T-helper cell type 2 (Th2) memory T cell-potentiating cytokine IL-25 has the potential to promote angiogenesis in asthma

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T-helper cell type 2 (Th2) memory T cell-potentiating cytokine IL-25 has the potential to promote angiogenesis in asthma. / Corrigan, Chris J.; Wang, Wei; Meng, Qiu et al.
In: Proceedings of the National Academy of Sciences of the United States of America, Vol. 108, No. 4, 25.01.2011, p. 1579-1584.

Research output: Contribution to Journal/Magazine › Journal article › peer-review

Harvard

Corrigan, CJ, Wang, W, Meng, Q, Fang, C, Wu, H, Reay, V, Lv, Z, Fan, Y, An, Y, Wang, Y-H, Liu, Y-J, Lee, TH & Ying, S 2011, 'T-helper cell type 2 (Th2) memory T cell-potentiating cytokine IL-25 has the potential to promote angiogenesis in asthma', Proceedings of the National Academy of Sciences of the United States of America, vol. 108, no. 4, pp. 1579-1584. https://doi.org/10.1073/pnas.1014241108

APA

Corrigan, C. J., Wang, W., Meng, Q., Fang, C., Wu, H., Reay, V., Lv, Z., Fan, Y., An, Y., Wang, Y.-H., Liu, Y.-J., Lee, T. H., & Ying, S. (2011). T-helper cell type 2 (Th2) memory T cell-potentiating cytokine IL-25 has the potential to promote angiogenesis in asthma. Proceedings of the National Academy of Sciences of the United States of America, 108(4), 1579-1584. https://doi.org/10.1073/pnas.1014241108

Vancouver

Corrigan CJ, Wang W, Meng Q, Fang C, Wu H, Reay V et al. T-helper cell type 2 (Th2) memory T cell-potentiating cytokine IL-25 has the potential to promote angiogenesis in asthma. Proceedings of the National Academy of Sciences of the United States of America. 2011 Jan 25;108(4):1579-1584. doi: 10.1073/pnas.1014241108

Author

Corrigan, Chris J. ; Wang, Wei ; Meng, Qiu et al. / T-helper cell type 2 (Th2) memory T cell-potentiating cytokine IL-25 has the potential to promote angiogenesis in asthma. In: Proceedings of the National Academy of Sciences of the United States of America. 2011 ; Vol. 108, No. 4. pp. 1579-1584.

Bibtex

@article{7af19ded5de94ca98ec829e4b84814a6,

title = "T-helper cell type 2 (Th2) memory T cell-potentiating cytokine IL-25 has the potential to promote angiogenesis in asthma",

abstract = "IL-25 (IL-17E) is a T-helper cell type 2 (Th2) cytokine best described as a potentiator of Th2 memory responses. Reports of expression of its receptor, IL-25R, on airways structural cells suggest a wider role for IL-25 in remodeling. We hypothesized that IL-25 stimulates local angiogenesis in the asthmatic bronchial mucosa. Immunoreactive IL-25(+), IL-25R(+), and CD31(+) (endothelial) cells in sections of bronchial biopsies from asthmatics and controls were detected by immunohistochemistry. The effect of IL-25 on angiogenesis was examined using an in vitro assay. Real-time PCR was used to detect expression of IL-25R and VEGF mRNA in cultured human vascular endothelial cells (HUVEC), and a cell proliferation kit (WST-8) was used to measure the effect of IL-25 on HUVEC proliferation. Immunostaining showed that IL-25(+), IL-25R(+), and CD31(+)/IL-25R(+) cells were significantly elevated in the bronchial mucosa of asthmatics compared with controls (P <0.003). In asthmatics, the numbers of IL-25(+) cells correlated inversely with the forced expiratory volume in 1 s (r = -0.639; P = 0.01). In vitro, HUVEC constitutively expressed IL-25R, which was up-regulated further by TNF-alpha. IL-25 and TNF-alpha also increased expression of VEGF and VEGF receptors. IL-25 increased HUVEC proliferation and the number, length, and area of microvessel structures in a concentration-dependent manner in vitro. VEGF blockade, the PI3K-specific inhibitor LY294002, and the MAPK/ERK1/2 (MEK1/2)-specific inhibitor U0126 all markedly attenuated IL-25-induced angiogenesis, and the inhibitors also reduced IL-25-induced proliferation and VEGF expression. Our findings suggest that IL-25 is elevated in asthma and contributes to angiogenesis, at least partly by increasing endothelial cell VEGF/VEGF receptor expression through PI3K/Akt and Erk/MAPK pathways.",

keywords = "THYMIC STROMAL LYMPHOPOIETIN, ENDOTHELIAL GROWTH-FACTOR, P38 MAP KINASE, IN-VIVO, ALLERGIC INFLAMMATION, KAPPA-B, EXPRESSION, INTERLEUKIN-25, ACTIVATION, CHEMOKINES",

author = "Corrigan, {Chris J.} and Wei Wang and Qiu Meng and Cailong Fang and Huifen Wu and Victoria Reay and Ze Lv and Yiqiang Fan and Yunqing An and Yui-Hsi Wang and Yong-Jun Liu and Lee, {Tak H.} and Sun Ying",

year = "2011",

month = jan,

day = "25",

doi = "10.1073/pnas.1014241108",

language = "English",

volume = "108",

pages = "1579--1584",

journal = "Proceedings of the National Academy of Sciences of the United States of America",

issn = "0027-8424",

publisher = "National Academy of Sciences",

number = "4",

}

RIS

TY - JOUR

T1 - T-helper cell type 2 (Th2) memory T cell-potentiating cytokine IL-25 has the potential to promote angiogenesis in asthma

AU - Corrigan, Chris J.

AU - Wang, Wei

AU - Meng, Qiu

AU - Fang, Cailong

AU - Wu, Huifen

AU - Reay, Victoria

AU - Lv, Ze

AU - Fan, Yiqiang

AU - An, Yunqing

AU - Wang, Yui-Hsi

AU - Liu, Yong-Jun

AU - Lee, Tak H.

AU - Ying, Sun

PY - 2011/1/25

Y1 - 2011/1/25

N2 - IL-25 (IL-17E) is a T-helper cell type 2 (Th2) cytokine best described as a potentiator of Th2 memory responses. Reports of expression of its receptor, IL-25R, on airways structural cells suggest a wider role for IL-25 in remodeling. We hypothesized that IL-25 stimulates local angiogenesis in the asthmatic bronchial mucosa. Immunoreactive IL-25(+), IL-25R(+), and CD31(+) (endothelial) cells in sections of bronchial biopsies from asthmatics and controls were detected by immunohistochemistry. The effect of IL-25 on angiogenesis was examined using an in vitro assay. Real-time PCR was used to detect expression of IL-25R and VEGF mRNA in cultured human vascular endothelial cells (HUVEC), and a cell proliferation kit (WST-8) was used to measure the effect of IL-25 on HUVEC proliferation. Immunostaining showed that IL-25(+), IL-25R(+), and CD31(+)/IL-25R(+) cells were significantly elevated in the bronchial mucosa of asthmatics compared with controls (P <0.003). In asthmatics, the numbers of IL-25(+) cells correlated inversely with the forced expiratory volume in 1 s (r = -0.639; P = 0.01). In vitro, HUVEC constitutively expressed IL-25R, which was up-regulated further by TNF-alpha. IL-25 and TNF-alpha also increased expression of VEGF and VEGF receptors. IL-25 increased HUVEC proliferation and the number, length, and area of microvessel structures in a concentration-dependent manner in vitro. VEGF blockade, the PI3K-specific inhibitor LY294002, and the MAPK/ERK1/2 (MEK1/2)-specific inhibitor U0126 all markedly attenuated IL-25-induced angiogenesis, and the inhibitors also reduced IL-25-induced proliferation and VEGF expression. Our findings suggest that IL-25 is elevated in asthma and contributes to angiogenesis, at least partly by increasing endothelial cell VEGF/VEGF receptor expression through PI3K/Akt and Erk/MAPK pathways.

AB - IL-25 (IL-17E) is a T-helper cell type 2 (Th2) cytokine best described as a potentiator of Th2 memory responses. Reports of expression of its receptor, IL-25R, on airways structural cells suggest a wider role for IL-25 in remodeling. We hypothesized that IL-25 stimulates local angiogenesis in the asthmatic bronchial mucosa. Immunoreactive IL-25(+), IL-25R(+), and CD31(+) (endothelial) cells in sections of bronchial biopsies from asthmatics and controls were detected by immunohistochemistry. The effect of IL-25 on angiogenesis was examined using an in vitro assay. Real-time PCR was used to detect expression of IL-25R and VEGF mRNA in cultured human vascular endothelial cells (HUVEC), and a cell proliferation kit (WST-8) was used to measure the effect of IL-25 on HUVEC proliferation. Immunostaining showed that IL-25(+), IL-25R(+), and CD31(+)/IL-25R(+) cells were significantly elevated in the bronchial mucosa of asthmatics compared with controls (P <0.003). In asthmatics, the numbers of IL-25(+) cells correlated inversely with the forced expiratory volume in 1 s (r = -0.639; P = 0.01). In vitro, HUVEC constitutively expressed IL-25R, which was up-regulated further by TNF-alpha. IL-25 and TNF-alpha also increased expression of VEGF and VEGF receptors. IL-25 increased HUVEC proliferation and the number, length, and area of microvessel structures in a concentration-dependent manner in vitro. VEGF blockade, the PI3K-specific inhibitor LY294002, and the MAPK/ERK1/2 (MEK1/2)-specific inhibitor U0126 all markedly attenuated IL-25-induced angiogenesis, and the inhibitors also reduced IL-25-induced proliferation and VEGF expression. Our findings suggest that IL-25 is elevated in asthma and contributes to angiogenesis, at least partly by increasing endothelial cell VEGF/VEGF receptor expression through PI3K/Akt and Erk/MAPK pathways.

KW - THYMIC STROMAL LYMPHOPOIETIN

KW - ENDOTHELIAL GROWTH-FACTOR

KW - P38 MAP KINASE

KW - IN-VIVO

KW - ALLERGIC INFLAMMATION

KW - KAPPA-B

KW - EXPRESSION

KW - INTERLEUKIN-25

KW - ACTIVATION

KW - CHEMOKINES

U2 - 10.1073/pnas.1014241108

DO - 10.1073/pnas.1014241108

M3 - Journal article

VL - 108

SP - 1579

EP - 1584

JO - Proceedings of the National Academy of Sciences of the United States of America

JF - Proceedings of the National Academy of Sciences of the United States of America

SN - 0027-8424

IS - 4

ER -

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