Bae, Seung Il;Jang, Jong Geol;Kim, Hun Tae;Ahn, Hee Yun;Kim, Min Jung;Kim, Hyun Je;Lee, Choong Ki;Hong, Young Hoon
Journal of Yeungnam Medical Science
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v.32
no.2
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pp.127-131
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2015
Churg-Strauss syndrome (CSS) is a necrotizing vasculitis with extra-, peri-vascular eosinophilic infiltration. Chronic symmetric polyarthritis with the presence of rheumatoid factor (RF) and anti-cyclic citrullinated peptide antibody are the mainstay of rheumatoid arthritis (RA) diagnosis. Mononeuritis multiplex is a peripheral neuropathy involving more than 2 separate nerve areas. A 62-year-old male patient was referred for left foot drop and polyarthritis of both hands and feet for 4 months. During evaluation, mononeuritis multiplex was detected on nerve conduction study and electromyography tests: vasculitis with neutrophil, eosinophil, and lymphocyte infiltration on peroneal nerve biopsy. A positive response to methacholin and bronchodilator was observed on the pulmonary function test. Radiologic tests showed peri-articular soft tissue swelling and osteopenia on both hand and foot. Marked peripheral eosinophilia, high RF, and positive perinuclear anti-neutrophil cytoplasmic antibody were detected on blood tests. Here, we report on a patient with overlap syndrome of CSS and RA with review of the relevant literature, from which a few references to overlap syndrome of CSS and RA were available.
Porcine juvenile pustular psoriasiform dermatitis (PJPPD) is a disease of young pigs and characterized by nonpruritic round eruption of skin. The cause of this disease is yet undetermined but is presumed to be genetic predisposition. There may be few opportunities for veterinarian to detect this disease compared with actual situation in field because these lesions resolve spontaneously in two months. The authors detected spontaneous PJPPD case and performed clinical and pathological studies on three pigs from one farm. The specific skin lesions were observed in the forty-day old pigs of mixed breed, which were produced by the sows received semen from the same boar, restrictively. However, there was no skin lesion of pigs in suckling or fattening periods. Grossly, lesions were commonly found on the ventral abdominal part as a papule and were spreaded to the skin of whole body. With the spreading of lesions centrifugally, skin was showed as a umbilicated plaques or mosaic pattern with a few pustules or crusts. Microscopically, the most prominent lesion was the psoriasiform hyperplasia with acanthosis, down growth of rete ridges, exocytosis of eosinophils and neutrophils, ballooning degeneration of superficial epidermis, and koilocytic degeneration of keratinocytes. Additionally, there were moderate dermal edema and severe mixed cellular infiltration, especially eosinophils. No infectious agent which can cause the skin lesion, was detected or cultured, and no lesion caused by infectious agents was also observed, pathologically. With pathological results of this study, it is supposed that pathogenesis or severity of PJPPD may be related to the infiltration of eosinophil or hypersensitivity.
Kim, So Jeong;Lee, Jinju;Choi, Woo Sun;Kim, Hyo Jeong;Kim, Mi-Yeon;Kim, Sun Chang;Kim, Hun Sik
Journal of Ginseng Research
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v.45
no.6
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pp.695-705
/
2021
Background: Ginsenosides have beneficial effects on several airway inflammatory disorders primarily through glucocorticosteroid-like anti-inflammatory activity. Among inflammatory cells, eosinophils play a major pathogenic role in conferring a risk of severe refractory diseases including chronic rhinosinusitis (CRS). However, the role of ginsenosides in reducing eosinophilic inflammation and CRS pathogenesis is unexplored. Methods: We investigated the therapeutic efficacy and underlying mechanism of ginsenoside F1 (G-F1) in comparison with those of dexamethasone, a representative glucocorticosteroid, in a murine model of CRS. The effects of G-F1 or dexamethasone on sinonasal abnormalities and infiltration of eosinophils and mast cells were evaluated by histological analyses. The changes in inflammatory cytokine levels in sinonasal tissues, macrophages, and NK cells were assessed by qPCR, ELISA, and immunohistochemistry. Results: We found that G-F1 significantly attenuated eosinophilic inflammation, mast cell infiltration, epithelial hyperplasia, and mucosal thickening in the sinonasal mucosa of CRS mice. Moreover, G-F1 reduced the expression of IL-4 and IL-13, as well as hematopoietic prostaglandin D synthase required for prostaglandin D2 production. This therapeutic efficacy was associated with increased NK cell function, without suppression of macrophage inflammatory responses. In comparison, dexamethasone potently suppressed macrophage activation. NK cell depletion nullified the therapeutic effects of G-F1, but not dexamethasone, in CRS mice, supporting a causal link between G-F1 and NK cell activity. Conclusion: Our results suggest that potentiating NK cell activity, for example with G-F1, is a promising strategy for resolving eosinophilic inflammation in CRS.
Background : Interleukin-5 (IL-5) is responsible for eosinophilia in allergic diseases. In allergic bronchial asthma, there is a correlation between the extent of eosinophil infiltration in bronchial mucosa and IL-5 concentrations. In addition, IL-2 concentration is elevated in the airways and associated with eosinophilia in symptomatic patients with bronchial asthma. In animal studies, IL-2 can induce eosinophilia by increasing the synthesis of IL-5, however, it is still unknown how IL-2 can induce eosinophila in human being. The aim of this study is to evaluation the effect and mechanism of IL-2 on prolongation of eosinophil survival. Methods : After purifiing the eosinophils from the venous blood of allergic patients with eosinophilia, we measured the survival rates of eosinophils using trypan blue dye exclusion test, and the number of eosinophils with Randolp's solution. We compared the survival rates of eosinophils in the presence of IL-2 or IL-5. Neutralizing antibody for IL-5 was added in IL-2 treated eosinophils to reveal whether IL-2 induced prolongation of eosinophil survival was mediated by IL-5. We checked IL-5 m-RNA expression of lymphocytes in the presence of IL-2 by using Reverse transcription-Polymerase chain reaction (RT-PCR) method to revealed the effect of IL-2 on IL-5 m-RNA expression on lymphocyte. $\alpha$ and $\beta$ IL-2 receptors were measured on eosinophils and lymphocytes with flow-cytometer after stimulated with IL-2. Results : 1) Eosinophil survival rates increased dose dependently on IL-5 and IL-2. 2) The eosinophil survival rates increased by IL-2 were not inhibited by the pretreatment with neutralizing antibody for IL-5. 3) IL-5 m-RNA was not expressed on lymphocytes by the treatment with IL-2 up to 96 hours. 4) IL-2 upregulate the expression of IL-$2R{\alpha}$ on eosinophils, instead of no effect on the expression of IL-$2R{\beta}$. Conclusion: Interleukin-2 had the enhancing effect on the survival rates of eosinophils. The mechanism behind IL-2 induced eosinophilia might be the increment of IL-2 receptors on eosinophils rather than IL-5 synthesis by lymphocytes.
Objectives : To study the effects of Kumsooyukkun-jeon on asthma. Methods : Asthma was induced to Balb/c mice with ovalbumin using the method of Hatfield et al. We measured the histological profiles of lung and trachea, numbers of cellular compartments in the bronchoalveolar lavage fluid (BALF), numbers and morphology of the mast cells in the trachea, numbers of mucous-secretory cells in the bronchus, morphology of the bronchus, ultramicroscopical appearance of surface of trachea and number of cilia and mucous-secretory cells by scanning electron microscope. Results : 1. Hypertrophy of mucous membrane of trachea and bronchus and bronchioles in the lung, peritracheal, peribronchus and peribronchiolar inflammatory cell infiltration, and mucoid exudate deposition the lumen were observed in control groups but these phenomena were recovered in the Kumsooyukkun-jeon groups. 2. Cellular compartments including neutrophil and eosinophil were increased in the BALF of control groups but these phenomena were recovered in the Kumsooyukkun-jeon groups. 3. Degranulation and decrease of the numbers of mast cells were detected in the trachea of control groups. However, these phenomena were recovered in the Kumsooyukkun-jeon groups. 4. Shedding, decrease of cilia cell and increase of mucous-secretory cells in the surface of the trachea were measured in control groups but these phenomena were recovered in the Kumsooyukkun-jeon groups. Conclusions : It is considered that Kumsooyukkun-jeon has somewhat favorable effects on asthma.
Hypereosinophilic syndrome (HES) is characterized by the presense of hypereosinophilia with evidence of target organ damage. We report a patient diagnosed with eosinophilic cystitis and HES. A 7 year old boy had hematuria, dysuria, and increased urinary frequency for 1 day. Laboratory examinations revealed hypereosinophilia (eosinophils, $2,058/{\mu}L$), hematuria, and proteinuria. Abdominal sonography revealed diffuse and severe wall thickening of the bladder. The patient was treated initially with antibiotics. However, his symptoms did not improve after 7 days. A computed tomography scan demonstrated severe wall thickening of the bladder and the hypereosinophilia persisted (eosinophils, $2,985/{\mu}L$). The patient complained of chest discomfort, dyspnea, epigastric pain, and vomiting on hospital day 10. Parasitic, allergic, malignancy, rheumatologic, and immune workups revealed no abnormal findings. Chest X-rays, electrocardiography, and a pulmonary function test were normal; however, the hypereosinophilia was aggravated (eosinophils, $3,934/{\mu}L$). Oral deflazacort was administered. A cystoscopic biopsy showed chronic inflammation with eosinophilic infiltration. The patient's respiratory, gastrointestinal, and urinary symptoms improved after 6 days of steroids, and he was discharged. The eosinophil count decreased dramatically ($182/{\mu}L$). The hypereosinophilia waxed and waned for 7 months, and the oral steroids were tapered and stopped. This case describes a patient diagnosed with eosinophilic cystitis and HES.
This study was carried out to investigate whether asian yellow sand dust (AS) has promoting effects of allergen-related airway inflammation and airway hyperresponsiveness, because the number of patient with allergic asthma and atopy, and with chronic bronchial inflammation and pneumonia have increased steadily in the cities of Korea. The appearance of AS collected was all round and flat, and the diameter was mostly below about 5 ${\mu}m$. When mice were treated with AS suspension by intratracheal instillation combined with ovalalbumin(OVA) sensitization chronically, the level of serum L-lactate dehydrogenase (LDH), IgE and histamine, and respiratory resistance was increased. Intratracheal instillation of AS and OVA also enhanced infiltration of eosinophils in the bronchoalveolar lavage fluid (BALF), IgE and eotaxin expression, and T helper type 2 cell derived cytokines of interleukin (IL)-4, IL-13 and IL-5 as major contributors to allergy and asthma. These results indicate that AS elevates allergen-related airway inflammation and airway hyperresponsiveness in mice and may play an important role in the aggravation of respiratory diseases in Korea.
Allergic rhinitis (AR), one of the most common inflammatory diseases, is caused by immunoglobulin E (IgE)-mediated reactions against inhaled allergens. AR involves mucosal inflammation driven by type 2 helper T (Th2) cells. Previously, it was shown that the Streptococcus pneumoniae pep27 mutant (Δpep27) could prevent and treat allergic asthma by reducing Th2 responses. However, the underlying mechanism of Δpep27 immunization in AR remains undetermined. Here, we investigated the role of Δpep27 immunization in the development and progression of AR and elucidated potential mechanisms. In an ovalbumin (OVA)-induced AR mice model, Δpep27 alleviated allergic symptoms (frequency of sneezing and rubbing) and reduced TLR2 and TLR4 expression, Th2 cytokines, and eosinophil infiltration in the nasal mucosa. Mechanistically, Δpep27 reduced the activation of the NLRP3 inflammasome in the nasal mucosa by down-regulating the Toll-like receptor signaling pathway. In conclusion, Δpep27 seems to alleviate TLR signaling and NLRP3 inflammasome activation to subsequently prevent AR.
Objective : This study was undertaken to investigate effects of Opuntia ficus-indica (OP)extract on an asthma murine model. Methods : The total number of cells and eosinophils in BALF and the infiltration of inflammatory cells into lung tissues were determined by hematoxylin and eosin staining. Results : The number of OVA-induced total cells and eosinophils, a phenomenon of asthma, were decreased by treatment of the animals with OP extract (200 mg/kg) (respectively, p < 0.001 and p<0.01). Furthermore, we showed that OP extract reduced the increased immune cell infiltration induced by ovalbumin (p < 0.01). The levels of interleukin (IL)-4 in BAL fluid were measured by enzyme-linked immunosorbent assay, because the eosinophilia is associated with a T helper (Th) 2 response including IL-4. The level of OVA-induced IL-4 was decreased by OP extract in BAL fluid (p < 0.05). We investigated whether OP extract reduced nitrite (NO) production on lipopolysaccharide (LPS)-stimulated RAW 264.7 sells, because asthma is an inflammatory disease. The level of LPS-induced NO production was decreased by OP extract (50, 100 and 200 mg/ml) on RAW 264.7 cells (respectively, p < 0.05, p<0.01 and p<0.05). Conclusions : Our results indicate that OP extract has an inhibitory effect on lung eosinophilia of asthma and suggest that OP extract is a therapeutic candidate in the treatment of inflammatory disease, including asthma.
The Journal of Korean Medicine Ophthalmology and Otolaryngology and Dermatology
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v.33
no.2
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pp.83-99
/
2020
Objectives : Atopic dermatitis is a chronic inflammatory skin disease with frequent relapses. This study was to investigate the effects of Gammakdaejo-tang(GMD) in DNCB induced atopic dermatitis mice. Methods : The study was divided into five comparion groups. 2,4-dinitrochlorobenzene(DNCB) solution was applied to Nc/Nga mice to induce atopic dermatitis, followed by normal group, negative control group with distilled water, positive control group with Dexamethasione and GMD 200mg/kg or 400mg/kg. The control group was orally administered 200㎕ once daily for 4 weeks. Visual skin condition, Immunoglobulin E, Histamine, Cytokine, Immune cells, Tissue biomarkers were observed. Results : As a result of the dermatitis score evaluation, it was confirmed that the GMD-administered group improved symptoms compared to the negative control group. As a result of measuring IgE, the GMD-administered group significantly decreased compared to the negative control group. As a result of measuring Histamine, GMD group except 200mg/kg of GMD significantly decreased compared to negative control group. As a result of measuring cytokine, GMD 200mg/kg significantly reduced IL-1β, IL-6 and TNF-α compared to the negative control. 400mg/kg significantly reduced IL-1β, IL-4, IL-5, IL-6, IL-10, TNF-α and significantly increased IL-2, IFNγ. As a result of confirming the immune cells, all experimental groups showed no difference in basophil, GMD group significantly reduced monocyte and eosinophil compared to negative control group, and GMD 400mg/kg group significantly reduced white blood cell and neutrophil. And significantly increased lymphocytes. As a result of measuring the gene expression level, all GMD group significantly increased TGF-β1 compared with the negative control group, and filaggrin, VEGF and EGF were significantly increased in GMD 400mg/kg group. Epidermis, dermis thickness, and eosinophil infiltration were found to be decreased in all GMD groups compared with the negative control group. Conclusions : GMD is effective in atopic dermatitis by reducing imbalance of immune response of T cells (Th1 / Th2) and reducing skin tissue damage and inflammatory response.
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