Published online before print June 14, 2004
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* Departments of Medical Microbiology and
Urology, Malmö University Hospital,
Cell and Molecular Biology, Lund University, and
Respiratory Medicine, University Hospital, Lund, Sweden
1 Correspondence: BMC B 14, Tornavägen 10, SE-221 84 Lund, Sweden. E-mail: Arne.Egesten{at}mikrobiol.mas.lu.se
Eosinophils participate in allergic inflammation, where expression of T helper cell type 2 (Th2) cytokines such as interleukin (IL)-4 and IL-5 are seen. However, eosinophils sometimes accumulate during disease with expression of Th1 cytokines [i.e., interferon-
(IFN-
), tumor necrosis factor
(TNF-
), and IL-1ß]. In this study, we investigated whether eosinophils can respond with expression of the IFN-inducible CXC chemokines monokine induced by IFN-
[MIG; CXC chemokine ligand 9 (CXCL9)], IFN-
-inducible protein (IP-10/CXCL10), and IFN-inducible T cell
chemoattractant (I-TAC/CXCL11). These chemokines share the ability to recruit and activate T cells and natural killer cells to sites of inflammation. We found that IFN-
induced rapid and sustained gene expression of MIG, IP-10, and I-TAC in eosinophils, as detected by quantitative reverse transcriptase-polymerase chain reaction. During incubation, IFN-
-stimulated eosinophils released MIG and IP-10, as detected by enzyme-linked immunosorbent assay, while I-TAC could not be detected in the medium. TNF-
but not IL-1ß enhanced the IFN-
-induced production of MIG and IP-10. Conversely, addition of the Th2 cytokine IL-4 down-regulated IFN-
-induced synthesis of MIG and IP10 in eosinophils. Crohns disease is characterized by a Th1-polarized inflammation and presence of eosinophils. In lesions from this disease, MIG was detected in eosinophils by immunohistochemistry. Taken together, the results point to immunoregulatory roles for eosinophils during some diseases with Th1-polarized inflammation.
Key Words: CXCL9 CXCL10 CXCL11 CXCR3
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