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Interleukin (IL)‐4 and to a lesser extent either IL‐13 or interferon‐gamma regulate the production of eotaxin‐2/CCL24 in nasal polyps
Author(s) -
LezcanoMeza D.,
DávilaDávila B.,
VegaMiranda A.,
NegreteGarcía M. C.,
Teran L. M.
Publication year - 2003
Publication title -
allergy
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.363
H-Index - 173
eISSN - 1398-9995
pISSN - 0105-4538
DOI - 10.1034/j.1398-9995.2003.00174.x
Subject(s) - eotaxin , nasal polyps , chemokine , cytokine , eosinophil , immunology , interleukin 5 , medicine , interleukin , endocrinology , immune system , asthma
Background: Eotaxin‐2/CCL24 is a potent eosinophil attractant that has been implicated in the recruitment of eosinophils in allergic disease. We have investigated whether the cytokines interleukin (IL)‐4, IL‐13, and interferon (IFN)‐gamma regulate eotaxin‐2/CCL24 in nasal polyps. Methods: Nasal polyps were cultured in the presence of the cytokines described above and the concentration of eotaxin‐2/CCL24 was measured in the culture supernatant. Results: IL‐4 was found to be the major stimulus for eotaxin‐2/CCL24 production from nasal polyps followed by IL‐13 and IFN‐gamma. IL‐4 induced eotaxin‐2/CCL24 in a dose‐dependent manner with concentrations as low as 0.1 ng/ml being able to induce eotaxin‐2/CCL24. By immunohistochemistry, eotaxin‐2/CCL24 immunoreactivity was localized to mononuclear cells in the IL‐4 stimulated nasal polyp tissue. Interestingly, nasal turbinates obtained from patients suffering from nonallergic rhinitis (vasomotor rhinitis) were also found to release eotaxin‐2/CCL24 both spontaneously and following cytokine stimulation with IL‐4 and IFN‐gamma being major inducers of this cytokine. Conclusions: All together these findings suggest that Th1 and Th2 cytokines may regulate eotaxin‐2/CCL24 production in nasal polyps and nonallergic rhinits.