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Interferon-gamma enhances human eosinophil effector functions induced by granulocyte-macrophage colony-stimulating factor or interleukin-5.
Immunol Lett. 2008 Jun 15; 118(1):88-95.IL

Abstract

T helper (Th) 2-type cytokines play a dominant role in allergic inflammation. Accumulating evidence suggests that Th1-type cytokines antagonize Th2-type cytokine responses; however, recent studies demonstrate that Th1 cytokines might enhance Th2 immune responses. We examined whether interferon (IFN)-gamma, a representative Th1 cytokine, modifies the effector functions of human eosinophils stimulated by granulocyte-macrophage colony-stimulating factor (GM-CSF) and interleukin (IL)-5. GM-CSF and IL-5 have significant functional homology, and contribute to the regulation of Th2 immunity. After the pretreatment of eosinophils with IFN-gamma, GM-CSF- or IL-5-induced eosinophil functions were examined, including superoxide anion generation, degranulation, adhesion, expression of GM-CSF receptor (R), IL-5R, or CD11b, and phosphorylation of intracellular signaling molecules. Superoxide anion generation was measured using the cytochrome c reduction method. Degranulation and cell adhesion were evaluated based on eosinophil-derived neurotoxin (EDN) contents in supernatants or adherent cells. Phosphorylation of signaling molecules was analyzed using a multiplex beads array system. Preincubation with IFN-gamma resulted in enhanced GM-CSF- or IL-5-induced superoxide anion generation and degranulation of human eosinophils, whereas stimulus-induced eosinophil adhesion was unaffected. In addition, IFN-gamma did not influence the expression of GM-CSFR, IL-5R, and CD11b. Furthermore, IFN-gamma upregulated GM-CSF- or IL-5-induced phosphorylation of extracellular signal-regulated kinase (ERK), p38 mitogen-activated protein kinase (MAPK), c-Jun N-terminal kinase (JNK), and activating transcription factor (ATF)-2. Finally, we confirmed that MAPK inhibitors blocked the enhancement of stimuli-induced superoxide anion generation of IFN-gamma treated eosinophils. In conclusion, IFN-gamma might upregulate ERK, p38, or JNK/ATF-2 phosphorylation induced by GM-CSF or IL-5, leading to enhanced cytokine-induced eosinophil superoxide generation and degranulation.

Authors+Show Affiliations

Gunma Prefectural Institute of Public Health and Environmental Sciences, Maebashi, Gunma, Japan.No affiliation info availableNo 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

18440651

Citation

Yamaguchi, Takafumi, et al. "Interferon-gamma Enhances Human Eosinophil Effector Functions Induced By Granulocyte-macrophage Colony-stimulating Factor or Interleukin-5." Immunology Letters, vol. 118, no. 1, 2008, pp. 88-95.
Yamaguchi T, Kimura H, Kurabayashi M, et al. Interferon-gamma enhances human eosinophil effector functions induced by granulocyte-macrophage colony-stimulating factor or interleukin-5. Immunol Lett. 2008;118(1):88-95.
Yamaguchi, T., Kimura, H., Kurabayashi, M., Kozawa, K., & Kato, M. (2008). Interferon-gamma enhances human eosinophil effector functions induced by granulocyte-macrophage colony-stimulating factor or interleukin-5. Immunology Letters, 118(1), 88-95. https://doi.org/10.1016/j.imlet.2008.03.005
Yamaguchi T, et al. Interferon-gamma Enhances Human Eosinophil Effector Functions Induced By Granulocyte-macrophage Colony-stimulating Factor or Interleukin-5. Immunol Lett. 2008 Jun 15;118(1):88-95. PubMed PMID: 18440651.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Interferon-gamma enhances human eosinophil effector functions induced by granulocyte-macrophage colony-stimulating factor or interleukin-5. AU - Yamaguchi,Takafumi, AU - Kimura,Hirokazu, AU - Kurabayashi,Masahiko, AU - Kozawa,Kunihisa, AU - Kato,Masahiko, Y1 - 2008/04/10/ PY - 2008/01/28/received PY - 2008/03/12/revised PY - 2008/03/17/accepted PY - 2008/4/29/pubmed PY - 2008/8/7/medline PY - 2008/4/29/entrez SP - 88 EP - 95 JF - Immunology letters JO - Immunol Lett VL - 118 IS - 1 N2 - T helper (Th) 2-type cytokines play a dominant role in allergic inflammation. Accumulating evidence suggests that Th1-type cytokines antagonize Th2-type cytokine responses; however, recent studies demonstrate that Th1 cytokines might enhance Th2 immune responses. We examined whether interferon (IFN)-gamma, a representative Th1 cytokine, modifies the effector functions of human eosinophils stimulated by granulocyte-macrophage colony-stimulating factor (GM-CSF) and interleukin (IL)-5. GM-CSF and IL-5 have significant functional homology, and contribute to the regulation of Th2 immunity. After the pretreatment of eosinophils with IFN-gamma, GM-CSF- or IL-5-induced eosinophil functions were examined, including superoxide anion generation, degranulation, adhesion, expression of GM-CSF receptor (R), IL-5R, or CD11b, and phosphorylation of intracellular signaling molecules. Superoxide anion generation was measured using the cytochrome c reduction method. Degranulation and cell adhesion were evaluated based on eosinophil-derived neurotoxin (EDN) contents in supernatants or adherent cells. Phosphorylation of signaling molecules was analyzed using a multiplex beads array system. Preincubation with IFN-gamma resulted in enhanced GM-CSF- or IL-5-induced superoxide anion generation and degranulation of human eosinophils, whereas stimulus-induced eosinophil adhesion was unaffected. In addition, IFN-gamma did not influence the expression of GM-CSFR, IL-5R, and CD11b. Furthermore, IFN-gamma upregulated GM-CSF- or IL-5-induced phosphorylation of extracellular signal-regulated kinase (ERK), p38 mitogen-activated protein kinase (MAPK), c-Jun N-terminal kinase (JNK), and activating transcription factor (ATF)-2. Finally, we confirmed that MAPK inhibitors blocked the enhancement of stimuli-induced superoxide anion generation of IFN-gamma treated eosinophils. In conclusion, IFN-gamma might upregulate ERK, p38, or JNK/ATF-2 phosphorylation induced by GM-CSF or IL-5, leading to enhanced cytokine-induced eosinophil superoxide generation and degranulation. SN - 0165-2478 UR - https://www.unboundmedicine.com/medline/citation/18440651/Interferon_gamma_enhances_human_eosinophil_effector_functions_induced_by_granulocyte_macrophage_colony_stimulating_factor_or_interleukin_5_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0165-2478(08)00090-4 DB - PRIME DP - Unbound Medicine ER -