CXCL14 Overexpression Attenuates Sepsis-Associated Acute Kidney Injury by Inhibiting Proinflammatory Cytokine Production
CXCL14 is a relatively novel chemokine with a wide spectrum of biological activities. The present study was designed to investigate whether CXCL14 overexpression attenuates sepsis-associated acute kidney injury (AKI) in mice. Sepsis model has been established by cecal ligation and puncture (CLP). CL...
Saved in:
| Main Authors: | , , , , |
|---|---|
| Format: | Article |
| Language: | English |
| Published: |
Wiley
2020-01-01
|
| Series: | Mediators of Inflammation |
| Online Access: | http://dx.doi.org/10.1155/2020/2431705 |
| Tags: |
Add Tag
No Tags, Be the first to tag this record!
|
| _version_ | 1832547186156503040 |
|---|---|
| author | Jing Lv Zhi-Lin Wu Zheng Gan Ping Gui Shang-Long Yao |
| author_facet | Jing Lv Zhi-Lin Wu Zheng Gan Ping Gui Shang-Long Yao |
| author_sort | Jing Lv |
| collection | DOAJ |
| description | CXCL14 is a relatively novel chemokine with a wide spectrum of biological activities. The present study was designed to investigate whether CXCL14 overexpression attenuates sepsis-associated acute kidney injury (AKI) in mice. Sepsis model has been established by cecal ligation and puncture (CLP). CLP induced AKI in mice as assessed by increased renal neutrophil gelatinase-associated lipocalin (NGAL) expression and serum creatinine levels. We found that renal CXCL14 expression in the kidney was significantly decreased at 12 hours after CLP. Correlation analysis demonstrated a negative association between renal CXCL14 expression and AKI markers including serum creatinine and renal NGAL. Moreover, CXCL14 overexpression reduced cytokine (TNF-α, IL-6, and IL-1β) production and NGAL expression in the kidney and decreased serum creatinine levels. In vivo and in vitro experiments found that CXCL14 overexpression inhibited M1 macrophage polarization but increased M2 polarization. Together, these results suggest that CXCL14 overexpression attenuates sepsis-associated AKI probably through the downregulation of macrophages-derived cytokine production. However, further studies are required to elucidate the underlying mechanism. |
| format | Article |
| id | doaj-art-dba7a46642c1451da7d9eaa8f949a3ab |
| institution | Kabale University |
| issn | 0962-9351 1466-1861 |
| language | English |
| publishDate | 2020-01-01 |
| publisher | Wiley |
| record_format | Article |
| series | Mediators of Inflammation |
| spelling | doaj-art-dba7a46642c1451da7d9eaa8f949a3ab2025-02-03T06:45:46ZengWileyMediators of Inflammation0962-93511466-18612020-01-01202010.1155/2020/24317052431705CXCL14 Overexpression Attenuates Sepsis-Associated Acute Kidney Injury by Inhibiting Proinflammatory Cytokine ProductionJing Lv0Zhi-Lin Wu1Zheng Gan2Ping Gui3Shang-Long Yao4Department of Anesthesiology, Institute of Anesthesiology and Critical Care Medicine, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, 1277 Jiefang Avenue, Wuhan, Hubei 430022, ChinaDepartment of Anesthesiology, Institute of Anesthesiology and Critical Care Medicine, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, 1277 Jiefang Avenue, Wuhan, Hubei 430022, ChinaDepartment of Anesthesiology, Institute of Anesthesiology and Critical Care Medicine, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, 1277 Jiefang Avenue, Wuhan, Hubei 430022, ChinaDepartment of Anesthesiology, Institute of Anesthesiology and Critical Care Medicine, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, 1277 Jiefang Avenue, Wuhan, Hubei 430022, ChinaDepartment of Anesthesiology, Institute of Anesthesiology and Critical Care Medicine, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, 1277 Jiefang Avenue, Wuhan, Hubei 430022, ChinaCXCL14 is a relatively novel chemokine with a wide spectrum of biological activities. The present study was designed to investigate whether CXCL14 overexpression attenuates sepsis-associated acute kidney injury (AKI) in mice. Sepsis model has been established by cecal ligation and puncture (CLP). CLP induced AKI in mice as assessed by increased renal neutrophil gelatinase-associated lipocalin (NGAL) expression and serum creatinine levels. We found that renal CXCL14 expression in the kidney was significantly decreased at 12 hours after CLP. Correlation analysis demonstrated a negative association between renal CXCL14 expression and AKI markers including serum creatinine and renal NGAL. Moreover, CXCL14 overexpression reduced cytokine (TNF-α, IL-6, and IL-1β) production and NGAL expression in the kidney and decreased serum creatinine levels. In vivo and in vitro experiments found that CXCL14 overexpression inhibited M1 macrophage polarization but increased M2 polarization. Together, these results suggest that CXCL14 overexpression attenuates sepsis-associated AKI probably through the downregulation of macrophages-derived cytokine production. However, further studies are required to elucidate the underlying mechanism.http://dx.doi.org/10.1155/2020/2431705 |
| spellingShingle | Jing Lv Zhi-Lin Wu Zheng Gan Ping Gui Shang-Long Yao CXCL14 Overexpression Attenuates Sepsis-Associated Acute Kidney Injury by Inhibiting Proinflammatory Cytokine Production Mediators of Inflammation |
| title | CXCL14 Overexpression Attenuates Sepsis-Associated Acute Kidney Injury by Inhibiting Proinflammatory Cytokine Production |
| title_full | CXCL14 Overexpression Attenuates Sepsis-Associated Acute Kidney Injury by Inhibiting Proinflammatory Cytokine Production |
| title_fullStr | CXCL14 Overexpression Attenuates Sepsis-Associated Acute Kidney Injury by Inhibiting Proinflammatory Cytokine Production |
| title_full_unstemmed | CXCL14 Overexpression Attenuates Sepsis-Associated Acute Kidney Injury by Inhibiting Proinflammatory Cytokine Production |
| title_short | CXCL14 Overexpression Attenuates Sepsis-Associated Acute Kidney Injury by Inhibiting Proinflammatory Cytokine Production |
| title_sort | cxcl14 overexpression attenuates sepsis associated acute kidney injury by inhibiting proinflammatory cytokine production |
| url | http://dx.doi.org/10.1155/2020/2431705 |
| work_keys_str_mv | AT jinglv cxcl14overexpressionattenuatessepsisassociatedacutekidneyinjurybyinhibitingproinflammatorycytokineproduction AT zhilinwu cxcl14overexpressionattenuatessepsisassociatedacutekidneyinjurybyinhibitingproinflammatorycytokineproduction AT zhenggan cxcl14overexpressionattenuatessepsisassociatedacutekidneyinjurybyinhibitingproinflammatorycytokineproduction AT pinggui cxcl14overexpressionattenuatessepsisassociatedacutekidneyinjurybyinhibitingproinflammatorycytokineproduction AT shanglongyao cxcl14overexpressionattenuatessepsisassociatedacutekidneyinjurybyinhibitingproinflammatorycytokineproduction |