IL-21 Modulates Release of Proinflammatory Cytokines in LPS-Stimulated Macrophages through Distinct Signaling Pathways
The aim of this study was to investigate the anti-inflammatory effect of IL-21 on LPS-induced mouse peritoneal macrophages. The results showed that IL-21 significantly inhibited LPS-induced mRNA expression of IL-1β, TNF-α, and IL-6 in macrophages, but not of IFN-γ, IL-10, CCL5, or CXCL2. ELISA analy...
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| Main Authors: | , , , , , , , , , , , , , |
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| Format: | Article |
| Language: | English |
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Wiley
2013-01-01
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| Series: | Mediators of Inflammation |
| Online Access: | http://dx.doi.org/10.1155/2013/548073 |
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| _version_ | 1832564721336713216 |
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| author | Su-nan Li Wei Wang Shou-peng Fu Jian-fa Wang Hong-mei Liu Shan-shan Xie Bing-run Liu Yang Li Qing-kang Lv Zhi-qiang Li Wen-jing Xue Bing-xu Huang Wei Chen Ju-xiong Liu |
| author_facet | Su-nan Li Wei Wang Shou-peng Fu Jian-fa Wang Hong-mei Liu Shan-shan Xie Bing-run Liu Yang Li Qing-kang Lv Zhi-qiang Li Wen-jing Xue Bing-xu Huang Wei Chen Ju-xiong Liu |
| author_sort | Su-nan Li |
| collection | DOAJ |
| description | The aim of this study was to investigate the anti-inflammatory effect of IL-21 on LPS-induced mouse peritoneal macrophages. The results showed that IL-21 significantly inhibited LPS-induced mRNA expression of IL-1β, TNF-α, and IL-6 in macrophages, but not of IFN-γ, IL-10, CCL5, or CXCL2. ELISA analysis showed that IL-21 also suppressed LPS-induced production of TNF-α and IL-6 in culture supernatants. Western blot analysis showed that IL-21 clearly inhibited ERK and IκBα phosphorylation and NF-κB translocation in LPS-stimulated macrophages, but it increased STAT3 phosphorylation. Flow cytometric and Western blot analysis showed that IL-21 decreased M1 macrophages surface markers expression of CD86, iNOS, and TLR4 in LPS-stimulated cells. All results suggested that IL-21 decreases IL-6 and TNF-α production via inhibiting the phosphorylation of ERK and translocation of NF-κB and promotes a shift from the M1 to M2 macrophage phenotype by decreasing the expression of CD86, iNOS, and TLR4 and by increasing STAT3 phosphorylation in LPS-stimulated cells. |
| format | Article |
| id | doaj-art-f9340692110c48cba12a7404e0981109 |
| institution | Kabale University |
| issn | 0962-9351 1466-1861 |
| language | English |
| publishDate | 2013-01-01 |
| publisher | Wiley |
| record_format | Article |
| series | Mediators of Inflammation |
| spelling | doaj-art-f9340692110c48cba12a7404e09811092025-02-03T01:10:30ZengWileyMediators of Inflammation0962-93511466-18612013-01-01201310.1155/2013/548073548073IL-21 Modulates Release of Proinflammatory Cytokines in LPS-Stimulated Macrophages through Distinct Signaling PathwaysSu-nan Li0Wei Wang1Shou-peng Fu2Jian-fa Wang3Hong-mei Liu4Shan-shan Xie5Bing-run Liu6Yang Li7Qing-kang Lv8Zhi-qiang Li9Wen-jing Xue10Bing-xu Huang11Wei Chen12Ju-xiong Liu13College of Veterinary Medicine, Jilin University, Changchun 130062, ChinaCollege of Veterinary Medicine, Jilin University, Changchun 130062, ChinaCollege of Veterinary Medicine, Jilin University, Changchun 130062, ChinaCollege of Veterinary Medicine, Jilin University, Changchun 130062, ChinaCollege of Veterinary Medicine, Jilin University, Changchun 130062, ChinaCollege of Veterinary Medicine, Jilin University, Changchun 130062, ChinaCollege of Veterinary Medicine, Jilin University, Changchun 130062, ChinaCollege of Veterinary Medicine, Jilin University, Changchun 130062, ChinaCollege of Veterinary Medicine, Jilin University, Changchun 130062, ChinaCollege of Veterinary Medicine, Jilin University, Changchun 130062, ChinaCollege of Veterinary Medicine, Jilin University, Changchun 130062, ChinaCollege of Veterinary Medicine, Jilin University, Changchun 130062, ChinaCollege of Veterinary Medicine, Jilin University, Changchun 130062, ChinaCollege of Veterinary Medicine, Jilin University, Changchun 130062, ChinaThe aim of this study was to investigate the anti-inflammatory effect of IL-21 on LPS-induced mouse peritoneal macrophages. The results showed that IL-21 significantly inhibited LPS-induced mRNA expression of IL-1β, TNF-α, and IL-6 in macrophages, but not of IFN-γ, IL-10, CCL5, or CXCL2. ELISA analysis showed that IL-21 also suppressed LPS-induced production of TNF-α and IL-6 in culture supernatants. Western blot analysis showed that IL-21 clearly inhibited ERK and IκBα phosphorylation and NF-κB translocation in LPS-stimulated macrophages, but it increased STAT3 phosphorylation. Flow cytometric and Western blot analysis showed that IL-21 decreased M1 macrophages surface markers expression of CD86, iNOS, and TLR4 in LPS-stimulated cells. All results suggested that IL-21 decreases IL-6 and TNF-α production via inhibiting the phosphorylation of ERK and translocation of NF-κB and promotes a shift from the M1 to M2 macrophage phenotype by decreasing the expression of CD86, iNOS, and TLR4 and by increasing STAT3 phosphorylation in LPS-stimulated cells.http://dx.doi.org/10.1155/2013/548073 |
| spellingShingle | Su-nan Li Wei Wang Shou-peng Fu Jian-fa Wang Hong-mei Liu Shan-shan Xie Bing-run Liu Yang Li Qing-kang Lv Zhi-qiang Li Wen-jing Xue Bing-xu Huang Wei Chen Ju-xiong Liu IL-21 Modulates Release of Proinflammatory Cytokines in LPS-Stimulated Macrophages through Distinct Signaling Pathways Mediators of Inflammation |
| title | IL-21 Modulates Release of Proinflammatory Cytokines in LPS-Stimulated Macrophages through Distinct Signaling Pathways |
| title_full | IL-21 Modulates Release of Proinflammatory Cytokines in LPS-Stimulated Macrophages through Distinct Signaling Pathways |
| title_fullStr | IL-21 Modulates Release of Proinflammatory Cytokines in LPS-Stimulated Macrophages through Distinct Signaling Pathways |
| title_full_unstemmed | IL-21 Modulates Release of Proinflammatory Cytokines in LPS-Stimulated Macrophages through Distinct Signaling Pathways |
| title_short | IL-21 Modulates Release of Proinflammatory Cytokines in LPS-Stimulated Macrophages through Distinct Signaling Pathways |
| title_sort | il 21 modulates release of proinflammatory cytokines in lps stimulated macrophages through distinct signaling pathways |
| url | http://dx.doi.org/10.1155/2013/548073 |
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