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[E. Immunology] E-12



                Ginsenoside Rg1 protects polymorphonuclear neutrophils


                 from suppression of immune function by mitochondrial


                              damage-associated molecular patterns




                                   #
         Mina Boo¹ , Hyo In Kim² , Woo Yong Park³, Gahee Song³, Ja Yeon Park³, Se Jin Jung³, Minji Choi¹,
                    #
                                 Jae-Young Um³,⁴, Hyun Jeong Kwak¹*, Jinbong Park³,⁴*

        ¹Department of Life Science, College of Natural Sciences, Kyonggi University, Suwon 16227, Korea, ²Department of

          Surgery, Beth Israel Deaconess Medical Center / Harvard Medical School, Boston 02215, USA, ³Department of
             Science in Korean Medicine, Graduate School, Kyung Hee University, Seoul 02447, Korea, ⁴Department of

         Pharmacology and Basic Research Laboratory for Comorbidity Research, College of Korean Medicine, Kyung Hee
                                               University, Seoul 02447, Korea




        Traumatic injuries affect the host immune system and thus increase the susceptibility to pneumonia. Nosocomial

        pneumonia is the most common cause of mortality in patients who survive their initial trauma. The underlying
        mechanisms  that  link  traumatic  injury  to  nosocomial  infection  remain  unclear,  but  reduced  polymorphonuclear

        neutrophil (PMN) function by mitochondrial damage-associated molecular patterns (mtDAMPs) is known to play a
        key role. Ginsenoside Rg1 (Rg1) is a saponin found in Panax ginseng which is well-known by its anti-inflammatory

        effect. We assayed the effects of Rg1 on PMN functions after exposure to an mtDAMP (the n-formyl peptide ND6)
        to mimic a post-traumatic environment. The respiratory burst, formation of neutrophil extracellular traps (NETs) and

        chemotaxis were studied. Interaction of PMN-FPR1 with mtDAMPs induced suppression of respiratory burst, NET
        formation  and  chemotactic  function  in  response  to  chemokines.  However,  ND6-suppressed  PMN  function  was

        restored by pre-treatment of Rg1. Post-treatment of Rg1, following exposure to ND6, did not restore chemotaxis
        but rescued PMN from suppression of respiratory burst and NET formation. Our study demonstrated that, in contrast

        to the previous literature, Rg1 can enhance the responses of PMN when subjected to mtDAMPs and lose proper
        immune functions.
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