[{"data":1,"prerenderedAt":-1},["ShallowReactive",2],{"detail-sidebar-cat-0-en-105":3,"doc-seo-456063-105":59,"doc-detail-456063-en":130},{"code":4,"msg":5,"data":6},0,"success",[7,13,18,23,28,33,38,43,48,51,55],{"id":8,"doc_module":4,"doc_module_name":9,"category_name":10,"show_sort_weight":11,"slug":12},1,"Document","Story & Novel",90,"story-novel",{"id":14,"doc_module":4,"doc_module_name":9,"category_name":15,"show_sort_weight":16,"slug":17},2,"Literature",80,"literature",{"id":19,"doc_module":4,"doc_module_name":9,"category_name":20,"show_sort_weight":21,"slug":22},4,"Exam",70,"exam",{"id":24,"doc_module":4,"doc_module_name":9,"category_name":25,"show_sort_weight":26,"slug":27},5,"Comic",60,"comic",{"id":29,"doc_module":4,"doc_module_name":9,"category_name":30,"show_sort_weight":31,"slug":32},6,"Technology",50,"technology",{"id":34,"doc_module":4,"doc_module_name":9,"category_name":35,"show_sort_weight":36,"slug":37},7,"Healthcare",40,"healthcare",{"id":39,"doc_module":4,"doc_module_name":9,"category_name":40,"show_sort_weight":41,"slug":42},8,"Research & Report",30,"research-report",{"id":44,"doc_module":4,"doc_module_name":9,"category_name":45,"show_sort_weight":46,"slug":47},9,"Religion & Spirituality",20,"religion-spirituality",{"id":46,"doc_module":4,"doc_module_name":9,"category_name":49,"show_sort_weight":46,"slug":50},"World Cup","world-cup",{"id":52,"doc_module":4,"doc_module_name":9,"category_name":53,"show_sort_weight":52,"slug":54},10,"Lifestyle","lifestyle",{"id":56,"doc_module":4,"doc_module_name":9,"category_name":57,"show_sort_weight":24,"slug":58},19,"General","general",{"code":4,"msg":60,"data":61},"ok",{"site_id":62,"language":63,"slug":64,"title":65,"keywords":66,"description":67,"schema_data":68,"social_meta":123,"head_meta":125,"extra_data":127,"updated_unix":129},105,"en","neutrophil-expression-of-decay-accelerating-factor-a-key-complement-regulator-has-no-impact-on-acute-kidney-injury-research-letter","Neutrophil Expression of Decay Accelerating Factor, a Key Complement Regulator, Has No Impact on Acute Kidney Injury - Research Letter","","AKI affects a substantial fraction of hospitalized and critically ill patients, and accumulating evidence links immune mechanisms—especially neutrophil recruitment—to disease onset and progression. In AA-induced AKI, neutrophil infiltration arises early and marks tubular injury, while complement signaling regulates neutrophil activation and migration. Decay accelerating factor (DAF/CD55) is a regulator of complement activation on cell membranes. However, in AA-challenged mice, DAF expression changes do not alter kidney neutrophil recruitment or AKI severity, suggesting DAF on neutrophils is dispensable for these outcomes.",{"@graph":69,"@context":122},[70,84,105],{"@type":71,"itemListElement":72},"BreadcrumbList",[73,77,79,82],{"item":74,"name":75,"@type":76,"position":8},"https://docshare.wps.com","Home","ListItem",{"item":78,"name":9,"@type":76,"position":14},"https://docshare.wps.com/document/",{"item":80,"name":35,"@type":76,"position":81},"https://docshare.wps.com/document/healthcare/",3,{"item":83,"name":65,"@type":76,"position":19},"https://docshare.wps.com/document/neutrophil-expression-of-decay-accelerating-factor-a-key-complement-regulator-has-no-impact-on-acute-kidney-injury-research-letter/456063/",{"url":83,"name":65,"@type":85,"image":86,"author":91,"headline":65,"publisher":94,"fileFormat":97,"inLanguage":63,"description":67,"dateModified":98,"datePublished":99,"encodingFormat":97,"isAccessibleForFree":100,"interactionStatistic":101},"DigitalDocument",{"url":87,"@type":88,"width":89,"height":90},"https://docshare.wps.com/thumbnails/neutrophil-expression-of-decay-accelerating-factor-a-key-complement-regulator-has-no-impact-on-acute-kidney-injury-research-letter/456063.png","ImageObject",300,407,{"name":92,"@type":93},"Cipher","Person",{"url":74,"name":95,"@type":96},"DocShare","Organization","application/pdf","2026-11-01","2026-09-30",true,{"@type":102,"interactionType":103,"userInteractionCount":29},"InteractionCounter",{"@type":104},"ViewAction",{"@type":106,"mainEntity":107},"FAQPage",[108,114,118],{"name":109,"@type":110,"acceptedAnswer":111},"What role do neutrophils play in acute kidney injury (AKI)?","Question",{"text":112,"@type":113},"Neutrophils infiltrate the kidney and contribute to tubular epithelial and endothelial injury through proinflammatory mediators and NETs, thereby amplifying immune cell recruitment and tissue damage.","Answer",{"name":115,"@type":110,"acceptedAnswer":116},"Why is decay accelerating factor (DAF/CD55) of interest in this study?",{"text":117,"@type":113},"DAF/CD55 regulates complement activation on cell membranes, and complement signaling is known to influence neutrophil activation and migration during inflammatory kidney diseases.",{"name":119,"@type":110,"acceptedAnswer":120},"Do changes in DAF expression on neutrophils affect AKI severity in mice?",{"text":121,"@type":113},"No. Although DAF expression in infiltrating renal neutrophils changes after AA administration, DAF deletion or overexpression did not change kidney neutrophil infiltration, histological lesions, or BUN levels, indicating DAF on neutrophils does not impact AA-induced AKI severity.","https://schema.org",{"og:url":83,"og:type":124,"og:title":65,"og:site_name":95,"og:description":67},"article",{"robots":126,"canonical":83},"index,follow",{"doc_id":128,"site_id":62},456063,1790792773,{"code":4,"msg":5,"data":131},{"doc_id":128,"user_id":132,"nickname":92,"user_avatar":133,"doc_module":4,"category_id":34,"category_name":35,"doc_title":65,"doc_description":67,"doc_content":134,"file_id":135,"file_url":136,"file_type":137,"file_size":138,"view_count":29,"is_deleted":4,"is_public":8,"is_downloadable":8,"audit_status":8,"page_count":81,"language":139,"language_code":63,"site_id":62,"html_lang":63,"table_of_contents":140,"faqs":141,"seo_title":142,"seo_description":67,"update_tm":143,"read_time":39,"preview_page_count":4},687208528416,"https://ap-avatar.wpscdn.com/davatar_9964176cb1d06d4a9deccf72a44ae3dc","Research Letter  \nNeutrophil Expression of Decay Accelerating Factor, a Key Complement Regulator, Has No Impact on Acute Kidney Injury  \nBarbara Franchin  and Paolo Cravedi   \nKidney360 6: 1790–1792, 2025. doi: [https://doi.org/10.34067/KID.0000000890](https://doi.org/10.34067/KID.0000000890)  \nAKI is a serious clinical condition affecting approximately 10%–15% of hospitalized individuals and up to 50% of critically ill patients in intensive care units. Increasing evidence highlights the role of the immune system in AKI onset and progression. Renal neutrophil infiltration is a common feature in mouse models of AKI model and in humans and correlates with disease severity.1 Neutrophils transmigrate from the circulation into the kidney interstitium, where they release proinflammatory molecules and neutrophil extracellular traps that induce tubular epithelial cell injury and death, endothelial dysfunction, and fuel further infiltration of immune cells.2  \nIn aristolochic acid (AA)-induced AKI, neutrophil infiltration occurs early and serves as a critical marker of tubular injury, as demonstrated by studies using neutrophil depletion strategies.2  \nComplement is strongly linked to neutrophil migration and activation in peripheral tissues, and blockade of C3a receptor ameliorates the severity of AA-induced AKI.3,4 Of note, decay accelerating factor (DAF or CD55) represents a key regulator of complement activation on cell membranes.  \nTo study the role of DAF on neutrophil activation and AKI severity, we administered AA (5 mg/kg, SigmaAldrich, 102501333) i.p. every other day for 5 days (day 1, 3 and 5) to 8-week-old C57BL/6J (B6, H-2b) male mice that were euthanize at 14 days after the first injection. Kidneys were processed to obtain single-cell suspensions (MACS dissociation kit, Miltenyi Biotec) for flow cytometric analyses.  \nWhen euthanized, AA-injected mice showed significantly more CD11b1Ly6g 1 neutrophils in the kidneys than control, PBS-injected mice (Figure 1A) . We next tested changes in DAF expression in neutrophils over time after AA injection (Figure 1B) . We found a stable decrease in  \nDAF expression in neutrophils infiltrating the kidneys, while DAF expression in splenic neutrophils initially raised on day 1 after AA followed by a reduction (Figure 1C), suggesting a mechanistic link among changes in DAF expression, neutrophil recruitment into the kidney, and renal injury (Supplemental Methods) .  \nTo formally test this hypothesis, we generated B6 mice that selectively lack (DAFDS100A8) or overexpress (DAFTgDS100A8) DAF in neutrophils.  \nFirst, we verified that DAF expression was selectively modified in neutrophils (Figure 1D) . We also found no significant differences in the number of Ly6g 1 neutrophils in the spleen or in the kidneys of DAFDS100A8 or DAF-TgDS100A8 mice at baseline (not shown) .  \nNext, we compared the severity of kidney injury upon AA injection across the groups. Contrary to our prediction, BUN levels at 7 and 14 days after AA injection did not differ among the three groups (Figure 1E) . Kidney neutrophil infiltration (Figure 1F) and histological lesions (Figure 1G) were also similar. Overall, these data suggest that DAF expression on neutrophils does not affect their renal recruitment or the severity of AKI in mice.  \nDAF is a key regulator of local complement activation and has been proposed as a therapeutic target to control complement activation locally. Prior studies by our group and others have demonstrated the critical role of DAF inglomerular diseases, where it limits complement activation and the generation of C3a and C5a, thereby modulating signaling through their respective receptors on glomerular cells.5 C5a/C5aR1 signaling in neutrophils is critical for their extravasation in vasculitides, and C5aR1 blockade is used clinically to prevent disease relapse in patients with ANCA-associated vasculitis.6 Therefore, we hypothesized that DAF overexpression would mitigate disease severity by restricting loc","cbCaivp0AT0KLjNO","https://ap.wps.com/l/cbCaivp0AT0KLjNO","pdf",368926,"English","# Background\n## Neutrophils and complement in AKI\n# Methods\n## AA-induced AKI model and DAF modulation\n# Results\n## DAF expression dynamics after AA injection\n## DAF loss or overexpression and AKI severity\n## Kidney recruitment, histology, and BUN readouts\n# Interpretation\n## DAF on neutrophils does not impact AA-induced AKI","[{\"question\":\"What role do neutrophils play in acute kidney injury (AKI)?\",\"answer\":\"Neutrophils infiltrate the kidney and contribute to tubular epithelial and endothelial injury through proinflammatory mediators and NETs, thereby amplifying immune cell recruitment and tissue damage.\"},{\"question\":\"Why is decay accelerating factor (DAF/CD55) of interest in this study?\",\"answer\":\"DAF/CD55 regulates complement activation on cell membranes, and complement signaling is known to influence neutrophil activation and migration during inflammatory kidney diseases.\"},{\"question\":\"Do changes in DAF expression on neutrophils affect AKI severity in mice?\",\"answer\":\"No. Although DAF expression in infiltrating renal neutrophils changes after AA administration, DAF deletion or overexpression did not change kidney neutrophil infiltration, histological lesions, or BUN levels, indicating DAF on neutrophils does not impact AA-induced AKI severity.\"}]","Neutrophil Expression of Decay Accelerating Factor, a Key Complement Regulator, Has No Impact on Acute Kidney Injury - Research Letter | PDF",1790745038]