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IL-25 regulates the expression of adhesion molecules on eosinophils: mechanism of eosinophilia in allergic inflammation.
Allergy. 2006 Jul; 61(7):878-85.A

Abstract

BACKGROUND

Interleukin-25 (IL-25) is a novel T-helper-2 (Th2) cytokine of the IL-17 family that plays a key role in allergic inflammation. Recent studies reported that over-expression of IL-25 in mouse induces eosinophilia. We investigated the effect of IL-25 on the expression of several adhesion molecules on human eosinophils and the underlying intracellular mechanisms.

METHODS

Viability of eosinophils was measured by annexin V-fluorescein isothiocyanate (FITC) assay. Gene expression and surface expression of intercellular adhesion molecule (ICAM)-1 (CD54), ICAM-3 (CD50), L-selectin (CD62L), leukocyte function-associated antigen (LFA-1) (CD11a/CD18) and very late antigen-4 (VLA-4, CD49d/CD29) on eosinophils were measured by reverse transcriptase-polymerase chain reaction (RT-PCR) and flow cytometry, respectively. Adhesion of eosinophils to fibronectin was assessed using the fibronectin-coated insert system.

RESULTS

Viability of eosinophils was significantly enhanced by IL-25 from 41% to 76% dose-dependently. IL-25 could significantly upregulate the surface expression of ICAM-1, but suppress those of ICAM-3 and L-selectin on eosinophils in a dose-dependent manner. Adhesion of eosinophils to fibronectin was also significantly enhanced by IL-25. Besides, pre-incubation with p38 mitogen-activated protein kinases (MAPK) inhibitor SB203580, C-Jun NH2-terminal protein kinases (JNK) inhibitor SP600125 and proteosome inhibitor MG-132 could significantly restrain the effects of IL-25 on surface expression of L-selectin, ICAM-1 and ICAM-3, respectively, and also on the adhesion of eosinophils onto fibronectin (all P < 0.05).

CONCLUSIONS

Our findings suggest an essential role of IL-25 in enhancing survival and regulating surface expression of ICAM-1, ICAM-3 and L-selectin on human eosinophils through the activation of p38 MAPK, JNK and nuclear factor (NF)-kappaB pathways, thereby shedding light on the molecular mechanisms of IL-25-induced eosinophilia in allergic inflammation.

Authors+Show Affiliations

Department of Chemical Pathology, The Chinese University of Hong Kong, Prince of Wales Hospital, NT, Hong Kong.No affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

16792588

Citation

Cheung, P F Y., et al. "IL-25 Regulates the Expression of Adhesion Molecules On Eosinophils: Mechanism of Eosinophilia in Allergic Inflammation." Allergy, vol. 61, no. 7, 2006, pp. 878-85.
Cheung PF, Wong CK, Ip WK, et al. IL-25 regulates the expression of adhesion molecules on eosinophils: mechanism of eosinophilia in allergic inflammation. Allergy. 2006;61(7):878-85.
Cheung, P. F., Wong, C. K., Ip, W. K., & Lam, C. W. (2006). IL-25 regulates the expression of adhesion molecules on eosinophils: mechanism of eosinophilia in allergic inflammation. Allergy, 61(7), 878-85.
Cheung PF, et al. IL-25 Regulates the Expression of Adhesion Molecules On Eosinophils: Mechanism of Eosinophilia in Allergic Inflammation. Allergy. 2006;61(7):878-85. PubMed PMID: 16792588.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - IL-25 regulates the expression of adhesion molecules on eosinophils: mechanism of eosinophilia in allergic inflammation. AU - Cheung,P F Y, AU - Wong,C K, AU - Ip,W K, AU - Lam,C W K, PY - 2006/6/24/pubmed PY - 2006/12/9/medline PY - 2006/6/24/entrez SP - 878 EP - 85 JF - Allergy JO - Allergy VL - 61 IS - 7 N2 - BACKGROUND: Interleukin-25 (IL-25) is a novel T-helper-2 (Th2) cytokine of the IL-17 family that plays a key role in allergic inflammation. Recent studies reported that over-expression of IL-25 in mouse induces eosinophilia. We investigated the effect of IL-25 on the expression of several adhesion molecules on human eosinophils and the underlying intracellular mechanisms. METHODS: Viability of eosinophils was measured by annexin V-fluorescein isothiocyanate (FITC) assay. Gene expression and surface expression of intercellular adhesion molecule (ICAM)-1 (CD54), ICAM-3 (CD50), L-selectin (CD62L), leukocyte function-associated antigen (LFA-1) (CD11a/CD18) and very late antigen-4 (VLA-4, CD49d/CD29) on eosinophils were measured by reverse transcriptase-polymerase chain reaction (RT-PCR) and flow cytometry, respectively. Adhesion of eosinophils to fibronectin was assessed using the fibronectin-coated insert system. RESULTS: Viability of eosinophils was significantly enhanced by IL-25 from 41% to 76% dose-dependently. IL-25 could significantly upregulate the surface expression of ICAM-1, but suppress those of ICAM-3 and L-selectin on eosinophils in a dose-dependent manner. Adhesion of eosinophils to fibronectin was also significantly enhanced by IL-25. Besides, pre-incubation with p38 mitogen-activated protein kinases (MAPK) inhibitor SB203580, C-Jun NH2-terminal protein kinases (JNK) inhibitor SP600125 and proteosome inhibitor MG-132 could significantly restrain the effects of IL-25 on surface expression of L-selectin, ICAM-1 and ICAM-3, respectively, and also on the adhesion of eosinophils onto fibronectin (all P < 0.05). CONCLUSIONS: Our findings suggest an essential role of IL-25 in enhancing survival and regulating surface expression of ICAM-1, ICAM-3 and L-selectin on human eosinophils through the activation of p38 MAPK, JNK and nuclear factor (NF)-kappaB pathways, thereby shedding light on the molecular mechanisms of IL-25-induced eosinophilia in allergic inflammation. SN - 0105-4538 UR - https://www.unboundmedicine.com/medline/citation/16792588/IL_25_regulates_the_expression_of_adhesion_molecules_on_eosinophils:_mechanism_of_eosinophilia_in_allergic_inflammation_ L2 - https://doi.org/10.1111/j.1398-9995.2006.01102.x DB - PRIME DP - Unbound Medicine ER -