scholarly journals Riemerella anatipestifer infection in ducks induces IL-17A production, but not IL-23p19

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Rochelle A. Flores ◽  
Cherry P. Fernandez-Colorado ◽  
Fahmida Afrin ◽  
Paula Leona T. Cammayo ◽  
Suk Kim ◽  
...  
Keyword(s):  
Mrna Expression ◽  
Proinflammatory Cytokines ◽  
Post Infection ◽  
Proinflammatory Cytokine ◽  
Th17 Cells ◽  
Critical Role ◽  
Splenic Lymphocytes ◽  
Expression Levels ◽  
Time Points ◽  
Mrna Expression Analysis

Abstract R. anatipestifer (RA) is one of the most harmful bacterial pathogens affecting the duck industry, and infection is associated with the production of proinflammatory cytokines, including IL-17A. Another proinflammatory cytokine, IL-23, is critical for the development of Th17 cells, which produce IL-17. However, IL-23 roles have not been studied in this infection. Here, we describe the identification and mRNA expression analysis of duck IL-23p19 (duIL-23p19) in splenic lymphocytes and macrophages stimulated with killed RA and in spleens of RA-infected ducks. Expression of duIL-23p19 transcript identified in this study was relatively high in livers of healthy ducks and was upregulated in mitogen-activated splenic lymphocytes as well as in splenic lymphocytes and macrophages stimulated with killed RA. In spleens of RA-infected ducks, expression levels of duIL-23p19 transcript were unchanged at all time points except on days 4 and 7 post-infection; however, duIL-17A and IL-17F expression levels were upregulated in both spleens of RA-infected ducks and splenic lymphocytes and macrophages stimulated with killed RA. In sera collected at 24 h after this infection, duIL-23p19 expression levels were unchanged, whereas IL-17A significantly upregulated. These results suggest that IL-23p19 does not play a critical role in the IL-17A response in early stages of RA-infected ducks.

scholarly journals Invasive Phenotype of Candida albicans Affects the Host Proinflammatory Response to Infection

2005 ◽  
Vol 73 (8) ◽  
pp. 4588-4595 ◽  
Author(s):  
C. C. Villar ◽  
H. Kashleva ◽  
A. P. Mitchell ◽  
A. Dongari-Bagtzoglou
Keyword(s):  
Endothelial Cells ◽  
Candida Albicans ◽  
Proinflammatory Cytokines ◽  
Proinflammatory Cytokine ◽  
Inflammatory Responses ◽  
Gene Knockout ◽  
Critical Role ◽  
Host Cells ◽  
Proinflammatory Response ◽  
Cytokine Responses

ABSTRACT Candida albicans is a major opportunistic pathogen in immunocompromised patients. Production of proinflammatory cytokines by host cells in response to C. albicans plays a critical role in the activation of immune cells and final clearance of the organism. Invasion of host cells and tissues is considered one of the virulence attributes of this organism. The purpose of this study was to investigate whether the ability of C. albicans to invade host cells and tissues affects the proinflammatory cytokine responses by epithelial and endothelial cells. In this study we used the invasion-deficient RIM101 gene knockout strain DAY25, the highly invasive strain SC5314, and highly invasive RIM101-complemented strain DAY44 to compare the proinflammatory cytokine responses by oral epithelial or endothelial cells. Using a high-throughput approach, we found both qualitative and quantitative differences in the overall inflammatory responses to C. albicans strains with different invasive potentials. Overall, the highly invasive strains triggered higher levels of proinflammatory cytokines in host cells than the invasion-deficient mutant triggered. Significant differences compared to the attenuated mutant were noted in interleukin-1α (IL-1α), IL-6, IL-8, and tumor necrosis factor alpha in epithelial cells and in IL-6, growth-related oncogene, IL-8, monocyte chemoattractant protein 1 (MCP-1), MCP-2, and granulocyte colony-stimulating factor in endothelial cells. Our results indicate that invasion of host cells and tissues by C. albicans enhances the host proinflammatory response to infection.

scholarly journals Changes in expression of NLRP3 inflamasome and IL-1β in the development of oxazolone-induced colitis in rats and on the background of administration of simvastatin and interleukin-1β receptor antagonist

Pathologia ◽  
2021 ◽  
Vol 18 (1) ◽  
pp. 58-65
Author(s):  
O. S. Zherebiatiev ◽  
N. M. Polishchuk
Keyword(s):  
Weight Loss ◽  
Receptor Antagonist ◽  
Mrna Expression ◽  
Nlrp3 Inflammasome ◽  
Proinflammatory Cytokine ◽  
Interleukin 1 ◽  
Clinical Signs ◽  
Histological Evaluation ◽  
Expression Levels ◽  
Interleukin 1 Receptor Antagonist

The aim. To study the expression of mRNA of the NLRP3 inflammasome and proinflammatory cytokine IL-1β in the inflamed colon of rats with experimental oxazolone-induced colitis and against the background of the introduction of simvastatin and antagonist of interleukin-1 receptors. Materials and methods. Experiments were carried out on male Wistar rats aged 8 months (body mass 120–150 g). Tissue samples were obtained from rats with experimental oxazolone-induced colitis (n = 20), rats with oxazolone-induced colitis treated with simvastatin (n = 20); rats with oxazolone-induced colitis treated with interleukin-1 receptor antagonist (n = 20) and control animals (n = 10). Clinical signs of colitis were evaluated by the clinical index of disease activity on the following parameters: weight loss, stool consistency and animal behavior. For macroscopic assessment of the development of colitis areas of inflammation and ulceration were investigated. For histological evaluation of lesions, sections of the intestine were stained with hematoxylin and eosin and cellular inflammatory infiltrates, epithelial hyperplasia, ulceration and loss of intestinal glands were studied. IL-1β and NLRP3 inflammasome mRNA expression was analyzed by real-time reverse transcriptase-polymerase chain reaction. Results. Animals treated with oxazolone rapidly developed colitis marked by weight loss and diarrhea peaking by day 2 after oxazolone administration and leading to death of 40 % of the rats by day 4. The histological observation showed inflammatory cell infiltration, including polymorphonuclear leukocytes and multiple erosive lesions in the large intestine. We determined that the expression level of the proinflammatory cytokine IL-1β is increased in colon samples of rats with oxazolone-induced colitis. IL-1β expression is increased 3.5‐fold in inflamed colon compared to uninflamed tissue. Administration of simvastatin and an interleukin-1 receptor antagonist to rats with oxazolone-induced colitis resulted in a 30 % and 2-fold decrease expression of IL-1β in colon samples. In addition, we examined NLRP3 expression in these tissues. RT‐PCR analysis demonstrates a 71‐fold increased expression of NLRP3 mRNA expression in colon samples tested. Administration of simvastatin and an interleukin-1 receptor antagonist to rats with oxazolone-induced colitis resulted in a 2.5- to 3.0-fold decrease expression of NLRP3 mRNA in colon samples. Conclusions. IL-1β and NLRP3 mRNA expression levels were elevated in the inflamed colon of rats with experimental oxazolone-induced colitis. Administration of simvastatin and an interleukin-1 receptor antagonist against the background of colitis caused a decrease in the expression levels of IL-1β and NLRP3 mRNA in the tissues of the intestine. Detection of abnormal expression of IL-1β and NLRP3 mRNA could provide insights into pathogenesis of Crohn's disease, and may help to identify future potential targets for therapeutic strategies in people with inflammatory bowel disease.

scholarly journals Tabetri™ (Tabebuia avellanedae Ethanol Extract) Ameliorates Atopic Dermatitis Symptoms in Mice

2018 ◽  
Vol 2018 ◽  
pp. 1-11
Author(s):  
Jae Gwang Park ◽  
Young-Su Yi ◽  
Sang Yun Han ◽  
Yo Han Hong ◽  
Sulgi Yoo ◽  
...  
Keyword(s):  
Atopic Dermatitis ◽  
Mrna Expression ◽  
Pharmacological Activity ◽  
Proinflammatory Cytokines ◽  
Proinflammatory Cytokine ◽  
Immunoglobulin E ◽  
Ethanol Extract ◽  
Underlying Mechanism ◽  
T Helper ◽  
T Helper 2

Tabebuia avellanedae has been traditionally used as an herbal remedy to alleviate various diseases. However, the plant’s pharmacological activity in allergic and inflammatory diseases and its underlying mechanism are not fully understood. Therefore, we investigated the pharmacological activity of Tabetri (T. avellanedae ethanol extract (Ta-EE)) in the pathogenesis of AD. Its underlying mechanism was explored using an AD mouse model and splenocytes isolated from this model. Ta-EE ameliorated the AD symptoms without any toxicity and protected the skin of 2,4-dinitrochlorobenzene- (DNCB-) induced AD mice from damage and epidermal thickness. Ta-EE reduced the secreted levels of allergic and proinflammatory cytokines, including histamine, immunoglobulin E (IgE), interleukin- (IL-) 4, and interferon-gamma (IFN-γ) in the DNCB-induced AD mice. Ta-EE suppressed the mRNA expression of T helper 2-specific cytokines, IL-4 and IL-5, and the proinflammatory cytokine IFN-γ in the atopic dermatitis skin lesions of AD mice. Moreover, Ta-EE suppressed the mRNA expression of IL-4, IL-5, IFN-γ, and another proinflammatory cytokine, IL-12, in the Con A-stimulated splenocytes. It also suppressed IL-12 and IFN-γ in the LPS-stimulated splenocytes. Taken together, these results suggest that Ta-EE protects against the development of AD through the inhibition of mRNA expression of T helper 2-specific cytokines and other proinflammatory cytokines.

scholarly journals High Expression of LTBP2 Contributes to Poor Prognosis in Colorectal Cancer Patients and Correlates with the Mesenchymal Colorectal Cancer Subtype

2019 ◽  
Vol 2019 ◽  
pp. 1-9 ◽  
Author(s):  
Ying Huang ◽  
Guihua Wang ◽  
Chunmei Zhao ◽  
Rong Geng ◽  
Shu Zhang ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Overall Survival ◽  
Protein Expression ◽  
Mrna Expression ◽  
Cell Lines ◽  
Critical Role ◽  
Prognostic Significance ◽  
Poor Overall Survival ◽  
Expression Levels ◽  
Mrna And Protein Expression

Colorectal cancer (CRC) is a complex and heterogeneous disease with four consensus molecular subtypes (CMS1-4). LTBP2 is a member of the fibrillin/LTBP super family and plays a critical role in tumorigenesis by activating TGF-β in the CMS4 CRC subtype. So far, the expression and prognostic significance of LTBP2 in CRC remains obscure. In this study, we aimed to analyze the mRNA and protein expression levels of LTBP2 in CRC tissues and then estimate their values as a potential prognostic biomarker. We detected the mRNA expression of LTBP2 in 28 cases of fresh CRC tissues and 4 CRC cell lines and the protein expression of LTBP2 in 483 samples of CRC tissues, matched tumor-adjacent tissues, and benign colorectal diseases. LTBP2 protein expression was then correlated to patients’ clinical features and overall survival. Both LTBP2 mRNA and protein expression levels in CRC tissues were remarkably superior to those in adjacent normal colorectal tissues (P=0.0071 and P<0.001, respectively), according to TCGA dataset of CRC. High LTBP2 protein expression was correlated with TNM stage (P<0.001), T stage (P<0.001), N stage (P<0.001), and M stage (P<0.001). High LTBP2 protein expression was related to poor overall survival in CRC patients and was an independent prognostic factor for CRC. LTBP2 mRNA expression was especially higher in the CMS4 subtype (P<0.001), which was confirmed in CRC cell lines. Our data suggested that LTBP2 may act as an oncogene in the development of colorectal cancer and have important significance in predicting CRC prognosis. LTBP2 could be a novel biomarker and potential therapeutic target for mesenchymal colorectal cancer and can improve the outcome of high-risk CRC.

scholarly journals Proinflammatory Cytokine IL-17 Shows a Significant Association with Helicobacter pylori Infection and Disease Severity

2017 ◽  
Vol 2017 ◽  
pp. 1-7 ◽  
Author(s):  
Piyumali Sandareka Arachchi ◽  
Neluka Fernando ◽  
Manjula Manoji Weerasekera ◽  
Bimalka Senevirathna ◽  
Deepaka D. Weerasekera ◽  
...  
Keyword(s):  
Immune Response ◽  
Helicobacter Pylori ◽  
Disease Severity ◽  
Inflammatory Cytokines ◽  
Proinflammatory Cytokines ◽  
Proinflammatory Cytokine ◽  
Th17 Cells ◽  
Sri Lankan ◽  
Healthy Controls ◽  
H Pylori

Background. The pro- and anti-inflammatory cytokines play an important role in the immune response against H. pylori infection. The proinflammatory cytokines of Th17 cells have been suggested to play a major role in H. pylori infection and resulting gastric inflammation. Objective. The objective of this study was to compare the expression of selected inflammatory cytokines (IL-10, IL-17, IL-21, IL-23, and TNF-α) in H. pylori-infected patients and healthy controls and to understand their association with H. pylori infection and disease severity. Results. The expression levels of IL-17 and IL-23 were significantly higher in H. pylori-infected patients. The expression of IL-21 was also higher in H. pylori-positive patients but there was no significant association with infection. IL-17 expression showed a significant increase with the severity of chronic gastritis. Conclusion. The proinflammatory cytokine, IL-17, shows a significant association with H. pylori infection and disease severity in a Sri Lankan dyspeptic patient population.

scholarly journals POS0005 THE EFFECT OF LKB1 INHIBITION IN RA PATHOGENESIS

2021 ◽  
Vol 80 (Suppl 1) ◽  
pp. 204.3-204
Author(s):  
H. R. Lee ◽  
J. Kim ◽  
S. J. Yoo ◽  
J. A. Park ◽  
S. W. Kang
Keyword(s):  
Rheumatoid Arthritis ◽  
Reactive Oxygen Species ◽  
Mrna Expression ◽  
Proinflammatory Cytokines ◽  
Critical Role ◽  
Nicotinamide Adenine Dinucleotide Phosphate ◽  
Reactive Oxygen ◽  
Migration And Invasion ◽  
Oxygen Species ◽  
Fibroblast Like Synoviocytes

Background:Liver kinase B1 (LKB1) is known as a tumor suppressor gene and also inhibits reactive oxygen species (ROS) levels. Intracellular ROS are catalyzed by the enzyme complex nicotinamide adenine dinucleotide phosphate (NADPH) oxidase (NOX). We previously reported that NOX4 induced the migration and invasion of fibroblast-like synoviocytes (FLS) in rheumatoid arthritis (RA). Although LKB1 is expected to alleviate synovial inflammation through ROS regulation, the role of LKB1 in RA has not been examined.Objectives:To explore whether LKB1 affects RA inflammation, we transfected LKB1 siRNA and analyzed related gene expressions in RA FLS.Methods:Synovial tissues were obtained from RA patients who were undergoing synovectomy or joint replacement. The isolated cells were cultured in Dulbecco’s modified Eagle’s medium (DMEM) supplemented with 10% fetal bovine serum, 100 U/ml penicillin and 100 mg/ml streptomycin and maintained in a 5% CO2 incubator at 37 °C. FLS were used for experiments after four to six passages. Cells were transfected with lipofectamine transfection reagent and LKB1 siRNA duplex targeting constructs. After incubation for 24 h, downregulation of target expression was evaluated by real-time PCR and western blot analysis.Results:RA FLS was transfected with LKB1 siRNA and 90% of LKB1 mRNA expression was decreased. LKB1 knock-down also caused the decreased expression of mechanistic target of rapamycin (mTOR; 0.38 fold) and serine/threonine kinase (AKT) 2 (0.40 fold), which are downstream targets of LKB1. NOX4 was significantly increased (4.94 fold) by LKB1 inhibition. On the other side, the down regulated NOX4 induced significantly elevated LKB1 mRNA expression in RA FLS. When the expressions of proinflammatory cytokines were examined, IL-1β, IL-6, TNF-α were highly increased by LKB1 deficiency. FLS migration-related chemokines, IL-8 and MMP-3 were also enhanced compared to control.Conclusion:There was a negative correlation between NOX4 and LKB1 in RA FLS. As LKB1 deficiency induced the expression of proinflammatory cytokines and migration related chemokines, LKB1 could play a critical role in RA pathogenesis.References:[1]Bartok B, Firestein GS. Fibroblast-like synoviocytes: key effector cells in rheumatoid arthritis. Immunol Rev. 2010;233(1):233–55.[2]Mateen S, Moin S, Khan AQ, Zafar A, Fatima N. Increased reactive oxygen species formation and oxidative stress in rheumatoid arthritis. PLoS One. 2016;11(4):e0152925.Disclosure of Interests:None declared.

scholarly journals Duck Interleukin-22: Identification and Expression Analysis in Riemerella anatipestifer Infection

2021 ◽  
Vol 2021 ◽  
pp. 1-12
Author(s):  
Rochelle A. Flores ◽  
Paula Leona T. Cammayo ◽  
Binh T. Nguyen ◽  
Cherry P. Fernandez-Colorado ◽  
Suk Kim ◽  
...  
Keyword(s):  
Mrna Expression ◽  
Expression Analysis ◽  
Cell Types ◽  
Splenic Lymphocytes ◽  
Cd4 Cells ◽  
Riemerella Anatipestifer ◽  
Interleukin 22 ◽  
Mrna Expression Analysis ◽  
Different Cell Types

Riemerella anatipestifer is one of the most devastating pathogens affecting the global duck farms. Infection is involved in secretion of proinflammatory cytokines, including interleukin- (IL-) 17A. During the immune response to infection, IL-22 and IL-17A are often produced concurrently and at high levels in inflamed tissues. Little is known about duck IL-22 (duIL-22) during R. anatipestifer infection. We describe the characterization of duIL-22 and its mRNA expression analysis in splenic lymphocytes and macrophages treated with heat-killed R. anatipestifer and in the spleens and livers of R. anatipestifer-infected ducks. Full-length cDNA of duIL-22 encoded 197 amino acids. The deduced amino acid sequence of duIL-22 shared a 30.4–40.5% similarity with piscine counterparts, 57.4–60.1% with mammalian homologs, and 93.4% similarity to the chicken. Duck IL-22 mRNA expression level was relatively high in the skin of normal ducks. It was increased in mitogen-stimulated splenic lymphocytes and in killed R. anatipestifer-activated splenic lymphocytes and macrophages. Compared with healthy ducks, IL-22 transcript expression was significantly upregulated in the livers and spleens on days 1 and 4 postinfection, but not on day 7. IL-17A was significantly increased in the spleens only on day 4 postinfection and in the livers at all time points. When splenic lymphocytes were stimulated with heat-killed R. anatipestifer, CD4+ cells predominantly produced IL-22 while IL-17A was expressed both by CD4+ and CD4- cells. These results suggested that IL-22 and IL-17A are likely expressed in different cell types during R. anatipestifer infection.

scholarly journals Real-Time Induction of Macrophage Apoptosis, Pyroptosis, and Necroptosis by Enterococcus faecalis OG1RF and Two Root Canal Isolated Strains

2021 ◽  
Vol 11 ◽  
Author(s):  
Danlu Chi ◽  
Xinwei Lin ◽  
Qingzhen Meng ◽  
Jiali Tan ◽  
Qimei Gong ◽  
...  
Keyword(s):  
Cell Death ◽  
Mrna Expression ◽  
Real Time ◽  
Enterococcus Faecalis ◽  
Virulence Factors ◽  
Post Infection ◽  
Root Canal ◽  
Caspase 3 ◽  
Ultrastructural Changes ◽  
Expression Levels

To investigate the effects of two Enterococcus faecalis root canal isolated strains (CA1 and CA2) and of the OG1RF strain on apoptosis, pyroptosis, and necroptosis in macrophages. The virulence factors of E. faecalis CA1 and CA2 pathogenic strains were annotated in the Virulence Factors Database (VFDB). E. faecalis CA1, CA2, and OG1RF strains were used to infect RAW264.7 macrophages (MOI, 100:1). We assessed the viability of intracellular and extracellular bacteria and of macrophages at 2, 6, and 12 h post-infection. We used a live cell imaging analysis system to obtain a dynamic curve of cell death after infection by each of the three E. faecalis strains. At 6 and 12 h post-infection, we quantified the mRNA expression levels of PANoptosis-related genes and proteins by RT-qPCR and western blot, respectively. We identified ultrastructural changes in RAW264.7 cells infected with E. faecalis OG1RF using transmission electron microscopy. We found 145 and 160 virulence factors in the CA1 and CA2 strains, respectively. The extracellular CA1 strains grew faster than the CA2 and OG1RF strains, and the amount of intracellular viable bacteria in the OG1RF group was highest at 6 and 12 h post-infection. The macrophages in the CA1 infection group were the first to reach the maximum PI-positivity in the cell death time point curve. We found the expressions of mRNA expression of caspase-1, GSDMD, caspase-3, MLKL, RIPK3, NLRP3, IL-1β and IL-18 and of proteins cleaved caspase-1, GSDMD, cleaved caspase-3 and pMIKL in the macrophages of the three infection groups to be upregulated (P&lt;0.05). We detected ultrastructural changes of apoptosis, pyroptosis, and necroptosis in macrophages infected with E. faecalis. The three E. faecalis strains induced varying degrees of apoptosis, pyroptosis, and necroptosis that were probably associated with PANoptosis in macrophages. The E. faecalis CA1 strain exhibited faster growth and a higher real-time MOI, and it induced higher expression levels of some PANoptosis-related genes and proteins in the infected macrophages than the other strains tested.

scholarly journals Activated cholangiocytes release macrophage-polarizing extracellular vesicles bearing the DAMP S100A11

2019 ◽  
Vol 317 (4) ◽  
pp. C788-C799 ◽  
Author(s):  
Tomohiro Katsumi ◽  
Maria Eugenia Guicciardi ◽  
Adiba Azad ◽  
Steven F. Bronk ◽  
Anuradha Krishnan ◽  
...  
Keyword(s):  
Mrna Expression ◽  
Cell Lines ◽  
Extracellular Vesicles ◽  
Proinflammatory Cytokines ◽  
Proinflammatory Cytokine ◽  
Inflammatory Diseases ◽  
Cell Communication ◽  
Cytokine Expression ◽  
Proinflammatory Cytokine Expression ◽  
Primary Mouse

In mouse models of biliary tract diseases, macrophages are recruited to the periductal milieu and promote injury and cholestasis. Although cell necrosis with release of biomolecules termed damage-associated molecular patterns (DAMPs) promotes recruitment and activation of macrophages, necrosis was not observed in these studies. Because extracellular vesicles (EVs) are important in cell-to-cell communication, we postulated that activated cholangiocytes may release EVs containing DAMPs as cargo. Both the human (NHC) and mouse cholangiocyte (603B) cell lines display constitutive activation with mRNA expression of chemokines. Proteomic analysis revealed that EVs from both cell lines contained the DAMP S100A11, a ligand for the receptor for advanced glycation end products (RAGE). Bone marrow-derived macrophages (BMDM) incubated with EVs derived from the mouse 603B cell line increased mRNA expression of proinflammatory cytokines. Genetic or pharmacologic inhibition of RAGE reduced BMDM expression of proinflammatory cytokines treated with EVs. RAGE signaling resulted in activation of the canonical NF-κB pathway, and consistently, proinflammatory cytokine expression was blunted by the IKKα/β inhibitor TPCA-1 in BMDM incubated with EVs. We also demonstrated that primary mouse cholangiocyte-derived organoids express chemokines indicating cholangiocyte activation, release EVs containing S100A11, and stimulate proinflammatory cytokine expression in BMDM by a RAGE-dependent pathway. In conclusion, these observations identify a non-cell death mechanism for cellular release of DAMPs by activated cholangiocytes, namely by releasing DAMPs as EV cargo. These data also suggest RAGE inhibitors may be salutary in macrophage-associated inflammatory diseases of the bile ducts.

scholarly journals Antiviral Effect of Hyunggaeyungyo-Tang on A549 Cells Infected with Human Coronavirus

2021 ◽  
Vol 2021 ◽  
pp. 1-10
Author(s):  
Seo-Young Won ◽  
In-Chan Seol ◽  
Ho-Ryong Yoo ◽  
Yoon-Sik Kim
Keyword(s):  
Herbal Medicine ◽  
Mrna Expression ◽  
Proinflammatory Cytokines ◽  
A549 Cells ◽  
Control Group ◽  
Inos Mrna ◽  
Mrna Levels ◽  
Expression Levels ◽  
Coronavirus Infection ◽  
Mrna Expression Levels

Background. Herbal medicine is widely recommended to treat viral infectious diseases. Over 123,000,000 individuals have been infected with the coronavirus since a worldwide pandemic was declared in March 2020. We conducted this research to confirm the potential of herbal medicine as a treatment for coronavirus. Methods. We infected the A549 cell line with betacoronavirus OC43 and then treated it with 100 μg/mL Hyunggaeyungyo-tang (HGYGT) or distilled water with a control of HGYGT. We measured the mRNA expression levels of proinflammatory cytokines and interferon stimulated genes (ISGs) to confirm the effectiveness of HGYGT upon coronavirus infection. Results. We found that the effects of HYGYT decrease the expression level of pPKR, peIF2α, IFI6, IFI44, IFI44L, IFI27, IRF7, OASL, and ISG15 when administered to cells with coronavirus infection. The expressions of IL-1, TNF-α, COX-2, NF-κB, iNOS, and IKK mRNA were also significantly decreased in the HGYGT group than in the control group. Conclusion. Through the reduction of the amount of coronavirus RNA, our research indicates that HGYGT has antiviral effects. The reduction of IKK and iNOS mRNA levels indicate that HGYGT reduces coronavirus RNA expression and may inhibit the replication of coronavirus by acting on NF-kB/Rel pathways to protect oxidative injury. In addition, decreases in mRNA expression levels of proinflammatory cytokines indicate that the HGYGT may relieve the symptoms of coronavirus infections.

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