Jun Guo
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Previous Organizations / Institutes
The organizations / institutes from the scholar's other articles in the past ten years
Research Subjects
Jun Guo has a total of 219 co-authors. Here are the top co-authors by number of shared publications:
Hongzeng Li
Department of Neurology Tangdu Hospital The Fourth Military Medical University Xi'an China
16 shared publicationsKaixi Ren
Department of Neurology Tangdu Hospital The Fourth Military Medical University Xi'an China
15 shared publicationsDaidi Zhao
Department of Neurology, Tangdu Hospital, The Fourth Military Medical University, Xi’an, China
13 shared publicationsJiaqi Ding
Department of Neurology, Tangdu Hospital, Fourth Military Medical University, Xi'an, China
10 shared publicationsJiarui Lu
Department of Neurology, Tangdu Hospital, Air Force Medical University, Xi'an, 710038, China
9 shared publicationsCong Zhao
Department of Neurology, Air Force Medical Center of PLA, Beijing, 100142, China
8 shared publications
Latest Publications
- Open Access
- 15 October 2026
- Published by Wiley in Advanced Science
- p. e78358
Gut Microbiota‐Derived Indole‐3‐Acetaldehyde Contributes to the Disease‐Alleviating Effects of Kurarinone in Experimental Autoimmune Encephalomyelitis
Multiple sclerosis (MS) is a central nervous system autoimmune disease primarily driven by Th1 and Th17 cells, whose onset and progression are closely associated with gut microbiota. Kurarinone (KU), an active component from Radix Sophora Flavescens , exhibits anti‐inflammatory, immunoregulatory and gut microbiota‐modulating properties. However, whether KU alleviates MS severity via a gut microbiota‐mediated mechanism remains unclear. Here, we demonstrate that KU ameliorates experimental autoimmune encephalomyelitis (EAE)‐an animal model of MS‐by modulating the gut microbiota, particularly via enriching Akkermansia muciniphila , and A. muciniphila is essential for the protective effects of KU in EAE. Furthermore, KU elevates levels of the tryptophan metabolite indole‐3‐acetaldehyde (IAAld). IAAld levels are positively correlated with the relative abundance of A. muciniphila and negatively correlated with EAE severity. In vitro, A. muciniphila alone is sufficient to facilitate tryptophan metabolism to produce IAAld. IAAld treatment ameliorates EAE and reduces the frequencies of pathogenic Th1 and Th17 cells in mice. Mechanistically, IAAld activates the aryl hydrocarbon receptor (AhR) and suppresses JAK/STAT signaling, thereby dampening Th1 and Th17 differentiation; these effects are abolished following AhR blockade. Collectively, this study identifies a novel mechanism by which KU mitigates EAE via the gut metabolite IAAld‐AhR‐immune axis and unveils potential therapeutic targets for MS.
- 15 October 2026
- Published by Wiley in Advanced Science
- p. e78358
Open AccessGut Microbiota‐Derived Indole‐3‐Acetaldehyde Contributes to the Disease‐Alleviating Effects of Kurarinone in Experimental Autoimmune Encephalomyelitis
Multiple sclerosis (MS) is a central nervous system autoimmune disease primarily driven by Th1 and Th17 cells, whose onset and progression are closely associated with gut microbiota. Kurarinone (KU), an active component from Radix Sophora Flavescens , exhibits anti‐inflammatory, immunoregulatory and gut microbiota‐modulating properties. However, whether KU alleviates MS severity via a gut microbiota‐mediated mechanism remains unclear. Here, we demonstrate that KU ameliorates experimental autoimmune encephalomyelitis (EAE)‐an animal model of MS‐by modulating the gut microbiota, particularly via enriching Akkermansia muciniphila , and A. muciniphila is essential for the protective effects of KU in EAE. Furthermore, KU elevates levels of the tryptophan metabolite indole‐3‐acetaldehyde (IAAld). IAAld levels are positively correlated with the relative abundance of A. muciniphila and negatively correlated with EAE severity. In vitro, A. muciniphila alone is sufficient to facilitate tryptophan metabolism to produce IAAld. IAAld treatment ameliorates EAE and reduces the frequencies of pathogenic Th1 and Th17 cells in mice. Mechanistically, IAAld activates the aryl hydrocarbon receptor (AhR) and suppresses JAK/STAT signaling, thereby dampening Th1 and Th17 differentiation; these effects are abolished following AhR blockade. Collectively, this study identifies a novel mechanism by which KU mitigates EAE via the gut metabolite IAAld‐AhR‐immune axis and unveils potential therapeutic targets for MS.
- Open Access
- 9 July 2026
- Published by Springer Nature in Journal of Neuroinflammation
- Vol. 23 (1)
Neutrophil extracellular traps exacerbate blood-brain barrier disruption in neuromyelitis optica spectrum disorder
Neuromyelitis optica spectrum disorder (NMOSD) is an autoimmune inflammatory disease of the central nervous system (CNS) characterized by recurrent optic n
- 9 July 2026
- Published by Springer Nature in Journal of Neuroinflammation
- Vol. 23 (1)
Open AccessNeutrophil extracellular traps exacerbate blood-brain barrier disruption in neuromyelitis optica spectrum disorder
Neuromyelitis optica spectrum disorder (NMOSD) is an autoimmune inflammatory disease of the central nervous system (CNS) characterized by recurrent optic n
- Open Access
- 23 June 2026
- Published by Wiley in Annals of Clinical and Translational Neurology
Clinical and Modifiable Factors Associated With Disability and Relapse in MOGAD : A Multicentre Cohort Study
Background: Factors associated with relapse course and disability in myelin oligodendrocyte glycoprotein antibody‐associated disease (MOGAD) remain incompletely understood. Objectives: To identify clinical and modifiable factors associated with relapse and disability in MOGAD. Methods: In this ambispective multicentre cohort study using data from the Chinese Neuroimmunological Diseases (NIDBase) cohort (21 Chinese centres; January 2020–December 2024), 173 MOGAD patients with ≥ 12‐month follow‐up were analysed. Time to first relapse and time to disability, defined as Expanded Disability Status Scale (EDSS) score ≥ 2 confirmed outside acute relapse periods, were analysed using Cox regression. Nonlinear associations were assessed using restricted cubic splines. Results: Older age at onset and smoking history were associated with increased disability risk. Smoking was also associated with relapse risk, although its association was attenuated and no longer statistically significant after adjustment. BMI showed nonlinear associations with both relapse and disability outcomes. Conclusions: In MOGAD, older age at onset, smoking, and BMI may influence prognosis. These findings support further investigation of modifiable lifestyle and metabolic factors in prognostic stratification.
- 23 June 2026
- Published by Wiley in Annals of Clinical and Translational Neurology
Open AccessClinical and Modifiable Factors Associated With Disability and Relapse in MOGAD : A Multicentre Cohort Study
Background: Factors associated with relapse course and disability in myelin oligodendrocyte glycoprotein antibody‐associated disease (MOGAD) remain incompletely understood. Objectives: To identify clinical and modifiable factors associated with relapse and disability in MOGAD. Methods: In this ambispective multicentre cohort study using data from the Chinese Neuroimmunological Diseases (NIDBase) cohort (21 Chinese centres; January 2020–December 2024), 173 MOGAD patients with ≥ 12‐month follow‐up were analysed. Time to first relapse and time to disability, defined as Expanded Disability Status Scale (EDSS) score ≥ 2 confirmed outside acute relapse periods, were analysed using Cox regression. Nonlinear associations were assessed using restricted cubic splines. Results: Older age at onset and smoking history were associated with increased disability risk. Smoking was also associated with relapse risk, although its association was attenuated and no longer statistically significant after adjustment. BMI showed nonlinear associations with both relapse and disability outcomes. Conclusions: In MOGAD, older age at onset, smoking, and BMI may influence prognosis. These findings support further investigation of modifiable lifestyle and metabolic factors in prognostic stratification.
- 17 February 2026
- Published by Elsevier in Clinical Immunology
- Vol. 284, 110682
Polymorphonuclear myeloid-derived suppressor cells inhibit natural killer cell function in neuromyelitis optica spectrum disorder via the CD155-TIGIT axis
- 17 February 2026
- Published by Elsevier in Clinical Immunology
- Vol. 284, 110682
Polymorphonuclear myeloid-derived suppressor cells inhibit natural killer cell function in neuromyelitis optica spectrum disorder via the CD155-TIGIT axis
- 1 February 2026
- Vol. 42 (2) , 159-163
[Research progress on the role of myeloid-derived suppressor cells in multiple sclerosis].
Myeloid-derived suppressor cells (MDSCs) are a heterogeneous group of cells composed of myeloid progenitor cells, immature granulocytes, monocytes, and dendritic cells. These cells were initially discovered in cancer research and have been confirmed to show immunosuppressive functions. In recent years, their role in autoimmune diseases has attracted more attention. Multiple sclerosis (MS) is a rare autoimmune disease of the central nervous system, which can lead to non-traumatic disability among young adults. However, the exact pathogenesis is still unclear, and there is no therapy to cure MS. Studies have shown that MDSCs can play an important immunomodulatory role in MS and experimental autoimmune encephalomyelitis (EAE) model through multiple pathways. This article reviews the origin and characteristics of MDSCs and their role in MS/EAE, with the aim of proposing new strategies for investigating the pathogenesis and treatment of MS.
- 1 February 2026
- Vol. 42 (2) , 159-163
[Research progress on the role of myeloid-derived suppressor cells in multiple sclerosis].
Myeloid-derived suppressor cells (MDSCs) are a heterogeneous group of cells composed of myeloid progenitor cells, immature granulocytes, monocytes, and dendritic cells. These cells were initially discovered in cancer research and have been confirmed to show immunosuppressive functions. In recent years, their role in autoimmune diseases has attracted more attention. Multiple sclerosis (MS) is a rare autoimmune disease of the central nervous system, which can lead to non-traumatic disability among young adults. However, the exact pathogenesis is still unclear, and there is no therapy to cure MS. Studies have shown that MDSCs can play an important immunomodulatory role in MS and experimental autoimmune encephalomyelitis (EAE) model through multiple pathways. This article reviews the origin and characteristics of MDSCs and their role in MS/EAE, with the aim of proposing new strategies for investigating the pathogenesis and treatment of MS.
- 3 December 2025
- Published by Elsevier in Multiple Sclerosis and Related Disorders
- Vol. 107, 106896
Dynamics of plasma fibrinogen unveils hepatic initiating role in the pathogenesis of multiple sclerosis
- 3 December 2025
- Published by Elsevier in Multiple Sclerosis and Related Disorders
- Vol. 107, 106896
Dynamics of plasma fibrinogen unveils hepatic initiating role in the pathogenesis of multiple sclerosis
- Open Access
- 23 May 2025
- Published by Springer Nature in Orphanet Journal of Rare Diseases
- Vol. 20 (1) , 1-9
Long-term efficacy and safety of low-dose rituximab strategy in neuromyelitis optica spectrum disorder: a retrospective cohort study on treatment compliance and clinical outcomes
Objective: To evaluate the efficacy and safety of low-dose rituximab (RTX) strategy in patients with neuromyelitis optica spectrum disorder (NMOSD) over a period exceeding 5 years and to investigate the impact of treatment compliance on clinical outcomes. Methods: We conducted a retrospective analysis of 81 NMOSD patients who received low-dose RTX at Tangdu Hospital from January 2014 to December 2019. The treatment protocol involved an induction phase of 100 mg weekly for three weeks, followed by maintenance doses of 100 mg every six months. Demographic characteristics, the expanded disability status scale (EDSS) scores, annualized relapse rates (ARR), number and date of attacks, and adverse events were collected. The influence of compliance on treatment efficacy was assessed using multivariable Cox regression and propensity score-weighted analysis. Results: Over the follow-up period, 32.1% of patients experienced relapses, with the ARR significantly reduced from a median of 1.5 before treatment to 0 after RTX therapy (p < 0.001). EDSS scores improved significantly from a median of 3.5 to 1.5 (p < 0.001). The relapse rate was significantly lower in the good compliance group compared to the poor compliance group (9.5% vs. 56.4%, p < 0.001), and good compliance was associated with a reduced risk of relapse (HR 0.07; 95% CI 0.02–0.25, p < 0.001). A total of 19 patients (23.5%) experienced mild adverse events, with no serious adverse events reported. Conclusion: Our findings support the long-term efficacy and safety of low-dose RTX strategy in treating NMOSD, highlighting the crucial role of treatment compliance in achieving favorable clinical outcomes.
- 23 May 2025
- Published by Springer Nature in Orphanet Journal of Rare Diseases
- Vol. 20 (1) , 1-9
Open AccessLong-term efficacy and safety of low-dose rituximab strategy in neuromyelitis optica spectrum disorder: a retrospective cohort study on treatment compliance and clinical outcomes
Objective: To evaluate the efficacy and safety of low-dose rituximab (RTX) strategy in patients with neuromyelitis optica spectrum disorder (NMOSD) over a period exceeding 5 years and to investigate the impact of treatment compliance on clinical outcomes. Methods: We conducted a retrospective analysis of 81 NMOSD patients who received low-dose RTX at Tangdu Hospital from January 2014 to December 2019. The treatment protocol involved an induction phase of 100 mg weekly for three weeks, followed by maintenance doses of 100 mg every six months. Demographic characteristics, the expanded disability status scale (EDSS) scores, annualized relapse rates (ARR), number and date of attacks, and adverse events were collected. The influence of compliance on treatment efficacy was assessed using multivariable Cox regression and propensity score-weighted analysis. Results: Over the follow-up period, 32.1% of patients experienced relapses, with the ARR significantly reduced from a median of 1.5 before treatment to 0 after RTX therapy (p < 0.001). EDSS scores improved significantly from a median of 3.5 to 1.5 (p < 0.001). The relapse rate was significantly lower in the good compliance group compared to the poor compliance group (9.5% vs. 56.4%, p < 0.001), and good compliance was associated with a reduced risk of relapse (HR 0.07; 95% CI 0.02–0.25, p < 0.001). A total of 19 patients (23.5%) experienced mild adverse events, with no serious adverse events reported. Conclusion: Our findings support the long-term efficacy and safety of low-dose RTX strategy in treating NMOSD, highlighting the crucial role of treatment compliance in achieving favorable clinical outcomes.
- Open Access
- 15 May 2025
- Published by Frontiers Media SA in Frontiers in Immunology
- Vol. 16, 1536740
Case Report: Anti-NMDAR encephalitis associated with neurobrucellosis: causality or coexistence?
Human brucellosis, caused by Brucella, is an infectious disease with specific endemic regions, especially in pastoral areas, and may affect multiple organ systems. Neurological involvement, namely neurobrucellosis, occurs in very few of these patients. Anti-N-methyl-D-aspartate receptor (NMDAR) encephalitis is the most frequent type of autoimmune encephalitis and is usually associated with tumors or herpes simplex virus infections. However, the link between the two disease entities is unknown. In this report, we present a rare case of a 29-year-old Chinese man with anti-NMDAR encephalitis associated with neurobrucellosis, with the detection of anti-NMDAR antibodies by cell-based assay and Brucella melitensis by metagenomic next-generation sequencing in his cerebrospinal fluid sample. The patient improved after antimicrobial treatment and immunotherapies, including steroids and intravenous immunoglobulin. This case implicates Brucella infection as a possible trigger for the production of anti-NMDAR antibodies, and prospective studies should reveal whether there is a casual relationship between brucellosis and anti-NMDAR antibodies.
- 15 May 2025
- Published by Frontiers Media SA in Frontiers in Immunology
- Vol. 16, 1536740
Open AccessCase Report: Anti-NMDAR encephalitis associated with neurobrucellosis: causality or coexistence?
Human brucellosis, caused by Brucella, is an infectious disease with specific endemic regions, especially in pastoral areas, and may affect multiple organ systems. Neurological involvement, namely neurobrucellosis, occurs in very few of these patients. Anti-N-methyl-D-aspartate receptor (NMDAR) encephalitis is the most frequent type of autoimmune encephalitis and is usually associated with tumors or herpes simplex virus infections. However, the link between the two disease entities is unknown. In this report, we present a rare case of a 29-year-old Chinese man with anti-NMDAR encephalitis associated with neurobrucellosis, with the detection of anti-NMDAR antibodies by cell-based assay and Brucella melitensis by metagenomic next-generation sequencing in his cerebrospinal fluid sample. The patient improved after antimicrobial treatment and immunotherapies, including steroids and intravenous immunoglobulin. This case implicates Brucella infection as a possible trigger for the production of anti-NMDAR antibodies, and prospective studies should reveal whether there is a casual relationship between brucellosis and anti-NMDAR antibodies.
- Open Access
- 22 November 2024
- Published by Frontiers Media SA in Frontiers in Nutrition
- Vol. 11, 1471981
Association between composite dietary antioxidant index and cognitive function impairment among the US older adults: a cross-sectional study based on the NHANES 2011–2014
Background: Cognitive function impairment (CFI) and the Composite Dietary Antioxidant Index (CDAI) were investigated in this study.Methods: Participants from the 2011–2014 cycles of the National Health and Nutrition Examination Survey were chosen to assess cognitive function using the Consortium to Establish a Registry for Alzheimer’s Disease Word Learning Test, the Animal Fluency Test, and the Digit Symbol Substitution Test. Participants scored below the 25% percentile of any of the three tests were defined as having cognitive function impairment. 24-h recalls of diet were collected to calculate CDAI.Results: 2,424 participants were included. The fully adjusted multivariate logistic regression model showed an increase of one CDAI unit reduced CFI risk by 5% (95% CI: 0.92 ~ 0.98, p = 0.004). When comparing individuals with the lowest CDAI in the first quartile (<−2.42), the adjusted odds ratio for CDAI and CFI were 0.81 (95% CI: 0.61 ~ 1.06, p = 0.125) in the second quartile, 0.69 (95% CI: 0.51 ~ 0.92, p = 0.012) in the third quartile, and 0.59 (95% CI: 0.43 ~ 0.82, p = 0.002) in the fourth quartile, respectively. Restricted cubic spline analysis revealed a steady negative linear correlation between CDAI and CFI, with a p-value for non-linearity of 0.122. Subgroup analysis did not reveal any significant interactions based on age, education level, family income, history of diabetes, hypertension, stroke, and depression.Conclusion: CDAI was inversely associated with CFI in a large representative American population. Further longitudinal studies are needed for causal inference.
- 22 November 2024
- Published by Frontiers Media SA in Frontiers in Nutrition
- Vol. 11, 1471981
Open AccessAssociation between composite dietary antioxidant index and cognitive function impairment among the US older adults: a cross-sectional study based on the NHANES 2011–2014
Background: Cognitive function impairment (CFI) and the Composite Dietary Antioxidant Index (CDAI) were investigated in this study.Methods: Participants from the 2011–2014 cycles of the National Health and Nutrition Examination Survey were chosen to assess cognitive function using the Consortium to Establish a Registry for Alzheimer’s Disease Word Learning Test, the Animal Fluency Test, and the Digit Symbol Substitution Test. Participants scored below the 25% percentile of any of the three tests were defined as having cognitive function impairment. 24-h recalls of diet were collected to calculate CDAI.Results: 2,424 participants were included. The fully adjusted multivariate logistic regression model showed an increase of one CDAI unit reduced CFI risk by 5% (95% CI: 0.92 ~ 0.98, p = 0.004). When comparing individuals with the lowest CDAI in the first quartile (<−2.42), the adjusted odds ratio for CDAI and CFI were 0.81 (95% CI: 0.61 ~ 1.06, p = 0.125) in the second quartile, 0.69 (95% CI: 0.51 ~ 0.92, p = 0.012) in the third quartile, and 0.59 (95% CI: 0.43 ~ 0.82, p = 0.002) in the fourth quartile, respectively. Restricted cubic spline analysis revealed a steady negative linear correlation between CDAI and CFI, with a p-value for non-linearity of 0.122. Subgroup analysis did not reveal any significant interactions based on age, education level, family income, history of diabetes, hypertension, stroke, and depression.Conclusion: CDAI was inversely associated with CFI in a large representative American population. Further longitudinal studies are needed for causal inference.
- 13 June 2024
- Published by Elsevier in Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease
- Vol. 1870 (7) , 167303
Follicular CD8+ T cells promote immunoglobulin production and demyelination in multiple sclerosis and a murine model
- 13 June 2024
- Published by Elsevier in Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease
- Vol. 1870 (7) , 167303
Follicular CD8+ T cells promote immunoglobulin production and demyelination in multiple sclerosis and a murine model