BACKGROUND: The induction of epithelial cytokines/chemokines is crucial in the migration of leukocytes, and its regulatory mechanisms remain incompletely defined. OBJECTIVE: To determine the role of IL-17, a CD4(+) T cell-derived cytokine, in modulation of primary bronchial epithelial cells, the expression of IL-6, IL-8, and intercellular adhesion molecule 1 (ICAM-1) and the potential involvement of mitogen-activated protein (MAP) kinases in IL-17-mediated signaling were examined. METHODS: The levels of gene expression and protein production for IL-6 and IL-8 in IL-17-treated cells, in the presence or absence of MAP kinase inhibitors, were analyzed by RT-PCR and ELISA, respectively, and activation of MAP kinases was determined by Western blot analyses. RESULTS: We showed first that IL-17 induced time-dependent expression of IL-6 and IL-8 but not of the chemokines eotaxin and RANTES. In addition, IL-17 induced activation of extracellular signal-regulated kinase 1/2 but not of p38 or JNK kinases. A selective MAP kinase kinase inhibitor, PD98059, inhibited IL-17-induced IL-6 and IL-8. A combination of IL-17 and each of the cytokines IL-4, IL-13, and IFN-gamma further enhanced IL-8 expression. IL-17 alone did not induce ICAM-1 expression and showed no effect on IL-4- or IL-13-induced ICAM-1 expression. In contrast, a combination of IL-17 and IFN-gamma augmented IL-6 and ICAM-1 expression. CONCLUSION: These findings suggest that IL-17, alone or in combination with other cytokines, modulates airway inflammation via-in part-the expression of epithelial IL-6, IL-8, and ICAM-1.
BACKGROUND: The induction of epithelial cytokines/chemokines is crucial in the migration of leukocytes, and its regulatory mechanisms remain incompletely defined. OBJECTIVE: To determine the role of IL-17, a CD4(+) T cell-derived cytokine, in modulation of primary bronchial epithelial cells, the expression of IL-6, IL-8, and intercellular adhesion molecule 1 (ICAM-1) and the potential involvement of mitogen-activated protein (MAP) kinases in IL-17-mediated signaling were examined. METHODS: The levels of gene expression and protein production for IL-6 and IL-8 in IL-17-treated cells, in the presence or absence of MAP kinase inhibitors, were analyzed by RT-PCR and ELISA, respectively, and activation of MAP kinases was determined by Western blot analyses. RESULTS: We showed first that IL-17 induced time-dependent expression of IL-6 and IL-8 but not of the chemokines eotaxin and RANTES. In addition, IL-17 induced activation of extracellular signal-regulated kinase 1/2 but not of p38 or JNK kinases. A selective MAP kinase kinase inhibitor, PD98059, inhibited IL-17-induced IL-6 and IL-8. A combination of IL-17 and each of the cytokines IL-4, IL-13, and IFN-gamma further enhanced IL-8 expression. IL-17 alone did not induce ICAM-1 expression and showed no effect on IL-4- or IL-13-induced ICAM-1 expression. In contrast, a combination of IL-17 and IFN-gamma augmented IL-6 and ICAM-1 expression. CONCLUSION: These findings suggest that IL-17, alone or in combination with other cytokines, modulates airway inflammation via-in part-the expression of epithelial IL-6, IL-8, and ICAM-1.
Authors: David I Weiss; Feiyang Ma; Alexander A Merleev; Emanual Maverakis; Michel Gilliet; Samuel J Balin; Bryan D Bryson; Maria Teresa Ochoa; Matteo Pellegrini; Barry R Bloom; Robert L Modlin Journal: J Immunol Date: 2019-06-24 Impact factor: 5.422
Authors: Ladislava Sebkova; Antonia Pellicanò; Giovanni Monteleone; Barbara Grazioli; Giovanni Guarnieri; Maria Imeneo; Francesco Pallone; Francesco Luzza Journal: Infect Immun Date: 2004-09 Impact factor: 3.441
Authors: Chun Kwok Wong; Shuiqing Hu; Karen Ming-Lam Leung; Jie Dong; Lan He; Yi Jun Chu; Ida Miu-Ting Chu; Huai-Na Qiu; Kelly Yan-Ping Liu; Christopher Wai-Kei Lam Journal: Cell Mol Immunol Date: 2013-03-25 Impact factor: 11.530