxin, an eosinophil chemoattractant [15].
  • In contrast, the mutants K26 (amino-terminus) E179 and E180 (ECL2) responded in chemotaxis assays to CCL11 and CCL24, but not to CCL26 [16].
  • Functional responsiveness to eotaxin was increased in IL5TG eosinophils as demonstrated by a 10x increase in its potency in producing actin polymerization and 3x increase in CD11b upregulation relative to WT [17].

Anatomical context of Ccl11

  • Consistent with its putative role in eosinophilic inflammation, eotaxin induces the selective infiltration of eosinophils when injected into the lung and skin [1].
  • High constitutive levels of eotaxin mRNA expression were observed in the lung, while the intestines, stomach, spleen, liver, heart, thymus, testes, and kidney expressed lower levels [1].
  • These latter effects would appear to be selective because no changes were observed when macrophage-inflammatory protein-1alpha, eotaxin, or MCP-3 were instilled into the airways of normal mice or when mast cells were treated in vitro [18].
  • Correlating with the decreased cellular infiltration, delta chain T-cell receptor-deficient (TCR delta(-/-)) mice exhibited substantially reduced levels of most of the chemokines analyzed (with the exception of eotaxin) [19].
  • We challenged wild-type (WT) BALB/c, CCL11 single knockout (SKO) and CCL11 IL-5 double knockout (DKO) mice with either T. spiralis muscle larvae or T. muris eggs in order to examine eosinophil recruitment to the small and large intestine during helminth infection [20].

Associations of Ccl11 with chemical compounds

  • Thus, eotaxin mRNA levels are increased in response to allergen challenge during the late phase response [1].
  • To investigate further contribution of CC chemokines, we administered a 35-kD CC chemokine neutralizing protein (vCKBP) in vivo. vCKBP inhibited the eosinophil accumulation induced by eotaxin and ovalbumin, but did not block that induced by LPS or LPW [21].
  • Alanine scanning mutagenesis of the chemokine receptor CCR3 reveals distinct extracellular residues involved in recognition of the eotaxin family of chemokines [16].
  • Taken together, these results demonstrate that expression of eotaxin and IL-5 in intestinal epithelium induces compartmentalized dysregulation of eosinophil trafficking and the important role of the beta(7) integrin in gastrointestinal allergic responses [10].
  • In addition, equivalent numbers of dispersed lung cells from L-NAME- and aminoguanidine-treated mice produced significantly higher levels of IL-4, monocyte chemoattractant protein (MCP)-1, and macrophage inflammatory protein (MIP)-1alpha and significantly lower levels of eotaxin compared with D-NAME-treated mice [22].

Physical interactions of Ccl11


Regulatory relationships of Ccl11


Other interactions of Ccl11

  • Moreover, IL-5 was found to be an eosinophil chemotactic factor by the checkerboard assay [26].
  • The adhesion molecule VCAM-1 and eotaxin have been implicated in extravasation and accumulation of eosinophils into tissue in animal models of asthma [27].
  • However, these cells were neither the main producers of the major eosinophilic chemokines eotaxin, RANTES, or MIP-1alpha, nor did they regulate the expression of these chemokines [28].
  • Unexpectedly, expression of only three chemokines, CCL11, CCL17, and CCL22, was STAT6 dependent, and many of the identified chemokines were overexpressed in STAT6-deficient mice, providing an explanation for the enhanced neutrophilic inflammation seen in these mice [29].
  • Messages encoding eotaxin, macrophage inflammatory protein (MIP)-1alpha, and MIP-2 were elevated after 4 and 24 h of exposure to 1 ppm ozone [30].

Analytical, diagnostic and therapeutic context of Ccl11


  1. Constitutive and allergen-induced expression of eotaxin mRNA in the guinea pig lung. Rothenberg, M.E., Luster, A.D., Lilly, C.M., Drazen, J.M., Leder, P. J. Exp. Med. (1995) [Pubmed]
  2. Pulmonary expression of interleukin-13 causes inflammation, mucus hypersecretion, subepithelial fibrosis, physiologic abnormalities, and eotaxin production. Zhu, Z., Homer, R.J., Wang, Z., Chen, Q., Geba, G.P., Wang, J., Zhang, Y., Elias, J.A. J. Clin. Invest. (1999) [Pubmed]
  3. Increased expression of chemokines in the skin of chronic proliferative dermatitis mutant mice. Renninger, M.L., Seymour, R., Lillard, J.W., Sundberg, J.P., HogenEsch, H. Exp. Dermatol. (2005) [Pubmed]
  4. Targeted disruption of the chemokine eotaxin partially reduces antigen-induced tissue eosinophilia. Rothenberg, M.E., MacLean, J.A., Pearlman, E., Luster, A.D., Leder, P. J. Exp. Med. (1997) [Pubmed]
  5. Expression and participation of eotaxin during mycobacterial (type 1) and schistosomal (type 2) antigen-elicited granuloma formation. Ruth, J.H., Lukacs, N.W., Warmington, K.S., Polak, T.J., Burdick, M., Kunkel, S.L., Strieter, R.M., Chensue, S.W. J. Immunol. (1998) [Pubmed]
  6. Mouse Eotaxin expression parallels eosinophil accumulation during lung allergic inflammation but it is not restricted to a Th2-type response. Ganzalo, J.A., Jia, G.Q., Aguirre, V., Friend, D., Coyle, A.J., Jenkins, N.A., Lin, G.S., Katz, H., Lichtman, A., Copeland, N., Kopf, M., Gutierrez-Ramos, J.C. Immunity (1996) [Pubmed]
  7. Intrinsic defect in T cell production of interleukin (IL)-13 in the absence of both IL-5 and eotaxin precludes the development of eosinophilia and airways hyperreactivity in experimental asthma. Mattes, J., Yang, M., Mahalingam, S., Kuehr, J., Webb, D.C., Simson, L., Hogan, S.P., Koskinen, A., McKenzie, A.N., Dent, L.A., Rothenberg, M.E., Matthaei, K.I., Young, I.G., Foster, P.S. J. Exp. Med. (2002) [Pubmed]
  8. The coordinated action of CC chemokines in the lung orchestrates allergic inflammation and airway hyperresponsiveness. Gonzalo, J.A., Lloyd, C.M., Wen, D., Albar, J.P., Wells, T.N., Proudfoot, A., Martinez-A, C., Dorf, M., Bjerke, T., Coyle, A.J., Gutierrez-Ramos, J.C. J. Exp. Med. (1998) [Pubmed]
  9. The eotaxin chemokines and CCR3 are fundamental regulators of allergen-induced pulmonary eosinophilia. Pope, S.M., Zimmermann, N., Stringer, K.F., Karow, M.L., Rothenberg, M.E. J. Immunol. (2005) [Pubmed]
  10. Enterocyte expression of the eotaxin and interleukin-5 transgenes induces compartmentalized dysregulation of eosinophil trafficking. Mishra, A., Hogan, S.P., Brandt, E.B., Wagner, N., Crossman, M.W., Foster, P.S., Rothenberg, M.E. J. Biol. Chem. (2002) [Pubmed]
  11. Inhibition of allergic airways inflammation and airway hyperresponsiveness in mice by dexamethasone: role of eosinophils, IL-5, eotaxin, and IL-13. Eum, S.Y., Maghni, K., Hamid, Q., Eidelman, D.H., Campbell, H., Isogai, S., Martin, J.G. J. Allergy Clin. Immunol. (2003) [Pubmed]
  12. IL-13 induces eosinophil recruitment into the lung by an IL-5- and eotaxin-dependent mechanism. Pope, S.M., Brandt, E.B., Mishra, A., Hogan, S.P., Zimmermann, N., Matthaei, K.I., Foster, P.S., Rothenberg, M.E. J. Allergy Clin. Immunol. (2001) [Pubmed]
  13. Inhibition of phosphodiesterase activity, airway inflammation and hyperresponsiveness by PDE4 inhibitor and glucocorticoid in a murine model of allergic asthma. Sun, J.G., Deng, Y.M., Wu, X., Tang, H.F., Deng, J.F., Chen, J.Q., Yang, S.Y., Xie, Q.M. Life Sci. (2006) [Pubmed]
  14. CD8 depletion-induced late airway response is characterized by eosinophilia, increased eotaxin, and decreased IFN-gamma expression in rats. Allakhverdi, Z., Lamkhioued, B., Olivenstein, R., Hamid, Q., Renzi, P.M. Am. J. Respir. Crit. Care Med. (2000) [Pubmed]
  15. Evidence that T-helper type 2 cell-derived cytokines and eosinophils contribute to acute rejection of orthotopic corneal xenografts in mice. Tanaka, K., Yamagami, S., Streilein, J.W. Transplantation (2005) [Pubmed]
  16. Alanine scanning mutagenesis of the chemokine receptor CCR3 reveals distinct extracellular residues involved in recognition of the eotaxin family of chemokines. Duchesnes, C.E., Murphy, P.M., Williams, T.J., Pease, J.E. Mol. Immunol. (2006) [Pubmed]
  17. Functional effects of eotaxin are selectively upregulated on IL-5 transgenic mouse eosinophils. Kudlacz, E., Whitney, C., Andresenl, C., Conklyn, M. Inflammation (2002) [Pubmed]
  18. Monocyte chemoattractant protein-1 mediates cockroach allergen-induced bronchial hyperreactivity in normal but not CCR2-/- mice: the role of mast cells. Campbell, E.M., Charo, I.F., Kunkel, S.L., Strieter, R.M., Boring, L., Gosling, J., Lukacs, N.W. J. Immunol. (1999) [Pubmed]
  19. CC chemokines mediate leukocyte trafficking into the central nervous system during murine neurocysticercosis: role of gamma delta T cells in amplification of the host immune response. Cardona, A.E., Gonzalez, P.A., Teale, J.M. Infect. Immun. (2003) [Pubmed]
  20. The role of Th2 cytokines, chemokines and parasite products in eosinophil recruitment to the gastrointestinal mucosa during helminth infection. Dixon, H., Blanchard, C., Deschoolmeester, M.L., Yuill, N.C., Christie, J.W., Rothenberg, M.E., Else, K.J. Eur. J. Immunol. (2006) [Pubmed]
  21. LPS induces eosinophil migration via CCR3 signaling through a mechanism independent of RANTES and Eotaxin. Penido, C., Castro-Faria-Neto, H.C., Vieira-de-Abreu, A., Figueiredo, R.T., Pelled, A., Martins, M.A., Jose, P.J., Williams, T.J., Bozza, P.T. Am. J. Respir. Cell Mol. Biol. (2001) [Pubmed]
  22. Collagen deposition in a non-fibrotic lung granuloma model after nitric oxide inhibition. Hogaboam, C.M., Gallinat, C.S., Bone-Larson, C., Chensue, S.W., Lukacs, N.W., Strieter, R.M., Kunkel, S.L. Am. J. Pathol. (1998) [Pubmed]
  23. T helper-2 immunity regulates bronchial hyperresponsiveness in eosinophil-associated gastrointestinal disease in mice. Forbes, E., Smart, V.E., D'Aprile, A., Henry, P., Yang, M., Matthaei, K.I., Rothenberg, M.E., Foster, P.S., Hogan, S.P. Gastroenterology (2004) [Pubmed]
  24. Chronic intestinal nematode infection induces Stat6-independent interleukin-5 production and causes eosinophilic inflammatory responses in mice. Sakamoto, Y., Hiromatsu, K., Ishiwata, K., Inagaki-Ohara, K., Ikeda, T., Nakamura-Uchiyama, F., Nawa, Y. Immunology (2004) [Pubmed]
  25. Murine eotaxin: an eosinophil chemoattractant inducible in endothelial cells and in interleukin 4-induced tumor suppression. Rothenberg, M.E., Luster, A.D., Leder, P. Proc. Natl. Acad. Sci. U.S.A. (1995) [Pubmed]
  26. Highly purified murine interleukin 5 (IL-5) stimulates eosinophil function and prolongs in vitro survival. IL-5 as an eosinophil chemotactic factor. Yamaguchi, Y., Hayashi, Y., Sugama, Y., Miura, Y., Kasahara, T., Kitamura, S., Torisu, M., Mita, S., Tominaga, A., Takatsu, K. J. Exp. Med. (1988) [Pubmed]
  27. Oncostatin-M up-regulates VCAM-1 and synergizes with IL-4 in eotaxin expression: involvement of STAT6. Fritz, D.K., Kerr, C., Tong, L., Smyth, D., Richards, C.D. J. Immunol. (2006) [Pubmed]
  28. Eosinophil recruitment to the lung in a murine model of allergic inflammation. The role of T cells, chemokines, and adhesion receptors. Gonzalo, J.A., Lloyd, C.M., Kremer, L., Finger, E., Martinez-A, C., Siegelman, M.H., Cybulsky, M., Gutierrez-Ramos, J.C. J. Clin. Invest. (1996) [Pubmed]
  29. Pulmonary chemokine expression is coordinately regulated by STAT1, STAT6, and IFN-gamma. Fulkerson, P.C., Zimmermann, N., Hassman, L.M., Finkelman, F.D., Rothenberg, M.E. J. Immunol. (2004) [Pubmed]
  30. Antioxidant and inflammatory response after acute nitrogen dioxide and ozone exposures in C57Bl/6 mice. Johnston, C.J., Reed, C.K., Avissar, N.E., Gelein, R., Finkelstein, J.N. Inhalation toxicology. (2000) [Pubmed]
  31. Cysteinyl-leukotrienes partly mediate eotaxin-induced bronchial hyperresponsiveness and eosinophilia in IL-5 transgenic mice. Hisada, T., Salmon, M., Nasuhara, Y., Chung, K.F. Am. J. Respir. Crit. Care Med. (1999) [Pubmed]
  32. Anti-inflammatory effects of high-dose montelukast in an animal model of acute asthma. Wu, A.Y., Chik, S.C., Chan, A.W., Li, Z., Tsang, K.W., Li, W. Clin. Exp. Allergy (2003) [Pubmed]
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