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Extracellular nucleoprotein exacerbates influenza viruspathogenesis by activating toll-like receptor 4 and the NLRP3inflammasome

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Cellular & Molecular Immunology 2022年第6期19卷 715-725页

作者： Chang-Ung Kim Yu-Jin Jeong Pureum Lee Moo-Seung Lee Jong-Hwan Park Young-Sang Kim Doo-Jin Kim Infectious Disease Research Center Korea Research Institute of Bioscience and Biotechnology(KRIBB)DaejeonSouth Korea Department of Biochemistry Chungnam National UniversityDaejeonSouth Korea Environmental Diseases Research Center Korea Research Institute of Bioscience and Biotechnology(KRIBB)DaejeonSouth Korea University of Science and Technology(UST) DaejeonSouth Korea College of Veterinary Medicine Chonnam National UniversityGwangjuSouth Korea

Host immune responses, such as those initiated by pattern recognition receptor (PRR) activation, are important for viralclearance and pathogenesis. However, little is known about the interactions of viral proteins with surface PRRs or, moreimportantly, the association of innate immune activation with viral pathogenesis. In this study, we showed that internalinfluenza virus proteins were released from infected cells. Among these proteins, nucleoprotein (NP) played a critical role inviral pathogenesis by stimulating neighboring cells through toll-like receptor (TLR)2, TLR4, and the NLR family pyrin domaincontaining 3 (NLRP3) inflammasome. Through the activation of these PRRs, NP induced the production of interleukin (IL)-1β andIL-6, which subsequently led to the induction of trypsin. Trypsin induced by NP increased the infectivity of influenza virus,leading to increases in viral replication and pathology upon subsequent viral infection. These results reveal the role of releasedNP in influenza pathogenesis and highlight the importance of the interactions of internal viral proteins with PRRs in theextracellular compartment during viral pathogenesis.

关键词： Influenza virus Viral protein release Nucleoprotein toll-like receptor Cyotkine-trypsin cycle

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The role of innate immunity in diabetic nephropathy and their therapeutic consequences

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Journal of Pharmaceutical Analysis 2024年第1期14卷 39-51页

作者： Min Yang Chun Zhang Department of Nephrology Union HospitalTongji Medical CollegeHuazhong University of Science and TechnologyWuhan430022China

Diabetic nephropathy (DN) is an enduring condition that leads to inflammation and affects a substantial number of individuals with diabetes worldwide. A gradual reduction in glomerular filtration and emergence of proteins in the urine are typical aspects of DN, ultimately resulting in renal failure. Mounting evidence suggests that immunological and inflammatory factors are crucial for the development of DN. Therefore, the activation of innate immunity by resident renal and immune cells is critical for initiating and perpetuating inflammation. toll-like receptors (TLRs) are an important group of receptors that identify patterns and activate immune responses and inflammation. Meanwhile, inflammatory responses in the liver, pancreatic islets, and kidneys involve inflammasomes and chemokines that generate pro-inflammatory cytokines. Moreover, the activation of the complement cascade can be triggered by glycated proteins. This review highlights recent findings elucidating how the innate immune system contributes to tissue fibrosis and organ dysfunction, ultimately leading to renal failure. This review also discusses innovative approaches that can be utilized to modulate the innate immune responses in DN for therapeutic purposes.

关键词： Innate immunity Diabetic nephropathy Inflammation toll-like receptor Inflammasomes

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General anesthetic agents induce neurotoxicity through astrocytes

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Neural Regeneration Research 2024年第6期19卷 1299-1307页

作者： Yanchang Yang Tiantian Liu Jun Li Dandan Yan Yuhan Hu Pin Wu Fuquan Fang Patrick M.McQuillan Wenxin Hang Jianhang Leng Zhiyong Hu Department of Anesthesiology The First Affiliated Hospital Zhejiang University School of Medicine Department of Anesthesiology Ningbo Women and Children's Hospital 3. Department of Anesthesiology Shulan (Hangzhou) Hospital Affiliated to Zhejiang Shuren University Shulan International Medical College 4. Cell Biology Department Yale University 5. Department of Anesthesiology Penn State Hershey Medical Centre Penn State College of Medicine 6. Department of Central Laboratory Affiliated Hangzhou First People's Hospital Zhejiang University School of Medicine

Neuroscientists have recognized the importance of astrocytes in regulating neurological function and their influence on the release of glial transmitters. Few studies, however, have focused on the effects of general anesthetic agents on neuroglia or astrocytes. Astrocytes can also be an important target of general anesthetic agents as they exert not only sedative, analgesic, and amnesic effects but also mediate general anesthetic-induced neurotoxicity and postoperative cognitive dysfunction. Here, we analyzed recent advances in understanding the mechanism of general anesthetic agents on astrocytes, and found that exposure to general anesthetic agents will destroy the morphology and proliferation of astrocytes, in addition to acting on the receptors on their surface, which not only affect Ca2+signaling, inhibit the release of brain-derived neurotrophic factor and lactate from astrocytes, but are even involved in the regulation of the pro-and anti-inflammatory processes of astrocytes. These would obviously affect the communication between astrocytes as well as between astrocytes and neighboring neurons, other neuroglia, and vascular cells. In this review, we summarize how general anesthetic agents act on neurons via astrocytes, and explore potential mechanisms of action of general anesthetic agents on the nervous system. We hope that this review will provide a new direction for mitigating the neurotoxicity of general anesthetic agents.

关键词： astrocytes brain-derived neurotrophic factor general anesthetic agents N-methyl-D-aspartate receptor neuron neurotoxicity perioperative neurocognition toll-like receptor γ-aminobutyric acid receptor

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Nuclear Factor-κB:Activation and Regulation during toll-like receptor Signaling

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Cellular & Molecular Immunology 2007年第1期4卷 31-41页

作者： Ruaidhrí J. Carmody Department of Pathology and Laboratory Medicine School of Medicine University of PennsylvaniaPhiladelphia PA 19104 USA 713A Stellar Chance Departmentof Pathology and Laboratory Medicine University of Pennsylvania Schoolof Medicine 422 Curie Blvd.Philadelphia PA 19104 USA

toll-like receptors （TLRs） recognize distinct microbial components to initiate the innate and adaptive immune responses. TLR activation culminates in the expression of appropriate pro-inflammatory and immunomodulatory factors to meet pathogenic challenges. The transcription factor NF-kB is the master regulator of all TLR-induced responses and its activation is the pivotal event in TLR-mediated activation of the innate immune response. Many of the key molecular events required for TLR-induced NF-r.B activation have been elucidated. However, much remain to be learned about the ability of TLRs to generate pathogen-specific responses using a limited number of transcription factors. This review will focus on our current understanding of NF-kB activation by TLRs and potential mechanisms for achieving a signal-specific response through NF-kB. Cellular ＆ Molecular Immunology. 2007;4（1）：31-41.

关键词： NF-kB toll-like receptor signal transduction innate immunity transcription

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Alcohol,nutrition and liver cancer:Role of toll-like receptor signaling

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World Journal of Gastroenterology 2010年第11期16卷 1344-1348页

作者： Samuel W French Joan Oliva Barbara A French Fawzia Bardag-Gorce Department of Pathology Harbor-UCLA Medical Center

This article reviews the evidence that ties the development of hepatocellular carcinoma (HCC) to the natural immune pro-inflammatory response to chronic liver disease, with a focus on the role of toll-like receptor (TLR) signaling as the mechanism of liver stem cell/progenitor transformation to HCC. Two exemplary models of this phenomenon are reviewed in detail. One model applies chronic ethanol/lipopolysaccharide feeding to the activated TLR4 signaling pathway. The other applies chronic feeding of a carcinogenic drug, in which TLR2 and 4 signaling pathways are activated. In the drug-induced model, two major methyl donors, S-adenosylmethionine and betaine, prevent the upregulation of the TLR signaling pathways and abrogate the stem cell/progenitor proliferation response when fed with the carcinogenic drug. This observation supports a nutritional approach to liver cancer prevention and treatment. The observation that upregulation of the TLR signaling pathways leads to liver tumor formation gives evidence to the popular concept that the chronic pro-inflammatory response is an important mechanism of liver oncogenesis. It provides a nutritional approach, which could prevent HCC from developing in many chronic liver diseases.

关键词： toll-like receptor Hepatocellular carcinoma Methyl donors, Epigenetic processes Inflammation Alcohol Drug toxicity Lipopolysaccharides

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Methylprednisolone inhibits activated CD4^+ T cell survival promoted by toll-like receptor ligands

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Hepatobiliary & Pancreatic Diseases International 2010年第4期9卷 376-383页

作者： Lu, You-Sheng Pu, Li-Yong Li, Xiang-Cheng Wang, Xue-Hao Nanjing Med Univ Affiliated Hosp 1 Liver Transplantat Ctr Peoples Hosp Jiangsu Prov Nanjing 210029 Peoples R China

BACKGROUND: Methylprednisolone (MP) can affect the survival of CD4(+) T lymphocytes and plays an important role in adaptive immune responses; however, its mechanism of action is not clear. Recent studies have shown that toll-like receptors (TLRs) on CD4(+) T cells can directly modulate adaptive immune responses by affecting the survival and proliferation of activated CD4(+) T cells. This study aimed to investigate the relationship between MP, TLRs and activated CD4(+) T cells. METHODS: We separated and purified CD4(+) T cells from mice, activated them in vitro, and co-cultured them with TLR ligands, MP or inhibitors of nuclear factor-kappa B (NF-kappa B) and activator protein 1 (AP-1). We then assessed CD4(+) T cell survival and proliferation and the expression of NF-kappa B and AP-1. RESULTS: Activated CD4(+) T cells showed increased TLR-3 and TLR-9 mRNA expression, but polyinosinic-polycytidylic acid (poly I:C) and MP had no effect on the expression of these mRNAs. Still, poly I:C and CpG oligodeoxynucleotides (CpG DNA) increased the survival of activated CD4(+) T cells, whereas MP reduced the survival of activated CD4(+) T cells and could inhibit the survival effects of poly I:C and CpG DNA. The NF-kappa B essential modifier-binding domain (NBD) inhibited the survival of activated CD4(+) T cells induced by poly I:C and CpG DNA, but the AP-1 inhibitor crucumin did not have the same effect. The increased expression of NF-kappa B induced by poly I:C and CpG DNA in activated CD4(+) T cells could be inhibited by MP, but the same was not true for the increased expression of AP-1 induced by poly I:C and CpG DNA. Finally, the proliferation of activated CD4(+) T cells was not affected by poly I:C or MP. CONCLUSION: The survival of activated CD4(+) T cells is promoted by TLR ligands, but this effect is inhibited by MP.

关键词： methylprednisolone toll-like receptor CD4(+) T lymphocytes NF-kappa B

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N-acetylcysteine inhibits activation of toll-like receptor 2 and 4 gene expression in the liver and lung after partial hepatic ischemia-reperfusion injury in mice

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Hepatobiliary & Pancreatic Diseases International 2007年第3期6卷 284-289页

作者： Jin, Xin Wang, Lin Wu, He-Shui Zhang, Lei Wang, Chun-You Tian, Yuan Zhang, Jing-Hui Huazhong Univ Sci & Technol Ctr Pancreat Surg Affiliated Union Hosp Tongji Med Coll Wuhan 430022 Peoples R China Huazhong Univ Sci & Technol Tongji Med Coll Affiliated Union Hosp Lab Gen Surg Wuhan 430022 Peoples R China

BACKGROUND: toll-like receptor 2 and 4 (TLR2/4) may play important roles in ischemia-reperfusion (I/R) injury, and N-acetylcysteine (NAC) can prevent the generation of reactive oxygen species (ROS) induced by I/R injury. This study aimed to investigate the changes in TLR2/4 gene expression in the liver and lung after I/R injury with or without NAC pretreatment. METHODS: BALB/c mice were used in a model of partial hepatic I/R injury and randomly assigned to a sham-operated control group (SH), a hepatic ischemia/reperfusion group (I/R) or a NAC pretreated, hepatic I/R group (I/R-NAC). The levels of TNF-alpha in the portal vein and plasma alanine aminotransferase (ALT) were measured at 1 and 3 hours after reperfusion. The lung wet-to-dry ratio was measured, and the expression of TLR2/4 mRNA and protein in the liver and lung were assessed with RT-PCR and Western blotting at the same time points. RESULTS: Compared with the I/R group, the expression of TLR2/4 mRNA and protein in the liver and lung in the I/R-NAC group was decreased at the same time point (P<0.05). The levels of portal vein TNF-a and plasma ALT increased continuously in the l/R group at I and 3 hours of reperfusion compared with the SH group; however, they declined significantly in the group pretreated with NAC (P<0.05). The extent of lung edema was relieved in the I/R-NAC group compared with the I/R group (P<0.05). CONCLUSIONS: TLR2/4 was activated in the liver and lung in the process of partial hepatic I/R injury. NAC inhibited the activation of TLR2/4 and the induction of TNF-alpha resulting from I/R injury via modulating the redox state, thus it may mitigate liver and lung injury following partial hepatic I/R in mice.

关键词： N-acetylcysteine ischemia-reperfusion lung injury toll-like receptor

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Upregulation of toll-like receptor 4 on T Cells in PBMCs Is Associated with Disease Aggravation of HBV-related Acute-on-chronic Liver Failure

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Journal of Huazhong University of Science and Technology(Medical Sciences) 2015年第6期35卷 910-915页

作者：徐春利郝友华卢银平唐宗生杨雪晟吴郡郑昕王宝菊刘嘉杨东亮 Department of Infectious Disease Union Hospital Tongji Medical College Huazhong University of Science and Technology Division of Clinical Immunology Tongji Hospital Tongji Medical College Huazhong University of Science and Technology

Summary： Immune-mediated inflammatory injury is an important feature of the disease aggravation of hepatitis B virus-related acute-on-chronic liver failure （ACLF）. toll-like receptors （TLRs） have been shown previously to play a pivotal role in the activation of innate immunity. The purpose of this study was.to characterize the TLR4 expression in peripheral blood mononuclear cells （PBMCs） of ACLF pa- tients and its possible role in the disease aggravation. Twelve healthy subjects, 15 chronic HBV-infected （CHB） patients and 15 ACLF patients were enrolled in this study. The TLR4 expression in PBMCs and T cells of all subjects was examined by real-time PCR and flow cytometry. The correlation of TLR4 ex- pression on T cells with the markers of disease aggravation was evaluated in ACLF patients. The ability of TLR4 ligands stimulation to induce inflammatory cytokine production in ACLF patients was ana- lyzed by flow cytometry. The results showed that TLR4 mRNA level was upregulated in PBMCs of ACLF patients compared to that in the healthy subjects and the CHB patients. Specifically, the expres- sion of TLR4 on CD4＋ and CD8＋ T cells of PBMCs was significantly increased in ACLF patients. The TLR4 levels on CD4＋ and CD8＋T cells were positively correlated with serum total bilirubin （TBIL）, direct bilirubin （DBIL）, international normalized ratio （INR） levels and white blood cells （WBCs）, and negatively correlated with serum albumin （ALB） levels in the HBV-infected patients, indicating TLR4 pathway may play a role in the disease aggravation of ACLF. In vitro TLR4 ligand stimulation on PBMCs of ACLF patients induced a strong TNF-α production by CD4＋ T cells, which was also posi- tively correlated with the serum markers for liver injury severity. It was concluded that TLR4 expression is upregulated on T cells in PBMCs, which is associated with the aggravation of ACLF.

关键词： toll-like receptor chronic hepatitis B hepatitis B-related acute-on-chronic liver failure pe-ripheral blood mononuclear cells

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The Expression of toll-like receptor 2 and 4 mRNA in Local Tissues of Model of Oropharyngeal Candidiasis in Mice

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Journal of Huazhong University of Science and Technology(Medical Sciences) 2004年第6期24卷 639-641页

作者：张少如李家文贾雪松邬炎卿 Department of Dermatology Union Hospital Tongji Medical College of Huazhong University of Science and Technology Wuhan 430022 China

Summary: To investigate the expression of toll-like receptor (TLR) 2 and 4 mRNA in local tissues of model of oropharyngeal candidiasis in mice and to explore the potential role of TLR2 and TLR4 in earlier period of immune response, a murine model of oropharyngeal candidiasis inoculated by cotton wool balls saturated with candida albicans was established. Mice were sacrificed at the indicated time points and the oropharyngeal tissues were excised. The expression of TLR2 and TLR4 mRNA was detected by RT-PCR. The results showed that low level of TLR2/4 mRNA could be detected in oropharyngeal tissues, but they were markedly up-regulated 6 h after inoculation, peaking after 12-24 h. Tissue TLR4 mRNA was gradually down-regulated 24-48 h, while TLR2 mRNA levels remained high up to the 72nd h. These data suggested that oropharyngeal infection of Candida albicans could result in up-regulation of TLR2/4 mRNA expression in local tissues, which might play important roles in earlier period of immune response.

关键词： Candida albicans oropharyngeal infection toll-like receptor

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toll-like receptor-Dependent Antiviral Responses at the Maternal-Fetal Interface

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Reproductive and Developmental Medicine 2020年第4期4卷 249-256页

作者： Liu Xiao-Rui Wei Xiao-Wei Lin Yi Department of Obstetrics and Gynecology Shanghai Key Laboratory of Embryo Original DiseasesSchool of MedicineInternational Peace Maternity and Child Health HospitalShanghai Jiao Tong UniversityShanghai 200030China

The maternal-fetal interface is a key barrier to protect the fetus from infection.toll-like receptors (TLRs) at the maternal-fetal interface are involved in antiviral responses.TLRs are expressed in both maternal decidua and fetal trophoblasts.Virus-induced activation of TLR signaling pathways triggers the release of interferon-related antiviral molecules and other inflammatory cytokines and/or chemokines by the host innate immune system,which may disrupt immune tolerance at the maternal-fetal interface and lead to pregnancy complications.In this review,we summarize the state of knowledge on the most common viral infections during pregnancy,antiviral TLR responses at the maternal-fetal interface,and TLR-associated pregnancy complications.

关键词： toll-like receptor Antiviral Response Maternal-Fetal Interface

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