• CELLMED
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• v.11 no.1
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• pp.1.1-1.4
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• 2021

Background: Amavata is a disease that occurs as a result of the error of metabolism. Poor dietary habits and faulty Dincharya (daily regimen) and ritucharya (seasonal regimen) leading to deranged metabolism and Agni (metabolic fire) which results in the formation of Ama(undigested product of metabolism). When Amaconceals with Vata(subtle energy associated with movement) and circulates in the body under the influence of Vyana Vayu (omnipresent air)it clogs the srotasas (microchannels) and initiates the inflammatory cascade. Amavata is commonly correlated with rheumatoid arthritis (RA) while other forms of auto-immune disorders can also be included in Amavata.Dysbiosis of the gut microbiota (GM) has been connected to the onset of diverse autoimmune diseases. In this study, it was hypothesized that Panchakarma (bio-purificatory methods) based intervention such as Virechana Karma (therapeutic purgation) may influence microbiota. Materials and Methods: Various Ayurvedic literature were reviewed for the etiopathogenesis of Amavata. Different databases were searched with research papers related to Gut Dysbiosis and autoimmunity and management of RA. A connecting link between Intestinal Dysbiosis with the autoimmune mechanisms was established and it was also found that the bowel cleansing introduced a change to the GM. Conclusion: It was concluded that Virechana karma is effective in gut flora Dysbiosis. This study aims to correlate the ancient Ayurvedic principles related to Agni Bala(metabolic energy) and biopurificatory treatment modalities like Virechana karma (therapeutic purgation)with the modern concept of gut microbiota and its role in the pathogenesis of various autoimmune disorders such as rheumatoid arthritis. The article creates an understanding about principles of Ayurveda and its rationality in today's scientific world and thereby opens newer vistas of research in therapeutics from Ayurveda, which may be helpful in the management of various immune-mediated Diseases through Ayurveda.

• Toxicological Research
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• v.34 no.1
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• pp.7-12
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• 2018

Laboratory animal models have been developed to investigate preventive or therapeutic effect of medicinal products, or occurrence or progression mechanism of atopic dermatitis (AD), a pruritic and persistent inflammatory skin disease. The murine model with immunologic phenomena resembling human AD was introduced, which demonstrated skewedness toward predominance of type-2 helper T cell reactivity and pathophysiological changes similar as human AD following 2,4-dinitrochlorobenzene (DNCB) sensitization and challenge. Molecular mechanism on the DNCB-mediated AD was further evaluated. Skin tissues were collected from mice treated with DNCB, and each tissue was equally divided into two sections; one for protein and the other for mRNA analysis. Expression of filaggrin, an important protein for keratinocyte integrity, was evaluated through SDS-PAGE. Level of mRNA expression for cytokines was determined through semi-quantitative reverse transcriptase polymerase chain reaction. Expression of filaggrin protein was significantly enhanced in the mice treated with DNCB compared with the vehicle (acetone : olive oil = 4 : 1 mixture) treatment group or the normal group without any treatment. Level of tumor necrosis factor-alpha and interleukin-18 mRNA expression, cytokines involved in activity of type-1 helper T ($T_H1$) cell, was significantly downregulated in the AD group compared with other control groups. These results suggest that suppression of $T_H1$ cell-mediated immune response could be reflected into the skin tissue of mice treated with DNCB for AD induction, and disturbance of keratinocyte integrity might evoke a compensatory mechanism.

• Journal of Physiology & Pathology in Korean Medicine
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• v.17 no.1
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• pp.165-176
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• 2003

The present study was carried out to examine the effects of Kami-hwal-hyeol-tang(KHHT) on the immune responses of synoviocyte cells prepared from the rheumatoid arthritis patients, and also on the collagen-mediated arthritis in mouse model. Several experiments were performed in vitro and in vivo to analyse the immunomodulatory effects of KHHT, and the major findings are summarized below: 1. KHHT did not show the cytotoxicity against mLFCs and hFLSs. 2. KHHT inhibited gene expression of IL-1β, IL-6, TNF-α, COX-2, NOS and GM-CSF in hFLSs. Furthermore, KHHT-treated hFLSs showed reduced production of pro-inflammatory cytokines such as IL-1β and IL-6 compared to the control cells. 3. KHHT treatment of hFLSs inhibited the binding activity of NF-kB and AP-1 to their consensus DNA sequences. 4. KHHT treatment(400 ㎍/㎖) of hFLSs significantly inhibited hFLSs proliferations compared to the control cells. 5. KHHT significantly reduced the production of ROS in hFLSs compared to the control cells. The present data show that KHHT plays an important role for the regulation of AP-1 and NF-kB gene expression. Also, it was found that KHHT has anti-arthritis effect. Further studies of KHHT in relation to RA therapeutics may provide important information to develop drugs to treat this disease.

• Journal of Yeungnam Medical Science
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• v.27 no.1
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• pp.42-46
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• 2010

Eosinophilic myositis is a rare idiopathic inflammatory muscle disease, and the patients with this malady present with diverse signs and symptoms such as muscle swelling, tenderness, pain, weakness, cutaneous lesions and eosinophilia. The etiology and pathogenesis of eosinophilic myositis remain elusive. Several drugs may occasionally initiate an immune mediated inflammatory myopathy, including eosinophilic myositis. We report here on a case a 17-year-old female patient who had taken anti-tuberculosis medicine for tuberculosis pleurisy. She presented with many clinical manifestations, including fever, skin rash, proximal muscle weakness, dyspnea, dysphagia and hypereosinophilia. She was diagnosed with eosinophilic myositis by the pathologic study. The muscle weakness progressed despite of stopping the anti-tuberculosis medicine, but the myositis promptly improved following the administration of glucocorticoid. Although drug induced myopathies may be uncommon, if a patient presents with muscular symptoms, then physicians have to consider the possibility of drug induced myopathies.

• Journal of the Korean Child Neurology Society
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• v.26 no.4
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• pp.284-287
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• 2018

Tuberous sclerosis complex (TSC) is an autosomal dominant disorder caused by mutation of one of two genes, TSC1 (encoding hamartin, 9q34) and TSC2 (encoding tuberin, 16p13). It invades the central nervous system and various parts of the body, causing various symptoms. Crohn's disease (CD) is a chronic immune-mediated disease that has not been clearly elucidated. It is thought to be caused by an excessive immune response of the body to bacteria that normally exist in the digestive tract with genetic factors. No cases have been reported in which both of the above-mentioned diseases occurred simultaneously. We report a case of CD in a patient with TSC. A 12-year-old boy was brought to our hospital because of abdominal pain. Skin lesions were observed in the TSC. Fundus examination revealed a hamartoma in the right retina. Brain magnetic resonance imaging revealed a subendothelial giant cell astrocytoma (SEGA). On the basis of these findings, he was diagnosed as having TSC. Blood test results showed increased levels of inflammatory markers. On abdominal ultrasonography, his colon walls were observed to be thickened with increased vascularity of the proximal ascending colon, ileocecal valve, and terminal ileum. Colonoscopy revealed discontinuous ulcerations and inflammations of the ileum, IC valve, and cecum, similar to those found in CD. Everolimus was administered orally for the SEGA but was discontinued frequently owing to the exacerbation of CD. The possibility of CD should be kept in mind in patients with TSC considering to undergo treatment for SEGA.

• Journal of Oral Medicine and Pain
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• v.44 no.4
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• pp.183-188
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• 2019

Erythema multiforme (EM) is an inflammatory immune-mediated mucosal disease. EM is classified as EM minor or EM major, depending on the severity of symptoms. Most patients with minor or major forms of EM have oral lesions. EM can occur as a result of adverse drug reactions but this is difficult to establish. Several indicators have been developed that can be used as a criterion of evaluation to ensure objectivity in identifying the causality of adverse drug reactions. The Naranjo algorithm was used in the evaluation to ensure objectivity in identifying the causality of adverse drug reactions. There were two cases of patients suspected of having EM induced by drugs. They were both assessed using the Naranjo algorithm to confirm the causality of the disease.

• Journal of Veterinary Science
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• v.23 no.4
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• pp.61.1-61.10
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• 2022

Background: Although there are growing demands for stem cell-based therapy for companion animals in various diseases, a few clinical trials have been reported. Moreover, most of them are the results from only one or a few times of stem cell injection. Objectives: The aim of this study is to describe a long-term treatment with allogeneic adipose-derived stem cells (ASCs) in a dog with rheumatoid arthritis (RA), which is a rare canine disease. Methods: The dog with RA received intravascular injection of allogeneic ASCs derived from two healthy donors once a month for 11 months. To assess therapeutic effects of ASCs, orthopedic examination and clinical evaluation was performed. Cytokines of tumor necrosis factor-α and interleukin-6 in the plasma were measured using ELISA analysis. Results: Despite this repeated and long-term administration of allogeneic ASCs, there were no side effects such as immunorejection responses or cell toxicity. The orthopedic examination score for the dog decreased after ASCs treatment, and the clinical condition of the dog and owner's satisfaction were very good Conclusions: Although ASCs has been suggested as one of the options for RA treatment because of its anti-inflammatory and immunosuppressive functions, it has never been used to treat RA in dogs. The present report describes a case of canine RA treated with allogeneic ASCs for long-term in which the dog showed clinical improvement without adverse effects.

• Journal of Physiology & Pathology in Korean Medicine
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• v.23 no.5
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• pp.1106-1115
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• 2009

Mori Ramulus has multiple applications in Korean traditional medicine prescription because it has antioxidant and anti-inflammatory effects by reducing macrophage activities. Yet, no studies on the anti-arthritic activity of EMR (extract of Mori Ramulus) have been reported in vitro and in vivo. Rheumatoid arthritis (RA) is a systemic autoimmune disease with chronic inflammation characterized by hyperplasia of synovial cells in affected joints, which ultimately leads to the destruction of cartilage and bone. Because collagen-induced arthritis (CIA) is similar to RA in pathological symptoms and immune reactions, there have been several reports concerning RA using CIA mouse model. Here, we investigated the effects of Mori Ramulus on RA using CIA mice. The importance of CD4+ Th1 cells in RA progress was previously indicated and studies further showed that Th17 cells play a prime role in severity of disease. Accordingly, the present study was focused on CIA associated with CD4+ Th1 cells and Th1 7 cells. DBA/1OlaHsd mice were immunized with bovine type II collagen (CII). After a second collagen immunization, mice were treated with EMR once a day for 4 weeks. The severity of arthritis within the paw joints was evaluated by histological assessment of cartilage destruction and pannus formation. Immune cells in peripheral blood mononuclear cells (PBMC), draining lymph node (DLN) and paw joints, cytokine production and gene expression were assessed from CIA mouse using ELISA, FACS and real-time PCR analysis. Administration of EMR significantly suppressed the progression of CIA and inhibited the production of TNF-$\alpha$, IL-6 and IL-17 in the serum. The erosion of cartilage was dramatically reduced in mouse knees after treatment with EMR. In conclusion, our results demonstrate that EMR significantly suppressed the progression of CIA and that this action was mediated by the decreased production of TNF-$\alpha$, IL-6, IL-17 and collagen II-specific antibody in the serum. EMR suppressed Th17 cells and reduced level of IL-6 via B cell suppression, and thus, the levels of autoantibodies produced from B cells were decreased. Furthermore, EMR suppressed NKT cells which directly stimulate B cells and develop imbalance of Th1/Th2 cell. Oral administration of EMR (100 mg/kg or 200 mg/kg) significantly suppressed the progression of CIA, which is comparable to that of methotrexate (MTX, 0.3 mg/kg) used as a positive control. We are currently studying the mechanism underlying the therapeutic role for EMR in CIA mice.

• Journal of Life Science
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• v.14 no.2
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• pp.275-279
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• 2004

Gene polymorphisms of cytokines and their receptors are attractive candidates as genetic factors in the pathogenesis of immune-mediated diseases and have been reported to be associated with disease susceptibility to autoimmune, inflammatory and infectious diseases. IL-29 is one of important candidate genes for complex trait of genetic diseases but there is no published survey of single nucleotide polymorphisms (SNPs) in this gene. In this study, for the first time, we have examined the full genomic sequence of IL-29 including the promoter regions to identify SNPs. We examined the frequencies of genotypes and alleles at the SNP site of IL-29 in allergic rhinitis patients and non-allergic rhinitis controls using the direct sequencing method to determine whether this IL-29 SNP is associated with allergic rhinitis in Korean population. We identified one novel SNP (1184C＞A) in the intron 2 and one novel variation site (-1842_-1841dupGA) in the promoter region of human IL-29 gene. The P values of SNP or variation site were not significant between the healthy controls and allergic rhinitis patients. Our results suggest that the 1184C＞A polymorphism and -1842_-1841dupGA variation site in human IL-29 gene were not associated to allergic rhinitis.

• Korean Journal of Radiology
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• v.25 no.5
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• pp.481-492
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• 2024

Objective: To evaluate the clinical and imaging characteristics of SARS-CoV-2 breakthrough infection in hospitalized immunocompromised patients in comparison with immunocompetent patients. Materials and Methods: This retrospective study analyzed consecutive adult patients hospitalized for COVID-19 who received at least one dose of the SARS-CoV-2 vaccine at two academic medical centers between June 2021 and December 2022. Immunocompromised patients (with active solid organ cancer, active hematologic cancer, active immune-mediated inflammatory disease, status post solid organ transplantation, or acquired immune deficiency syndrome) were compared with immunocompetent patients. Multivariable logistic regression analysis was performed to evaluate the effect of immune status on severe clinical outcomes (in-hospital death, mechanical ventilation, or intensive care unit admission), severe radiologic pneumonia (≥ 25% of lung involvement), and typical CT pneumonia. Results: Of 2218 patients (mean age, 69.5 ± 16.1 years), 274 (12.4%), and 1944 (87.6%) were immunocompromised an immunocompetent, respectively. Patients with active solid organ cancer and patients status post solid organ transplantation had significantly higher risks for severe clinical outcomes (adjusted odds ratio = 1.58 [95% confidence interval {CI}, 1.01-2.47], P = 0.042; and 3.12 [95% CI, 1.47-6.60], P = 0.003, respectively). Patient status post solid organ transplantation and patients with active hematologic cancer were associated with increased risks for severe pneumonia based on chest radiographs (2.96 [95% CI, 1.54-5.67], P = 0.001; and 2.87 [95% CI, 1.50-5.49], P = 0.001, respectively) and for typical CT pneumonia (9.03 [95% CI, 2.49-32.66], P < 0.001; and 4.18 [95% CI, 1.70-10.25], P = 0.002, respectively). Conclusion: Immunocompromised patients with COVID-19 breakthrough infection showed an increased risk of severe clinical outcome, severe pneumonia based on chest radiographs, and typical CT pneumonia. In particular, patients status post solid organ transplantation was specifically found to be associated with a higher risk of all three outcomes than hospitalized immunocompetent patients.