• Childhood Kidney Diseases
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• v.8 no.1
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• pp.80-85
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• 2004

The systemic lupus erythematosus(SLE) is a systemic inflammatory disease caused by autoimmune mechanism, involving blood cells, the kidney, the central nervous system, and etc. The heart is one of the frequently involved organs but it is rare as an initial manifestation. Therefore, early suspicion and accurate diagnosis followed by aggressive immunosuppressive therapy including corticosteroid is mandatory for heart-involved patients. We experienced a case of pericardial effusion as an initial manifestation of childhood SLE, which showed immediate response to corticosteroid.

• Journal of Chest Surgery
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• v.47 no.6
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• pp.523-528
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• 2014

Background: Numerous statistical models have been developed to accurately predict outcomes in multiple trauma patients. However, such trauma scoring systems reflect the patient's physiological condition, which can only be determined to a limited extent, and are difficult to use when performing a rapid initial assessment. We studied the predictive ability of the systemic inflammatory response syndrome (SIRS) score compared to other scoring systems. Methods: We retrospectively reviewed 229 patients with multiple trauma combined with chest injury from January 2006 to June 2011. A SIRS score was calculated for patients based on their presentation to the emergency room. The patients were divided into two groups: those with an SIRS score of two points or above and those with an SIRS score of one or zero. Then, the outcomes between the two groups were compared. Furthermore, the ability of the SIRS score and other injury severity scoring systems to predict mortality was compared. Results: Hospital death occurred in 12 patients (5.2%). There were no significant differences in the general characteristics of patients, but the trauma severity scores were significantly different between the two groups. The SIRS scores, number of complications, and mortality rate were significantly higher in those with a SIRS score of two or above (p<0.001). In the multivariant analysis, the SIRS score was the only independent factor related to mortality. Conclusion: The SIRS score is easily calculated on admission and may accurately predict mortality in patients with multiple traumas.

• BMB Reports
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• v.55 no.10
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• pp.473-480
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• 2022

Neutrophils, the most abundant innate immune cells, play essential roles in the innate immune system. As key innate immune cells, neutrophils detect intrusion of pathogens and initiate immune cascades with their functions; swarming (arresting), cytokine production, degranulation, phagocytosis, and projection of neutrophil extracellular trap. Because of their short lifespan and consumption during immune response, neutrophils need to be generated consistently, and generation of newborn neutrophils (granulopoiesis) should fulfill the environmental/systemic demands for training in cases of infection. Accumulating evidence suggests that neutrophils also play important roles in the regulation of adaptive immunity. Neutrophil-mediated immune responses end with apoptosis of the cells, and proper phagocytosis of the apoptotic body (efferocytosis) is crucial for initial and post resolution by producing tolerogenic innate/adaptive immune cells. However, inflammatory cues can impair these cascades, resulting in systemic immune activation; necrotic/pyroptotic neutrophil bodies can aggravate the excessive inflammation, increasing inflammatory macrophage and dendritic cell activation and subsequent T_H1/T_H17 responses contributing to the regulation of the pathogenesis of autoimmune disease. In this review, we briefly introduce recent studies of neutrophil function as players of immune response.

• The Journal of Korean Medicine Ophthalmology and Otolaryngology and Dermatology
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• v.31 no.4
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• pp.22-30
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• 2018

Objectives : The aim of this study is to investigate the relationship between chronic low grade inflammation theory, psoriasis, and herbal medicine. Methods : We reviewed recent studies on the relationship between chronic low-grade inflammation, psoriasis, and herbal medicine through Pubmed. Results : The pathological basis for psoriasis is the action of inflammatory mediators by the activation of the immune response, which can be a cause of various cardiovascular, metabolic and psychological symptoms of psoriasis patients, in addition to skin lesions. The herbal medicines improve these inflammatory conditions and improve local lesions through herbal medicine such as Qingdai, which have a strong inhibitory effect on IL-17,22 production. Conclusions : Herbal medicines used in psoriasis are thought to be effective not only for the improvement of local psoriasis lesions through anti-inflammatory effect but also for the improvement of systemic inflammation associated with chronic low grade inflammation.

• Korean Journal of Acupuncture
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• v.20 no.4
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• pp.53-63
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• 2003

Objective : Experimental studies were done to research the clinical effects of Herba Patriniae(HP) aqua-acupuncture ($BL_{13},\;BL_{17},\;BL_{13}{\cdot}BL_{17}$ and free points) on the anti-allergic inflammatory response. Methods : We measured active systemic anaphylatic shock induced by compound 48/80 and microvascular permeability increased by acetic acid. And we measured total IgE and plasma WBC level, serum total protein, albumin, immunoglobulin and NO levels induced by egg albumin. Results : HP aqua-acupuncture pretreatments at all acupoints inhibited active systemic anaphylatic shock induced by compound 48/80 and microvascular permeability increased by acetic acid. Total IgE and plasma WBC level inhibited by HP aqua-acupuncture pretreatment at $BL_{13}\;BL_{17}$ and free points. However, HP aqua-acupuncture didn't effect serum total protein, albumin, immunoglobulin and NO levels. Conclusion : These results suggest that HP aqua-acupuncture may be beneficial in the regulation of type Ⅰ allergic reaction, but is further required immunological studies on the allergic reaction.

• IMMUNE NETWORK
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• v.16 no.3
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• pp.159-164
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• 2016

IL-33 is a multifunctional cytokine that is released in response to a variety of intrinsic and extrinsic stimuli. The role of IL-33 in Candida albicans infections is just beginning to be revealed. This cytokine has beneficial effects on host defense against systemic C. albicans infections, and it promotes resistance mechanisms by which the immune system eliminates the invading fungal pathogens; and it also elevates host tolerance by reducing the inflammatory response and thereby, potentially, tissue damage. Thus, IL-33 is classified as a cytokine that has evolved functionally to protect the host from damage by pathogens and immunopathology.

• Advances in Traditional Medicine
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• v.3 no.1
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• pp.46-50
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• 2003

We studied the inhibitory effect of Green Life Enzyme (GLE) on compound 48/80-induced anaphylactic response in a murine model. GLE inhibited compound 48/80-induced systemic anaphylactic shock at the dose of 10 g/kg by 87.5%. When GLE was given as pre-treatment at concentrations ranging from 0.01 to 1.0 g/kg, it inhibited passive cutaneous anaphylaxis activated by anti-dinitrophenyl (DNP) IgE. In addition, GLE (0.1 mg/ml) inhibited anti-DNP IgE-induced tumor necrosis $factor-{\alpha}$ production from mast cells by 69% compared to saline value. These results indicate that GLE may possess anti-anaphylactic and anti-inflammatory activity.

• Biomolecules & Therapeutics
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• v.12 no.2
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• pp.62-67
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• 2004

Trauma remains one of the important sources leading to systemic inflammatory response anti sub-sequent multiple organ failure. Although hepatic microvascular dysfunction occurs during trauma, the mechanism responsible remains unclear. The aim of this study was to investigate the effect of trauma on hepatic vascular stress gene expression. Femur fracture (EFx) was induced by torsion to the femur at midshaft. Liver samples were taken for RT-PCR analysis of mRNA for gtenes of interest: endothelin-1 (ET-1), its receptors $ET_A$ and $ET_B$, nitric oxide synthases (iNOS and eNOS), cyclooxygenase-2 (COX-2), heme oxygenase-1 (HO-1), and tumor necrosis tactor-${\alpha}$ (TNF-${\alpha}$). The expression of ET-1 mRNA was significantly increased by FFx. Expression of mRNA in FFx group showed no change in $ET_A$, $ET_B$, iNOS and HO-1 and showed a slight increase of 2.2-fold and 2.7-fold for eNOS tll1d COX-2, respectively. The level of TNF-${\alpha}$ mRNA significantly increased in FFx group. In conclusion, mild trauma alone causes little change in expression of vasoactive mediators.

• Journal of Ginseng Research
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• v.43 no.3
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• pp.335-341
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• 2019

Background: Inflammation is a host-defensive innate immune response to protect the body from pathogenic agents and danger signals induced by cellular changes. Although inflammation is a host-defense mechanism, chronic inflammation is considered a major risk factor for the development of a variety of inflammatory autoimmune diseases, such as rheumatic diseases. Rheumatic diseases are systemic inflammatory and degenerative diseases that primarily affect connective tissues and are characterized by severe chronic inflammation and degeneration of connective tissues. Ginseng and its bioactive ingredients, genocides, have been demonstrated to have antiinflammatory activity and pharmacological effects on various rheumatic diseases by inhibiting the expression and production of inflammatory mediators. Methods: Literature in this review was searched in a PubMed site of National Center for Biotechnology Information. Results: The studies reporting the preventive and therapeutic effects of ginseng and ginsenosides on the pathogenesis of rheumatic diseases were discussed and summarized. Conclusion: Ginseng and ginsenosides play an ameliorative role on rheumatic diseases, and this review provides new insights into ginseng and ginsenosides as promising agents to prevent and treat rheumatic diseases.

• Biomolecules & Therapeutics
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• v.24 no.4
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• pp.387-394
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• 2016

Sepsis, a serious clinical problem, is characterized by a systemic inflammatory response to infection and leads to organ failure. Toll-like receptor (TLR) signaling is intimately implicated in hyper-inflammatory responses and tissue injury during sepsis. Histone deacetylase (HDAC) inhibitors have been reported to exhibit anti-inflammatory properties. The aim of this study was to investigate the hepatoprotective mechanisms of trichostatin A (TSA), a HDAC inhibitor, associated with TLR signaling pathway during sepsis. The anti-inflammatory properties of TSA were assayed in lipopolysaccharide (LPS)-stimulated RAW264.7 cells. Polymicrobial sepsis was induced in mice by cecal ligation and puncture (CLP), a clinically relevant model of sepsis. The mice were intraperitoneally received TSA (1, 2 or 5 mg/kg) 30 min before CLP. The serum and liver samples were collected 6 and 24-h after CLP. TSA inhibited the increased production of tumor necrosis factor (TNF)-${\alpha}$ and interleukin (IL)-6 in LPS-stimulated RAW264.7 cells. TSA improved sepsis-induced mortality, attenuated liver injury and decreased serum TNF-${\alpha}$ and IL-6 levels. CLP increased the levels of TLR4, TLR2 and myeloid differentiation primary response protein 88 (MyD88) protein expression and association of MyD88 with TLR4 and TLR2, which were attenuated by TSA. CLP increased nuclear translocation of nuclear factor kappa B and decreased cytosolic inhibitor of kappa B ($I{\kappa}B$) protein expression, which were attenuated by TSA. Moreover, CLP decreased acetylation of $I{\kappa}B$ kinase (IKK) and increased association of IKK with $I{\kappa}B$ and TSA attenuated these alterations. Our findings suggest that TSA attenuates liver injury by inhibiting TLR-mediated inflammatory response during sepsis.