• Molecules and Cells
• /
• v.44 no.6
• /
• pp.384-391
• /
• 2021

The recent appearance of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has affected millions of people around the world and caused a global pandemic of coronavirus disease 2019 (COVID-19). It has been suggested that uncontrolled, exaggerated inflammation contributes to the adverse outcomes of COVID-19. In this review, we summarize our current understanding of the innate immune response elicited by SARS-CoV-2 infection and the hyperinflammation that contributes to disease severity and death. We also discuss the immunological determinants behind COVID-19 severity and propose a rationale for the underlying mechanisms.

• BMB Reports
• /
• v.53 no.7
• /
• pp.385-390
• /
• 2020

Inflammatory Bowel Disease is caused by an acute or chronic dysfunction of the mucosal inflammatory system in the intestinal tract. In line with the results of our previous study, wherein we found that the PKCα-LSD1-NF-κB signaling plays a critical role in the prolonged activation of the inflammatory response, we aimed to investigate the effect of signaling on colitis in the present study. Lsd1 S112A knock-in (Lsd1^SA/SA) mice, harboring a deficiency in phosphorylation by PKCα, exhibited less severe colitis symptoms and a relatively intact colonic epithelial lining in dextran sulfate sodium (DSS)-induced colitis models. Additionally, a reduction in pro-inflammatory gene expression and immune cell recruitment into damaged colon tissues in Lsd1^SA/SA mice was observed upon DSS administration. Furthermore, LSD1 inhibition alleviated colitis symptoms and reduced colonic inflammatory responses. Both LSD1 phosphorylation and its activity jointly play a role in the progression of DSS-induced colitis. Therefore, the inhibition of LSD1 activity could potentially protect against the colonic inflammatory response.

• Journal of Haehwa Medicine
• /
• v.9 no.2
• /
• pp.315-324
• /
• 2001

To investigate the capacity of anti-inflammatory cytokines and biological response modifiers (BRMs) to induce IL-$1{\beta}$, IL-6, TNF-${\alpha}$ gene overexpression from mouse macrophages, we isolated the resident peritoneal macrophages from BALB/c mouse (8 week old) and incubated for 6 h with lipopolysaccaride (LPS) and Moschus moschiferus (MOMS) extracts. Analysis of inflammatory cytokines gene expression was carried out by RT-PCR amplification. Amplified PCR products were electrophoresed on 1.2% agarose gel, and the analysis (Ht) was used to 1D-density program. 1. LPS and MOMS extract treatments resulted in a significant decrease in IL-$1{\beta}$, IL-6, TNF-${\alpha}$ mRNA expression level compared with the LPS treatment. 2. Among four sample of MOMS, Inhibitory effects of MOMS-A and MOMS-D for inflammatory cytokines gene expression were to be fine compared with the MOMS-Band MOMS-C. According to the above data, Because the anti- tumoral and anti-inflammatory response activities of macrophage are known to be dependent on the production of inflammatory cytokines (IL-$1{\beta}$, IL-6, TNF-${\alpha}$) by macrophages, we suggest that evaluations of BRM for the reduction of inflammatory cytokines production by macrophages are important for clinical application.

• Journal of Physiology & Pathology in Korean Medicine
• /
• v.36 no.1
• /
• pp.28-34
• /
• 2022

Echinacea purpurea (Asteraceae family) is widely used in the European countries and the United States due to its proven immune enhancement and anti-inflammatory effects. Echinacea purpurea has been reported prevent and treat upper respiratory tract infections and common cold, but the underlying molecular mechanisms are not well understood. In the present study, we examined the anti-inflammatory effects and molecular mechanisms of Echinacea purpurea (EP) extract using lipopolysaccharide (LPS)-stimulated signal pathways in RAW264.7 cells. Our results suggest that EP extract exerts anti-inflammatory effects by down-regulating the expression of LPS-induced toll-like receptor 4 (TLR4), subsequently inhibiting the activation of nuclear factor (NF)-κB and mitogen-activated protein kinase (MAPK) signaling pathways and suppression of the release of pro-inflammatory cytokines. These results suggest that EP extract is a potential therapeutic agent for inflammatory diseases.

• Journal of Chest Surgery
• /
• v.37 no.11
• /
• pp.922-924
• /
• 2004

A 55 year old male was admitted for dyspnea. The patient was diagnosed as acute myocardiac infarction, and coronary artery bypass grafting was performed with cardiopulmonary bypass. At postoperative day ＃1, Systemic Inflammatory Response Syndrome was developed with fever, leukocytosis, tachycardia, tachypnea and low systemic vascular resistance. The patient was recovered after being treated with high dose of (36 $\mug/min)$ norepinephrine, and was discharged.

• IMMUNE NETWORK
• /
• v.22 no.6
• /
• pp.46.1-46.25
• /
• 2022

T-helper-17 (Th17) cells and related IL-17-producing (type17) lymphocytes are abundant at the epithelial barrier. In response to bacterial and fungal infection, the signature cytokines IL-17A/F and IL-22 mediate the antimicrobial immune response and contribute to wound healing of injured tissues. Despite their protective function, type17 lymphocytes are also responsible for various chronic inflammatory disorders, including inflammatory bowel disease (IBD) and colitis associated cancer (CAC). A deeper understanding of type17 regulatory mechanisms could ultimately lead to the discovery of therapeutic strategies for the treatment of chronic inflammatory disorders and the prevention of cancer. In this review, we discuss the current understanding of the development and function of type17 immune cells at the intestinal barrier, focusing on the impact of microbiota-immune interactions on intestinal barrier homeostasis and disease etiology.

• Biomedical Science Letters
• /
• v.20 no.2
• /
• pp.96-102
• /
• 2014

Staphylococcal enterotoxin B (SEB) is bacterial toxin that induces the activation of immune cells. Because the inhibition of pro-inflammatory effect of SEB can resolve the inflammation, I determined the influence of functional or structural change of SEB on immune cells. The post translational modification of protein occurs through carbamylation. Carbamylation can change the structure of proteins and can modify the biological activity of protein. In the present study, I investigated the effect of carbamylated SEB (CSEB) on the inflammatory response mediated by LPS in HL-60 cells. To determine the anti-inflammatory effect of CSEB, I produced carbamylated SEB using potassium cyanate (KCN) and then examined whether CSEB involved in cytokine releases and apoptosis of LPS-stimulated HL-60 cells. Although CSEB had not any effect on the LPS-stimulated HL-60 cells, the protein levels of IL-8, TNF-${\alpha}$ and IL-$1{\beta}$ were significantly decreased by CSEB without cytotoxicity. CSEB also blocked Akt and NF-${\kappa}B$ activation. These results indicate that the suppressive effect of CSEB in LPS-stimulated cytokine releases is occurred by inhibition of Akt and NF-${\kappa}B$ activity. Through further studies, CSEB may be used as anti-inflammatory molecule that makes the immune system more efficient.

• Journal of Integrative Natural Science
• /
• v.17 no.1
• /
• pp.21-30
• /
• 2024

Several anti-inflammatory small molecules have been found in the process of the inflammatory response, and these small molecules have been used to treat some inflammatory and autoimmune diseases. Numerous tools for predicting anti-inflammatory peptides (AIPs) have emerged in recent years. However, conducting experimental validations in the lab is both resource-intensive and time-consuming. Current therapies for inflammatory and autoimmune disorders often involve nonspecific anti-inflammatory drugs and immunosuppressants, often with potential side effects. AIPs have been used in treating inflammatory illnesses like Alzheimer's disease and can limit the expression of inflammatory promoters. Recent advances in adverse incident predictions (AIPs) have been made, but it is crucial to acknowledge limitations and imperfections in existing methodologies.

• Journal of Yeungnam Medical Science
• /
• v.40 no.4
• /
• pp.435-441
• /
• 2023

Pheochromocytomas and paragangliomas (PPGLs) may secrete hormones or bioactive neuropeptides such as interleukin-6 (IL-6), which can mask the clinical manifestations of catecholamine hypersecretion. We report the case of a patient with delayed diagnosis of paraganglioma due to the development of IL-6-mediated systemic inflammatory response syndrome (SIRS). A 58-year-old woman presented with dyspnea and flank pain accompanied by SIRS and acute cardiac, kidney, and liver injuries. A left paravertebral mass was incidentally observed on abdominal computed tomography (CT). Biochemical tests revealed increased 24-hour urinary metanephrine (2.12 mg/day), plasma norepinephrine (1,588 pg/mL), plasma normetanephrine (2.27 nmol/L), and IL-6 (16.5 pg/mL) levels. ¹⁸F-fluorodeoxyglucose (FDG) positron emission tomography/CT showed increased uptake of FDG in the left paravertebral mass without metastases. The patient was finally diagnosed with functional paraganglioma crisis. The precipitating factor was unclear, but phendimetrazine tartrate, a norepinephrine-dopamine release drug that the patient regularly took, might have stimulated the paraganglioma. The patient's body temperature and blood pressure were well controlled after alpha-blocker administration, and the retroperitoneal mass was surgically resected successfully. After surgery, the patient's inflammatory, cardiac, renal, and hepatic biomarkers and catecholamine levels improved. In conclusion, our report emphasizes the importance of IL-6-producing PPGLs in the differential diagnosis of SIRS.

• Journal of Physiology & Pathology in Korean Medicine
• /
• v.34 no.1
• /
• pp.7-13
• /
• 2020

Sanyeoleumja (SY) is the traditional Korean medicinal prescription for the treatment of inflammatory diseases of eyes. In this study, the anti-inflammatory effects of SY water extract were investigated. To measure the anti-inflammatory effects of SY, we examined the productions of inflammatory factor including nitric oxide (NO), prostaglandin E2 (PGE₂), inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2), interleukin-6 (IL-6), interleukin-1β (IL-1β) in lipopolysaccharide (LPS)-induced RAW 264.7 cells. SY inhibited NO and PGE₂ production in a dose dependent manner and decreased the protein and mRNA expression of iNOS and COX-2. Also, SY decreased the mRNA expression of interleukin-6 (IL-6) and interleukin-1β (IL-1β). In conclusion, SY downregulated LPS-induced inflammatory factor productions, which could be a clinical basis for inflammatory diseases.