• 제목/요약/키워드: inflammatory disorder

검색결과 299건 처리시간 0.026초

Ibuprofen이 원인으로 추정되는 호산구성 폐렴 1예 (A Case of Eosinophilic Pneumonia with Ibuprofen as the Suspected Etiology)

  • 조성연;이양덕;조용선;김정념;한민수
    • Tuberculosis and Respiratory Diseases
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    • 제55권2호
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    • pp.206-210
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    • 2003
  • 호산구성 폐렴은 폐 간질내에 호산구의 침윤을 보이는 질환으로 말초 혈액에서의 호산구증을 동반하기도 한다. 많은 약제가 호산구성 폐렴을 유발할 수 있지만 비스테로이드성 소염제에 의한 증례는 드물다. 하지만, 비전문의약품으로 분류되는 비스테로이드성 소염제의 종류가 많아지고 이의 오용과 남용이 증가하여 이에 의한 호산구성 폐렴의 발생도 증가하리라 사료된다. 저자들은 기침을 주소로 내원한 남자 환자에서 ibuprofen이 원인으로 추정되는 호산구성 폐렴 1예를 경험하였기에 문헌고찰과 함께 보고하는 바이다.

Effects of Orally-Administered Bifidobacterium animalis subsp. lactis Strain BB12 on Dextran Sodium Sulfate-Induced Colitis in Mice

  • Chae, Jung Min;Heo, Wan;Cho, Hyung Taek;Lee, Dong Hun;Kim, Jun Ho;Rhee, Min Suk;Park, Tae-Sik;Kim, Yong Ki;Lee, Jin Hyup;Kim, Young Jun
    • Journal of Microbiology and Biotechnology
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    • 제28권11호
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    • pp.1800-1805
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    • 2018
  • Inflammatory bowel disease, including Crohn's disease and ulcerative colitis (UC), is a chronically relapsing inflammatory disorder of the gastrointestinal tract. Intestinal epithelial cells (IECs) constitute barrier surfaces and play a critical role in maintaining gut health. Dysregulated immune responses and destruction of IECs disrupt intestinal balance. Dextran sodium sulfate (DSS) is the most widely used chemical for inducing colitis in animals, and its treatment induces colonic inflammation, acute diarrhea, and shortening of the intestine, with clinical and histological similarity to human UC. Current treatments for this inflammatory disorder have poor tolerability and insufficient therapeutic efficacy, and thus, alternative therapeutic approaches are required. Recently, dietary supplements with probiotics have emerged as promising interventions by alleviating disturbances in the indigenous microflora in UC. Thus, we hypothesized that the probiotic Bifidobacterium animalis subsp. lactis strain BB12 could protect against the development of colitis in a DSS-induced mouse model of UC. In the present study, oral administration of BB12 markedly ameliorated DSS-induced colitis, accompanied by reduced tumor necrosis factor-${\alpha}$-mediated IEC apoptosis. These findings indicate that the probiotic strain BB12 can alleviate DSS-induced colitis and suggest a novel mechanism of communication between probiotic microorganisms and intestinal epithelia, which increases intestinal cell survival by modulating pro-apoptotic cytokine expression.

Impact of Upper Limb Joint Fluid Variation on Inflammatory Diseases Diagnosis

  • Hari, Krishnan G.;Ananda, Natarajan R.;Nanda, Anima
    • Journal of Electrical Engineering and Technology
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    • 제9권6호
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    • pp.2114-2117
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    • 2014
  • Joint pain is generally a common disorder not only for the old aged people but also for the immunocompromised patients. The present proposed study reveals the presence of inflammatory diseases in joint generally diagnosed by removing synovial fluid and changes in the volume and composition are examined for the presence of WBC and crystals. This study implement a non-invasive approach to identify the changes in joint fluid by measuring the changes in electrical property of the synovial tissue under the influence of electrical current signal with frequency range between 100 kHz to 300 kHz. The response of tissue for the current signal was measured in terms of potential drop across the tissue. The hardware system design consists of input and output sections. The input section which applies current signal to upper limb joint region is made of ICL8038 function generator IC with amplifier and voltage to current converter. The output section picks voltage variation using metal surface electrode, amplifier, ADC, PIC microcontroller and LCD interface. 100 patient inclusive of normal and disease affected patients where examined for upper limb synovial fluid variation and inflammatory diseases were identified.

Inflammasomes: Molecular Regulation and Implications for Metabolic and Cognitive Diseases

  • Choi, Alexander J.S.;Ryter, Stefan W.
    • Molecules and Cells
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    • 제37권6호
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    • pp.441-448
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    • 2014
  • Inflammasomes are specialized signaling platforms critical for the regulation of innate immune and inflammatory responses. Various NLR family members (i.e., NLRP1, NLRP3, and IPAF) as well as the PYHIN family member AIM2 can form inflammasome complexes. These multiprotein complexes activate inflammatory caspases (i.e., caspase-1) which in turn catalyze the maturation of select pro-inflammatory cytokines, including interleukin (IL)-$1{\beta}$ and IL-18. Activation of the NLRP3 inflammasome typically requires two initiating signals. Toll-like receptor (TLR) and NOD-like receptor (NLR) agonists activate the transcription of pro-inflammatory cytokine genes through an NF-${\kappa}B$-dependent priming signal. Following exposure to extracellular ATP, stimulation of the P2X purinoreceptor-7 ($P2X_7R$), which results in $K^+$ efflux, is required as a second signal for NLRP3 inflammasome formation. Alternative models for NLRP3 activation involve lysosomal destabilization and phagocytic NADPH oxidase and /or mitochondria-dependent reactive oxygen species (ROS) production. In this review we examine regulatory mechanisms that activate the NLRP3 inflammasome pathway. Furthermore, we discuss the potential roles of NLRP3 in metabolic and cognitive diseases, including obesity, type 2 diabetes mellitus, Alzheimer's disease, and major depressive disorder. Novel therapeutics involving inflammasome activation may result in possible clinical applications in the near future.

A Review on Chemical-Induced Inflammatory Bowel Disease Models in Rodents

  • Randhawa, Puneet Kaur;Singh, Kavinder;Singh, Nirmal;Jaggi, Amteshwar Singh
    • The Korean Journal of Physiology and Pharmacology
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    • 제18권4호
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    • pp.279-288
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    • 2014
  • Ulcerative colitis and Crohn's disease are a set of chronic, idiopathic, immunological and relapsing inflammatory disorders of the gastrointestinal tract referred to as inflammatory bowel disorder (IBD). Although the etiological factors involved in the perpetuation of IBD remain uncertain, development of various animal models provides new insights to unveil the onset and the progression of IBD. Various chemical-induced colitis models are widely used on laboratory scale. Furthermore, these models closely mimic morphological, histopathological and symptomatical features of human IBD. Among the chemical-induced colitis models, trinitrobenzene sulfonic acid (TNBS)-induced colitis, oxazolone induced-colitis and dextran sulphate sodium (DSS)-induced colitis models are most widely used. TNBS elicits Th-1 driven immune response, whereas oxazolone predominantly exhibits immune response of Th-2 phenotype. DSS-induced colitis model also induces changes in Th-1/Th-2 cytokine profile. The present review discusses the methodology and rationale of using various chemical-induced colitis models for evaluating the pathogenesis of IBD.

The Ameliorative Effect of Rubi Fructus on DSS-induced Colitis in Mice

  • Myung, Noh-Yil
    • 한국자원식물학회지
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    • 제34권3호
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    • pp.216-222
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    • 2021
  • Ulcerative colitis (UC) is an inflammatory bowel disease and a chronic gastrointestinal disorder. Rubi Fructus (RF), the fruit of Rubus coreanus Miquel, is known to exert several pharmacological effects including anti-oxidative, anti-obesity and anti-inflammatory properties. However, the improving effect and mechanism of RF on intestinal inflammation is not been fully understood. The purpose of this study was to investigate the regulatory effect of RF on dextran sulfate sodium (DSS)-induced colitis in mice. We evaluated the effects of RF on DSS-induced clinical signs by analyzing weight loss and colon length. The inhibitory effects of RF on inflammatory mediators such as prostaglandin E2 (PGE2), cyclooxygenase (COX)-2, as well as the activation of nuclear factor-κB (NF-κB), were determined in colitis tissue. Our data indicated that mice treated with DSS showed clinical symptoms of colitis, including weight loss, colon length decrease and diarrhea. However, we observed that RF treatment significantly improved these clinical symptoms of weight loss, colon length decrease and diarrhea induced by DSS. RF inhibited the enhanced levels of COX-2 and PGE2 caused by DSS. We also showed that the anti-inflammatory mechanism of RF by suppressing the activation of NF-kB in DSS-treated colon tissues. Collectively, the findings of this study indicate the prospect of developing new drugs from RF for UC treatment.

만성 피부 염증소견을 보인 개의 면역학적 특성 분석 연구 (Analysis of Immune Response in Dogs with Chronic Inflammatory Skin Disease)

  • 조선주;고민수;정복기;고재형;윤소라;한동운;이봉주
    • 한국임상수의학회지
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    • 제26권5호
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    • pp.433-440
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    • 2009
  • High levels of inflammatory cytokines were proposed contributors to the pathogenesis of a various inflammatory skin disorders. Therefore, investigating the immune response of the inflammatory skin disorder allows a better understanding of pathogenesis of a various inflammatory skin disorders and therapeutic approaches. The aim of this study was to analyze of the immune response in dogs with chronic inflammatory skin disease. To this aim, the present study evaluated relative mRNA expression of canine $IFN-{\gamma}$, IL-4, $TGF-{\beta}$ and IL-10 using TaqMan realtime PCR assays and semi-quantitative RT-PCR in freshly isolated peripheral blood mononuclear cells from twenty dogs with chronic inflammatory skin disease and ten normal dogs. The relative mRNA expression levels of IL-4 mRNA were significantly higher in dogs with chronic inflammatory skin disease than those in normal dogs (P < 0.01). The results of present study also showed a tendency towards increased expression of IL-10 transcripts in dogs with chronic inflammatory skin disease. However, there were no significant differences in the levels $IFN-{\gamma},\;TGF-{\beta}$ between normal and chronically inflammed dogs. In addition, the concentration of serum IgE was significantly increased in dogs with chronic inflammatory skin disease compared with those in normal dogs (P < 0.01). In histopathological examination, we found that there were markedly increased mast cell counts in chronically inflammed dogs (P < 0.05). These results suggest that the pathogenesis of chronic inflammatory skin disease might be associated with a T-cell mediated inflammatory responses characterized by a Th2-skewed immune response. Based on these results, the modulation of Th1/Th2 balance may be an effective therapeutic strategy for the treatment of chronic inflammatory skin disease.

염증 반응과 수면 장애 (Inflammation and Insufficient or Disordered Sleep)

  • 이석준;김진관
    • 대한임상검사과학회지
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    • 제47권3호
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    • pp.97-104
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    • 2015
  • 수면현상은 인간의 삶의 1/3을 차지하는 중요한 생리적 현상으로 인간의 수면은 신체의 기능을 유지하기 위한 중요한 생리적 기능뿐 아니라 수면을 통한 휴식을 통하여 신체 건강을 유지하고 성장을 유지하는 중요한 역할을 한다. 최근의 급격한 산업화와 정보화로 인하여 급격한 사회 생활구조의 변화를 유발하여 성인뿐 아니라 소아에서도 평균수면 시간의 감소와 다양한 스트레스 환경으로 인한 수면의 질적 저하로 인한 다양한 수면 문제가 사회적 문제로 대두되고 있다. 단순히 수면 부족 또는 수면의 질적 저하뿐 아니라 수면 장애, 특히 폐쇄성 수면 무호흡증은 심혈관 질환뿐 아니라 비만, 대사증후군, 심혈관 질환, 뇌혈관 질환 등 의 다양한 만성 질병의 발생과 깊은 연관성이 있는 것으로 보고하고 있다. 특히 이러한 만성질환을 유발하는 핵심기전으로 염증 반응이 관여하고 있는 것으로 알려져 있으며, 따라서 수면 현상과 다양한 수면 장애에 대한 관심이 급격히 증가하고 있는 실정이다. 비록 수면 무호흡증으로 인한 이러한 질병의 이환에 대한 기전은 다양한 요인이 복합적으로 작용하는 것으로 알려져 있지만 핵심 기전으로 알려진 염증반응의 활성화가 병태 생리학적으로 중요한 역할을 하는 것으로 추측하고 있다. 따라서 최근 수면 무호흡증을 낮은 수준의 만성 염증 질환으로 인식되고 있으며, 더불어 비만과 수면무호흡증으로 인한 연관된 질병의 이환을 더욱 증가시키는 것으로 보고되고 있다. 따라서 본 종설에는 수면의 질적 또는 양적 저하뿐 아니라 폐쇄성 수면 무호흡증으로 인한 염증성 반응의 활성화가 인간의 신체 면역 과정 미치는 영향을 중심으로 최근의 연구 결과 및 수면 무호흡증과 비만의 잠재적 상호작용에 대하여 서술하고자 한다

6-Shogaol reduces progression of experimental endometriosis in vivo and in vitro via regulation of VGEF and inhibition of COX-2 and PGE2-mediated inflammatory responses

  • Wang, Dan;Jiang, Yiling;Yang, Xiaoxin;Wei, Qiong;Wang, Huimin
    • The Korean Journal of Physiology and Pharmacology
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    • 제22권6호
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    • pp.627-636
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    • 2018
  • Endometriosis (EM) is one of the most common gynaecological disorder affecting women in their reproductive age. Mechanisms involved in the pathogenesis of EM remains poorly understood, however inflammatory responses have been reported to be significantly involved. The efficacy of 6-shogaol on proliferation of endometriotic lesions and inflammatory pathways in experimentally-induced EM model was explored in this study. EM was stimulated in Sprague-Dawley rats by implantation of autologous endometrium onto the peritoneum abdominal wall. Separate groups were treated with 6-shogaol (50, 100 or 150 mg/kg b.wt/day) via oral gavage for one month period. Gestrinone (GTN) group received GTN (0.5 mg/kg/day) as positive control. Five weeks after implantation, the spherical volume of ecto-uterine tissues was determined. Treatment with 6-shogaol significantly reduced the implant size. Histological analysis reported atrophy and regression of the lesions. 6-shogaol administration effectively down-regulated $NF-{\kappa}B$ signaling, VEGF and VEGFR-2 (Flk-1) expression in the endometriotic lesions. Excess production of $IL-1{\beta}$ and IL-6 (pro-inflammatory cytokines), PGE2 and nitric oxide (NO) were reduced. Overall, the results of the study reveal the efficacy of 6-shogaol against endometriosis via effectively suppressing proliferation of the lesions and modulating angiogenesis and $COX-2/NF-{\kappa}B$-mediated inflammatory cascades.

대장 상피세포에서 p-Hydroxycinnamic Acid의 항염증 효과와 염증성 장질환에 대한 치료 효과 (Anti-inflammatory Effect of p-Hydroxycinnamic Acid on HT-29 Intestinal Cells and Its Therapeutic Effect of Immune Bowel Disease)

  • 이현수;이승호;최혁재;정길생
    • 생약학회지
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    • 제51권2호
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    • pp.107-114
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    • 2020
  • Inflammatory bowel disease (IBD) is a chronic inflammatory disorder on the large intestine that has been considered as an incurable not only in Western society but also in Eastern Asia in recent years. Despite enormous efforts to develop novel therapeutics for this disease, strategy using bioactive compounds from natural product is still considered as important. p-hydroxycinnamic acid (HCA) is an intermediate substance found in several plants and has been known to possess anti-inflammation but little evidence is reported whether HCA has an inhibitory effect on intestinal inflammation. In the present study, we observed HCA does not show cytotoxic and apoptotic in HT-29 cells. Quantitative PCR analysis revealed that HCA effectively blocks the activity of HT-29 cells stimulated with TNF-α treatment. HCA inhibits translocation of p65 and MAPK pathways in activated HT-29 cells by TNF-α treatment. Besides, oral administration of HCA attenuates manifestation of DSS-induced inflammatory disease in vivo. Histological analysis exhibited that oral administration of HCA recovers IBD symptoms. The expression of pro-inflammatory cytokines were reduced by oral administration of HCA on intestinal tissues. Therefore, these results suggest that HCA has a potent anti-inflammatory effect on intestinal cells as well as show a therapeutic potential for treating IBD in vivo.