SIGNR3‐dependent immune regulation by Lactobacillus acidophilus surface layer protein A in colitis |
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| Authors: | Yaíma L Lightfoot Kurt Selle Tao Yang Yong Jun Goh Bikash Sahay Mojgan Zadeh Jennifer L Owen Natacha Colliou Eric Li Timo Johannssen Bernd Lepenies Todd R Klaenhammer Mansour Mohamadzadeh |
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| Affiliation: | 1. Department of Infectious Diseases and Pathology, University of Florida, Gainesville, FL, USA;2. Division of Gastroenterology, Hepatology & Nutrition, Department of Medicine, University of Florida, Gainesville, FL, USA;3. Department of Food, Bioprocessing and Nutrition Sciences, and Genomic Sciences Program, North Carolina State University, Raleigh, NC, USA;4. Department of Physiological Sciences, College of Veterinary Medicine, University of Florida, Gainesville, FL, USA;5. Division of Infectious Diseases and Global Medicine, Department of Medicine, University of Florida, Gainesville, FL, USA;6. Department of Biomolecular Systems, Max Planck Institute of Colloids and Interfaces, Potsdam, Germany;7. Institute of Chemistry and Biochemistry, Freie Universit?t Berlin, Berlin, Germany |
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| Abstract: | ![]()
Intestinal immune regulatory signals govern gut homeostasis. Breakdown of such regulatory mechanisms may result in inflammatory bowel disease (IBD). Lactobacillus acidophilus contains unique surface layer proteins (Slps), including SlpA, SlpB, SlpX, and lipoteichoic acid (LTA), which interact with pattern recognition receptors to mobilize immune responses. Here, to elucidate the role of SlpA in protective immune regulation, the NCK2187 strain, which solely expresses SlpA, was generated. NCK2187 and its purified SlpA bind to the C-type lectin SIGNR3 to exert regulatory signals that result in mitigation of colitis, maintenance of healthy gastrointestinal microbiota, and protected gut mucosal barrier function. However, such protection was not observed in Signr3−/− mice, suggesting that the SlpA/SIGNR3 interaction plays a key regulatory role in colitis. Our work presents critical insights into SlpA/SIGNR3-induced responses that are integral to the potential development of novel biological therapies for autoinflammatory diseases, including IBD. |
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| Keywords: | colitis immune regulation
Lactobacillus acidophilus
SIGNR3 surface layer protein A |
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