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The complement system is mainly liver-derived and serum-operative, yet complement-mediated defense at mucosal surfaces is increasingly recognized. Focusing on Complement Factor B (CFB), the alternative pathway’s constitutively active amplifier, the study shows that human colonic CFB is increased in active inflammatory bowel disease. Mouse models lacking circulating but retaining gut CFB reveal that locally synthesized CFB protects against colitis. Single-cell and cell-specific deletions identify epithelial and stromal sources, supported by pharmacologic inhibition.",{"@graph":69,"@context":123},[70,84,106],{"@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/mucosally-sourced-complement-factor-b-modulates-the-host-response-to-colitis/451610/",{"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/mucosally-sourced-complement-factor-b-modulates-the-host-response-to-colitis/451610.png","ImageObject",300,407,{"name":92,"@type":93},"supergirl","Person",{"url":74,"name":95,"@type":96},"DocShare","Organization","application/pdf","2026-11-10","2026-09-30",true,{"@type":102,"interactionType":103,"userInteractionCount":105},"InteractionCounter",{"@type":104},"ViewAction",11,{"@type":107,"mainEntity":108},"FAQPage",[109,115,119],{"name":110,"@type":111,"acceptedAnswer":112},"What role does Complement Factor B (CFB) play in the intestine?","Question",{"text":113,"@type":114},"CFB is part of the alternative complement pathway and is shown to be produced in the human colon. Locally synthesized CFB mitigates colitis by functioning as a locally regulated mucosal defense system.","Answer",{"name":116,"@type":111,"acceptedAnswer":117},"How were the local versus liver-derived sources of CFB studied?",{"text":118,"@type":114},"The study used mouse models that lack circulating, liver-derived CFB while retaining intact CFB expression in the gut. In comparison with global CFB deficiency, liver-specific knockout mice were more resistant to colitis.",{"name":120,"@type":111,"acceptedAnswer":121},"Which gut cell types contribute to CFB production?",{"text":122,"@type":114},"Single-cell analyses identify enterocytes and fibroblasts as key CFB producers in the gut, and compartment-specific CFB deletion from epithelial or stromal cells removes mucosal protection.","https://schema.org",{"og:url":83,"og:type":125,"og:title":65,"og:site_name":95,"og:description":67},"article",{"robots":127,"canonical":83},"index,follow",{"doc_id":129,"site_id":62},451610,1791149957,{"code":4,"msg":5,"data":132},{"doc_id":129,"user_id":133,"nickname":92,"user_avatar":134,"doc_module":4,"category_id":34,"category_name":35,"doc_title":65,"doc_description":67,"doc_content":135,"file_id":136,"file_url":137,"file_type":138,"file_size":139,"view_count":105,"is_deleted":4,"is_public":8,"is_downloadable":8,"audit_status":8,"page_count":140,"language":141,"language_code":63,"site_id":62,"html_lang":63,"table_of_contents":142,"faqs":143,"seo_title":144,"seo_description":67,"update_tm":145,"read_time":146,"preview_page_count":4},962088121634,"https://ap-avatar.wpscdn.com/davatar_9964176cb1d06d4a9deccf72a44ae3dc","bioRxiv preprint doi: [https://doi.org/10.64898/2025.12.31.697141](https://doi.org/10.64898/2025.12.31.697141); this version posted January 1, 2026. The copyright holder for this preprint (which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is made  \navailable under aCC-BY-NC-ND 4.0 International license.  \n1 Title: Mucosally sourced complement factor B modulates the host response to colitis. 2  \n3  \n4 Authors: Aayusha Thapa1* , Aasritha Nallapu1* , Nnenna Mougboh 1 , Swathi Nedunchezian 1 , 5 Khushi Talati5 , Brian Yang1 , Jungheun Hyun1 , John Michael Sanchez1 , Christopher S. Seet1,2 , 6 Hon Wai Koon1 , Zhaoping Li,1,3,4 Matthew A. Ciorba5 , Kathrin Michelsen6 , Hrishikesh. S.  \n7 Kulkarni1,2 \\# and Devesha H. Kulkarni 1,2,3\\# 8  \n9  \n10 Affiliations:  \n11 1 Department of Medicine, David Geffen School of Medicine at the University of California-Los  \n12 Angeles, Los Angeles, CA, USA.  \n13  \n14 2Jonsson Comprehensive Cancer Center (JCCC), David Geffen School of Medicine, University of  \n15 California, Los Angeles, Los Angeles, CA 90095, 16  \n17 3Center for Human Nutrition, David Geffen School of Medicine, Department of Medicine, 18 University of California, Los Angeles, Los Angeles, CA 90095, USA.  \n19  \n20 4 Department of Medicine, VA Greater Los Angeles HealthCare System, Los Angeles, CA 90073,  \n21 USA.  \n22  \n23 5 Department of Medicine, Washington University School of Medicine, St. Louis, MO, USA. 24  \n25 6 F. Widjaja Inflammatory Bowel Disease Institute (IBDI), Departments of Medicine and Biomedical  \n26 Sciences, Cedars-Sinai Medical Center, Los Angeles, CA, USA.  \n27  \n28 * these authors have equal contribution 29  \n30  \n31 \\# Corresponding Authors: 32  \n33 Hrishikesh S. Kulkarni, MD, MSCI  \n34 Division of Pulmonary, Critical Care and Sleep Medicine,  \n35 David Geffen School of Medicine, 36 University of California, Los Angeles, 37 Los Angeles, CA 90095  \n38 Email: [hskulkarni@mednet.ucla.edu](hskulkarni@mednet.ucla.edu)  \n39  \n40 Devesha Kulkarni, PhD  \n41 Division of Clinical Nutrition, Department of Medicine,  \n42 David Geffen School of Medicine, 43 University of California, Los Angeles, 44 Los Angeles, CA 90095  \n45 [Email:](Email: DHKulkarni@mednet.ucla.edu)[ ](Email: DHKulkarni@mednet.ucla.edu)[DHKulkarni@mednet.ucla.edu](Email: DHKulkarni@mednet.ucla.edu)[ ](Email: DHKulkarni@mednet.ucla.edu)46  \n47  \n48  \n49 Conflict of interest statement: The authors have declared that no conflict of interest exists. 50  \n51  \nbioRxiv preprint doi: [https://doi.org/10.64898/2025.12.31.697141](https://doi.org/10.64898/2025.12.31.697141); this version posted January 1, 2026. The copyright holder for this preprint (which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is made  \navailable under aCC-BY-NC-ND 4.0 International license.  \n1 ABSTRACT  \n2 Distinct host factors maintain intestinal homeostasis but are incompletely understood. The  \n3 complement system is primarily liver-derived and serum-operative. However, there is growing  \n4 recognition for complement-mediated host defense at mucosal surfaces. The alternative pathway, 5 which is constitutively active at low levels and amplifies complement activation independent of  \n6 antibodies, requires Complement Factor B (CFB) . Despite its evolutionary conservation, the  \n7 spatial, cellular, and functional roles of CFB in the intestine are poorly understood. Here, we show  \n8 that CFB is produced in the human colon and is increased in patients with active inflammatory  \n9 bowel disease. To isolate the role of local CFB in mucosal responses, we interrogated a mouse  \n10 strain that has no circulating, liver-derived CFB but retains intact CFB expression in the gut. Global  \n11 CFB-deficient mice succumb to colitis compared to these liver-specific knockout mice, suggesting  \n12 that locally synthesized CFB mitiga","cbCais4I176TNNIm","https://ap.wps.com/l/cbCais4I176TNNIm","pdf",6463846,35,"English","# Abstract\n## Brief Summary\n# Introduction","[{\"question\":\"What role does Complement Factor B (CFB) play in the intestine?\",\"answer\":\"CFB is part of the alternative complement pathway and is shown to be produced in the human colon. Locally synthesized CFB mitigates colitis by functioning as a locally regulated mucosal defense system.\"},{\"question\":\"How were the local versus liver-derived sources of CFB studied?\",\"answer\":\"The study used mouse models that lack circulating, liver-derived CFB while retaining intact CFB expression in the gut. In comparison with global CFB deficiency, liver-specific knockout mice were more resistant to colitis.\"},{\"question\":\"Which gut cell types contribute to CFB production?\",\"answer\":\"Single-cell analyses identify enterocytes and fibroblasts as key CFB producers in the gut, and compartment-specific CFB deletion from epithelial or stromal cells removes mucosal protection.\"}]","Mucosally sourced complement factor B modulates the host response to colitis | PDF",1790735527,88]