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Erdenebileg Uyangaa,최진영,류형원,오세량,어성국 대한면역학회 2015 Immune Network Vol.15 No.2
Herpes simplex virus (HSV) is a common causative agent of genital ulceration and can lead to subsequent neurological disease in some cases. Here, using a genital infection model, we tested the efficacy of vinegar-processed flos of Daphne genkwa (vp-genkwa) to modulate vaginal inflammation caused by HSV-1 infection. Our data revealed that treatment with optimal doses of vp-genkwa after, but not before, HSV-1 infection provided enhanced resistance against HSV-1 infection, as corroborated by reduced mortality and clinical signs. Consistent with these results, treatment with vp-genkwa after HSV-1 infection reduced viral replication in the vaginal tract. Furthermore, somewhat intriguingly, treatment of vp-genkwa after HSV-1 infection increased the frequency and absolute number of CD3−NK1.1+NKp46+ natural killer (NK) cells producing interferon (IFN)-γ and granyzme B, which indicates that vp-genkwa treatment induces the activation of NK cells. Supportively, secreted IFN-γ was detected at an increased level in vaginal lavages of mice treated with vp-genkwa after HSV-1 infection. These results indicate that enhanced resistance to HSV-1 infection by treatment with vp-genkwa is associated with NK cell activation. Therefore, our data provide a valuable insight into the use of vp-genkwa to control clinical severity in HSV infection through NK cell activation.
Erdenebileg Uyangaa,어성국,이헌구 대한면역학회 2012 Immune Network Vol.12 No.5
Besides their role as building blocks of protein, there are growing evidences that some amino acids have roles in regulating key metabolic pathways that are necessary for maintenance,growth, reproduction, and immunity. Here, we evaluated the modulatory functions of several amino acids in protective immunity against mucosal infection of herpes simplex virus type 1 (HSV-1). We found that glutamine (Gln) and leucine (Leu) showed enhanced protective immunity to HSV-1mucosal infection when two administration of Gln and single administration of Leu per day, but not when administered in combinations. Ameliorated clinical signs of HSV-1 challenged mice by the intraperitoneal administration of Gln and Leu were closely associated with viral burden and IFN-γ production in the vaginal tract at 2 and 4 days post-infection. In addition, the enhanced production of vaginal IFN-γ appeared to be caused by NK and HSV-1 antigen-specific Th1-type CD4+ T cells recruited into vaginal tract of mice treated with Gln and Leu, which indicates that IFN-γ, produced by NK and Th1-type CD4+ T cells, may be critical to control the outcome of diseases caused by HSV-1 mucosal infection. Collectively, our results indicate that intraperitoneal administration of Gln and Leu following HSV-1 mucosal infection could provide beneficial effects for the modulation of protective immunity, but dosage and frequency of administration should be carefully considered, because higher frequency and overdose of Gln and Leu, or their combined treatment,showed detrimental effects to protective immunity. Besides their role as building blocks of protein, there are growing evidences that some amino acids have roles in regulating key metabolic pathways that are necessary for maintenance,growth, reproduction, and immunity. Here, we evaluated the modulatory functions of several amino acids in protective immunity against mucosal infection of herpes simplex virus type 1 (HSV-1). We found that glutamine (Gln) and leucine (Leu) showed enhanced protective immunity to HSV-1mucosal infection when two administration of Gln and single administration of Leu per day, but not when administered in combinations. Ameliorated clinical signs of HSV-1 challenged mice by the intraperitoneal administration of Gln and Leu were closely associated with viral burden and IFN-γ production in the vaginal tract at 2 and 4 days post-infection. In addition, the enhanced production of vaginal IFN-γ appeared to be caused by NK and HSV-1 antigen-specific Th1-type CD4+ T cells recruited into vaginal tract of mice treated with Gln and Leu, which indicates that IFN-γ, produced by NK and Th1-type CD4+ T cells, may be critical to control the outcome of diseases caused by HSV-1 mucosal infection. Collectively, our results indicate that intraperitoneal administration of Gln and Leu following HSV-1 mucosal infection could provide beneficial effects for the modulation of protective immunity, but dosage and frequency of administration should be carefully considered, because higher frequency and overdose of Gln and Leu, or their combined treatment,showed detrimental effects to protective immunity.
Erdenebileg Uyangaa,Ajit Mahadev Patil,어승국 대한면역학회 2014 Immune Network Vol.14 No.4
Herpes simplex virus types 1 and 2 (HSV-1 and HSV-2) are the most common cause of genital ulceration in humans worldwide. Typically, HSV-1 and 2 infections via mucosal route result in a lifelong latent infection after peripheral replication in mucosal tissues, thereby providing potential transmission to neighbor hosts in response to reactivation. To break the transmission cycle, immunoprophylactics and therapeutic strategies must be focused on prevention of infection or reduction of infectivity at mucosal sites. Currently, our understanding of the immune responses against mucosal infection of HSV remains intricate and involves a balance between innate signaling pathways and the adaptive immune responses. Numerous studies have demonstrated that HSV mucosal infection induces type I interferons (IFN) via recognition of Toll-like receptors (TLRs) and activates multiple immune cell populations, including NK cells, conventional dendritic cells (DCs), and plasmacytoid DCs. This innate immune response is required not only for the early control of viral replication at mucosal sites, but also for establishing adaptive immune responses against HSV antigens. Although the contribution of humoral immune response is controversial, CD4+ Th1 T cells producing IFN-γ are believed to play an important role in eradicating virus from the hosts. In addition, the recent experimental successes of immunoprophylactic and therapeutic compounds that enhance resistance and/or reduce viral burden at mucosal sites have accumulated. This review focuses on attempts to modulate innate and adaptive immunity against HSV mucosal infection for the development of prophylactic and therapeutic strategies. Notably, cells involved in innate immune regulations appear to shape adaptive immune responses. Thus, we summarized the current evidence of various immune mediators in response to mucosal HSV infection, focusing on the importance of innate immune responses.
Uyangaa, Erdenebileg,Lee, Hern-Ku,Eo, Seong Kug The Korean Association of Immunobiologists 2012 Immune Network Vol.12 No.5
Besides their role as building blocks of protein, there are growing evidences that some amino acids have roles in regulating key metabolic pathways that are necessary for maintenance, growth, reproduction, and immunity. Here, we evaluated the modulatory functions of several amino acids in protective immunity against mucosal infection of herpes simplex virus type 1 (HSV-1). We found that glutamine (Gln) and leucine (Leu) showed enhanced protective immunity to HSV-1 mucosal infection when two administration of Gln and single administration of Leu per day, but not when administered in combinations. Ameliorated clinical signs of HSV-1 challenged mice by the intraperitoneal administration of Gln and Leu were closely associated with viral burden and IFN-${\gamma}$ production in the vaginal tract at 2 and 4 days post-infection. In addition, the enhanced production of vaginal IFN-${\gamma}$ appeared to be caused by NK and HSV-1 antigen-specific Th1-type CD4+ T cells recruited into vaginal tract of mice treated with Gln and Leu, which indicates that IFN-${\gamma}$, produced by NK and Th1-type CD4+ T cells, may be critical to control the outcome of diseases caused by HSV-1 mucosal infection. Collectively, our results indicate that intraperitoneal administration of Gln and Leu following HSV-1 mucosal infection could provide beneficial effects for the modulation of protective immunity, but dosage and frequency of administration should be carefully considered, because higher frequency and overdose of Gln and Leu, or their combined treatment, showed detrimental effects to protective immunity.
Saruul Erdenebileg,Yang-Ju Son,Myungsuk Kim,Sarangerel Oidovsambuu,Kwang Hyun Cha,Jaeyoung Kwon,Da Seul Jung,Chu Won Nho 한국한의학연구원 2023 Integrative Medicine Research Vol.12 No.4
Background: The root of Saposhnikovia divaricata (Turcz.) Schischk is a well-known traditional medicinal plant, containing various bioactive compounds with anti-inflammatory, antioxidant, and analgesic properties. However, no scientific studies have validated its clinical use as an anti-inflammatory agent against inflammatory bowel disease (IBD). This study aimed to investigate whether the root extract of S. divaricata ameliorates IBD and induces gut microbial alteration, using a RAW 264.7 cell line and a DSS-induced colitis mouse model. Methods: To investigate the anti-inflammatory effects and alleviation of IBD, using a methanol extract of Saposhnikovia divaricata (Turcz.) Schischk. root (MESD), RAW 264.7, murine macrophages and a dextran sodium sulfate (DSS)-induced colitis mouse model were employed. 16S rRNA gene sequencing was conducted to determine the alterations in the gut microbiota of mice with DSS-induced colitis. Results: MESD significantly decreased nitric oxide (NO) and inflammatory cytokine levels in lipopolysaccharide (LPS)-induced RAW 264.7 cells in vitro. Oral administration of MESD reduced the expression of inflammatory cytokines in the colons of mice with DSS-induced colitis. Additionally, MESD inhibited the abundance of Clostridium sensu stricto 1 and enhanced the predicted functional pathways, including l-glutamate degradation VIII (to propanoic acid). Seven compounds with anti-inflammatory properties were isolated from the MESD. Among them, 3′-O-acetylhamaudol and 3′-O-angeloylhamaudol exhibited strong anti-inflammatory effects in vitro. Conclusion: Overall, MESD may be a potential natural product for the treatment of IBD by lowering inflammatory cytokine levels and altering gut microbiota composition.
Otgonchimeg Erdenebileg,조성준(Sung Jun Jo) 중앙대학교 한국인적자원개발전략연구소 2021 역량개발학습연구 Vol.16 No.4
본 연구는 임시직 근로자가 자신의 일에 몰입하는데 영향을 미치는 포용적 리더십의 역할을 연구하였다. 포용적 리더가 근로자의 업무몰입에 미치는 영향은 직원 개개인의 심리적 임파워먼트에 의해 매개되고, 근로자의 고용형태 (정규직 혹은 임시직)에 의해 조절된다는 가설을 세우고 이를 검증하였다. 이러한 연구목적을 달성하기 위해 횡단면적 연구를 시행하였으며, 온라인 기반의 설문 조사 도구를 활용하여 다양한 작업 분야에 종사하는 252명으로부터 표본 데이터를 수집하여 분석에 활용하였다. 분석결과, 포용적 리더십과 근로자의 업무몰입 간에 유의한 정의 관계가 검증되었으며, 포용적 리더십과 심리적 임파워먼트, 그리고 심리적 임파워먼트와 업무몰입 간에도 유의한 정의 관계가 발견되어, 심리적 임파워먼트의 부분적 매개효과가 확인되었다. 고용형태는 포용적 리더십이 심리적 임파워먼트와 업무몰입에 미치는 정의 효과를 조절하였는데, 포용적 리더십의 효과는 비정규직 근로자에게 더욱 강하게 나타났다. 이러한 연구결과는 변화의 속도가 빠르고, 경쟁이 치열한 환경에서 리더는 포용적 태도로 직원들이 보다 책임감 있는 자세로 업무를 수행하며, 참여감을 높여야 함을 시사한다. 유연한 고용관계가 더욱 확산되고 있는 오늘날 포용적 리더십의 역할은 더욱 강조되어야 할 필요가 있다. This study aimed to explore the associations between individual employees’ perception of inclusive leadership (IL) and employee work engagement (EWE) with a mediating effect of individual employees’ perception of psychological empowerment (PE) and a moderating role of employment status (permanent vs. temporary). The cross-sectional study utilized online-based survey tools to distribute to employees in a variety of working fields. Out of received 256 responses of the employees, 252 responses were found to be useful for analysis. Significant and positive relationships were found between IL and PE, PE and EWE, IL and EWE. The relationship between IL and EWE was partially mediated by PE and employment status moderated relationships between IL and PE, and IL and EWE. The positive effect of IL was stronger for temporary employees. The paper contributes both to the body of literature and managerial practice. In order to be successful in an agile, highly competitive environment, managers should recognize that they could encourage their employees to be engaged in their work through inclusive approaches. The paper found IL could be one of the effective ways of boosting employees’ EWE by utilizing PE.
Uyangaa, Erdenebileg,Kim, Jin Hyoung,Patil, Ajit Mahadev,Choi, Jin Young,Kim, Seong Bum,Eo, Seong Kug Public Library of Science 2015 PLoS pathogens Vol.11 No.11
<▼1><P>Type I interferon (IFN-I)-dependent orchestrated mobilization of innate cells in inflamed tissues is believed to play a critical role in controlling replication and CNS-invasion of herpes simplex virus (HSV). However, the crucial regulators and cell populations that are affected by IFN-I to establish the early environment of innate cells in HSV-infected mucosal tissues are largely unknown. Here, we found that IFN-I signaling promoted the differentiation of CCL2-producing Ly-6C<SUP>hi</SUP> monocytes and IFN-γ/granzyme B-producing NK cells, whereas deficiency of IFN-I signaling induced Ly-6C<SUP>lo</SUP> monocytes producing CXCL1 and CXCL2. More interestingly, recruitment of Ly-6C<SUP>hi</SUP> monocytes preceded that of NK cells with the levels peaked at 24 h post-infection in IFN-I–dependent manner, which was kinetically associated with the CCL2-CCL3 cascade response. Early Ly-6C<SUP>hi</SUP> monocyte recruitment was governed by CCL2 produced from hematopoietic stem cell (HSC)-derived leukocytes, whereas NK cell recruitment predominantly depended on CC chemokines produced by resident epithelial cells. Also, IFN-I signaling in HSC-derived leukocytes appeared to suppress Ly-6G<SUP>hi</SUP> neutrophil recruitment to ameliorate immunopathology. Finally, tissue resident CD11b<SUP>hi</SUP>F4/80<SUP>hi</SUP> macrophages and CD11c<SUP>hi</SUP>EpCAM<SUP>+</SUP> dendritic cells appeared to produce initial CCL2 for migration-based self-amplification of early infiltrated Ly-6C<SUP>hi</SUP> monocytes upon stimulation by IFN-I produced from infected epithelial cells. Ultimately, these results decipher a detailed IFN-I–dependent pathway that establishes orchestrated mobilization of Ly-6C<SUP>hi</SUP> monocytes and NK cells through CCL2-CCL3 cascade response of HSC-derived leukocytes and epithelium-resident cells. Therefore, this cascade response of resident–to-hematopoietic–to-resident cells that drives cytokine–to-chemokine–to-cytokine production to recruit orchestrated innate cells is critical for attenuation of HSV replication in inflamed tissues.</P></▼1><▼2><P><B>Author Summary</B></P><P>Herpes simplex virus type 1 and 2 (HSV-1 and HSV-2) are the most common cause of genital ulceration in humans worldwide with lifelong latent infection after peripheral replication in mucosal tissues. Furthermore, acquisition of human immunodeficiency virus (HIV) is increased in HSV-infected individuals, underscoring the contribution of this virus in facilitating increased susceptibility to other microbial pathogens. Therefore, it is imperative to characterize the host defense to HSV infection and identify key components that regulate virus resistance, in order to devise therapeutic strategy. Although type I interferon (IFN-I)-dependent orchestrated mobilization of innate cells in inflamed tissues is considered a key player to control replication and CNS-invasion of HSV, the regulators and cell population that are affected by IFN-I to establish the orchestrated environment of innate cells in HSV-infected tissues are largely unknown. In the present study, we demonstrate that IFN-I signal governs the sequential recruitment of Ly-6C<SUP>hi</SUP> monocytes and then NK cells into mucosal tissues, depending on CCL2-CCL3 cascade mediated by HSC-derived leukocytes and epithelial resident cells, respectively. Also, tissue resident CD11b<SUP>hi</SUP>F4/80<SUP>hi</SUP> macrophages and CD11c<SUP>hi</SUP>EpCAM<SUP>+</SUP> dendritic cells were involved in producing the initial CCL2 for migration-based self-amplification of rapidly infiltrated Ly-6C<SUP>hi</SUP> monocytes through stimulation by IFN-I produced from infected epithelial cells. This study deciphers detailed IFN-I-dependent pathway that establishes orchestrated mobilization of Ly-6C<SUP>hi</SUP> monocytes and NK cells through CCL2-CCL3 cascade.</P></▼2>
Uyangaa, Erdenebileg,Patil, Ajit Mahadev,Eo, Seong Kug The Korean Association of Immunobiologists 2014 Immune Network Vol.14 No.4
Herpes simplex virus types 1 and 2 (HSV-1 and HSV-2) are the most common cause of genital ulceration in humans worldwide. Typically, HSV-1 and 2 infections via mucosal route result in a lifelong latent infection after peripheral replication in mucosal tissues, thereby providing potential transmission to neighbor hosts in response to reactivation. To break the transmission cycle, immunoprophylactics and therapeutic strategies must be focused on prevention of infection or reduction of infectivity at mucosal sites. Currently, our understanding of the immune responses against mucosal infection of HSV remains intricate and involves a balance between innate signaling pathways and the adaptive immune responses. Numerous studies have demonstrated that HSV mucosal infection induces type I interferons (IFN) via recognition of Toll-like receptors (TLRs) and activates multiple immune cell populations, including NK cells, conventional dendritic cells (DCs), and plasmacytoid DCs. This innate immune response is required not only for the early control of viral replication at mucosal sites, but also for establishing adaptive immune responses against HSV antigens. Although the contribution of humoral immune response is controversial, $CD4^+$ Th1 T cells producing IFN-${\gamma}$ are believed to play an important role in eradicating virus from the hosts. In addition, the recent experimental successes of immunoprophylactic and therapeutic compounds that enhance resistance and/or reduce viral burden at mucosal sites have accumulated. This review focuses on attempts to modulate innate and adaptive immunity against HSV mucosal infection for the development of prophylactic and therapeutic strategies. Notably, cells involved in innate immune regulations appear to shape adaptive immune responses. Thus, we summarized the current evidence of various immune mediators in response to mucosal HSV infection, focusing on the importance of innate immune responses.
Uyangaa, Erdenebileg,Choi, Jin Young,Ryu, Hyung Won,Oh, Sei-Ryang,Eo, Seong Kug The Korean Association of Immunobiologists 2015 Immune Network Vol.15 No.2
Herpes simplex virus (HSV) is a common causative agent of genital ulceration and can lead to subsequent neurological disease in some cases. Here, using a genital infection model, we tested the efficacy of vinegar-processed flos of Daphne genkwa (vp-genkwa) to modulate vaginal inflammation caused by HSV-1 infection. Our data revealed that treatment with optimal doses of vp-genkwa after, but not before, HSV-1 infection provided enhanced resistance against HSV-1 infection, as corroborated by reduced mortality and clinical signs. Consistent with these results, treatment with vp-genkwa after HSV-1 infection reduced viral replication in the vaginal tract. Furthermore, somewhat intriguingly, treatment of vp-genkwa after HSV-1 infection increased the frequency and absolute number of $CD3^-NK1.1^+NKp46^+$ natural killer (NK) cells producing interferon (IFN)-${\gamma}$ and granyzme B, which indicates that vp-genkwa treatment induces the activation of NK cells. Supportively, secreted IFN-${\gamma}$ was detected at an increased level in vaginal lavages of mice treated with vp-genkwa after HSV-1 infection. These results indicate that enhanced resistance to HSV-1 infection by treatment with vp-genkwa is associated with NK cell activation. Therefore, our data provide a valuable insight into the use of vp-genkwa to control clinical severity in HSV infection through NK cell activation.