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Inhibition of SLPI ameliorates disease activity in experimental autoimmune encephalomyelitis
André Müller, Esther Jun, Hana Conlon, Saud Sadiq
BMC Neuroscience , 2012, DOI: 10.1186/1471-2202-13-30
Abstract: To investigate the pathophysiological effects of SLPI within EAE, we induced SLPI-neutralizing antibodies in mice and rats to determine the clinical severity of the disease. In addition we studied the effects of SLPI on the anti-inflammatory cytokine TGF-β.The induction of SLPI neutralizing antibodies resulted in a milder disease course in mouse and rat EAE. SLPI neutralization was associated with increased serum levels of TGF-β and increased numbers of FoxP3+ CD4+ T cells in lymph nodes. In vitro, the addition of SLPI significantly decreased the number of functional FoxP3+ CD25hi CD4+ regulatory T cells in cultures of naive human CD4+ T cells. Adding recombinant TGF-β to SLPI-treated human T cell cultures neutralized SLPI's inhibitory effect on regulatory T cell differentiation.In EAE, SLPI exerts potent pro-inflammatory actions by modulation of T-cell activity and its neutralization may be beneficial for the disease.The secretory leukocyte protease inhibitor (SLPI) is an 11.7 kDa protein originally identified in bodily secretions such as saliva, seminal fluid, and in the mucus of cervical, nasal and bronchial passages [1]. It was later found in neutrophils, peritoneal macrophages, astrocytes and neurons [2,3] as well as in activated regulatory T cells [4], and was shown to be strongly upregulated in the CNS as a consequence of ischemic stroke [2], spinal cord injury [5] and experimental autoimmune encephalomyelitis (EAE) [3]. SLPI is a potent inhibitor of leukocyte serine proteases, including elastase and cathepsin G from neutrophils, chymase and tryptase from mast cells, and trypsin and chymotrypsin from pancreatic acinar cells [6]. In addition, SLPI suppresses bacterial growth [7], inhibits HIV-1 infection of macrophages [8] and exerts anti-inflammatory functions in macrophages, neutrophils and B cells by inhibition of IκBα degradation [9,10]. Finally, SLPI diminishes inflammatory gene expression and inflammatory cell accumulation after hepatic and lung injuries
Rituximab Therapy Reduces Organ-Specific T Cell Responses and Ameliorates Experimental Autoimmune Encephalomyelitis  [PDF]
Nancy L. Monson,Petra Cravens,Rehana Hussain,Christopher T. Harp,Matthew Cummings,Maria de Pilar Martin,Li-Hong Ben,Julie Do,Jeri-Anne Lyons,Amy Lovette-Racke,Anne H. Cross,Michael K. Racke,Olaf Stüve,Mark Shlomchik,Todd N. Eagar
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0017103
Abstract: Recent clinical trials have established B cell depletion by the anti-CD20 chimeric antibody Rituximab as a beneficial therapy for patients with relapsing-remitting multiple sclerosis (MS). The impact of Rituximab on T cell responses remains largely unexplored. In the experimental autoimmune encephalomyelitis (EAE) model of MS in mice that express human CD20, Rituximab administration rapidly depleted peripheral B cells and strongly reduced EAE severity. B cell depletion was also associated with diminished Delayed Type Hypersensitivity (DTH) and a reduction in T cell proliferation and IL-17 production during recall immune response experiments. While Rituximab is not considered a broad immunosuppressant, our results indicate a role for B cells as a therapeutic cellular target in regulating encephalitogenic T cell responses in specific tissues.
A Nonsecosteroidal Vitamin D Receptor Modulator Ameliorates Experimental Autoimmune Encephalomyelitis without Causing Hypercalcemia  [PDF]
Songqing Na,Yanfei Ma,Jingyong Zhao,Clint Schmidt,Qing Q. Zeng,Srinivasan Chandrasekhar,William W. Chin,Sunil Nagpal
Autoimmune Diseases , 2011, DOI: 10.4061/2011/132958
Abstract: Vitamin D receptor (VDR) agonists are currently the agents of choice for the treatment of psoriasis, a skin inflammatory indication that is believed to involve an autoimmune component. 1,25-dihydroxyvitamin D3 [1,25-(OH)2D3], the biologically active metabolite of vitamin D, has shown efficacy in animal autoimmune disease models of multiple sclerosis, rheumatoid arthritis, inflammatory bowel disease, and type I diabetes. However, the side effect of 1,25-(OH)2D3 and its synthetic secosteroidal analogs is hypercalcemia, which is a major impediment in their clinical development for autoimmune diseases. Hypercalcemia develops as a result of the action of VDR agonists on the intestine. Here, we describe the identification of a VDR modulator (VDRM) compound A that was transcriptionally less active in intestinal cells and as a result exhibited less calcemic activity in vivo than 1,25-(OH)2D3. Cytokine analysis indicated that the VDRM not only modulated the T-helper cell balance from Th1 to Th2 effector function but also inhibited Th17 differentiation. Finally, we demonstrate that the oral administration of compound A inhibited the induction and progress of experimental autoimmune encephalomyelitis in mice without causing hypercalcemia. 1. Introduction Experimental autoimmune encephalomyelitis (EAE), an inflammatory demyelinating disease induced in mice by immunization with myelin components, displays pathological and clinical resemblances to the human demyelinating disease multiple sclerosis (MS). EAE and MS are characterized clinically by neurodegeneration and paralysis and pathologically by demyelination and infiltration of lymphocytes and monocytes into the CNS [1]. Epidemiological studies have shown a global north-south gradient of MS incidence and mortality rates. In other words, geographic distribution of MS prevalence increases with increasing latitude on both sides of the equator [2, 3]. A strong correlation between latitude and MS incidence could be explained by the decreased exposure of susceptible population to UV radiation. Since UV light is required for vitamin D synthesis in the skin, a number of studies have explored the connection between vitamin D and MS. In a prospective epidemiological study (Nurses’ Health Study) involving 187,000 women from 1980 to 2001, intake of vitamin D from supplements was inversely associated with the risk of MS [4]. The notion that vitamin D could be involved in the regulation of disease activity of MS is further strengthened from the observation that lower serum 25-hydroxyvitamin D levels were observed during MS
Artemisinin Analogue SM934 Ameliorates Murine Experimental Autoimmune Encephalomyelitis through Enhancing the Expansion and Functions of Regulatory T Cell  [PDF]
Xin Li, Tian-Tian Li, Xiao-Hui Zhang, Li-Fei Hou, Xiao-Qian Yang, Feng-Hua Zhu, Wei Tang, Jian-Ping Zuo
PLOS ONE , 2013, DOI: 10.1371/journal.pone.0074108
Abstract: Background Artemisinin analogue SM934 was previously reported to possess immunosuppressive properties. The aim of this study was to determine the effects and the underlying mechanisms of SM934 in murine experimental autoimmune encephalomyelitis (EAE). Methods Female C57BL/6 mice immunized with MOG35–55 were treated with or without SM934, then the clinical scores and other relevant parameters were assessed. Th1, Th17 and regulatory T (Treg) cell profiles were determined through ELISA, qRT-PCR, flow cytometry and BrdU incorporation assay. The effects of SM934 on Th1, Th17 and Treg cells differentiation were explored through intracellular staining and flow cytometry examination. Results In vivo, administration of SM934 significantly inhibited the development of EAE and suppressed the elevation of serum IL-17. Ex vivo, upon antigen-recall stimulation, IL-2, IFN-γ, IL-17 and IL-6 production were decreased, whereas IL-10 and TGF-β production were increased from the splenocytes isolated from SM934-treated mice. Consistently, both flow cytometry and qRT-PCR results showed that SM934 treatment significantly increased the Treg, while strongly suppressed the Th17 and Th1, responses in the peripheral. Furthermore, in the spinal lesion, SM934 treatment dramatically decreased the infiltration of CD4+ T cells, within which the Treg cells percentage was enlarged, whereas the Th17, but not Th1 percentage, was significantly decreased comparing with the vehicle-treated groups. Finally, both BrdU incorporation and in vitro Treg differentiation assays revealed that SM934 treatment could directly promote the expansion of Treg cells in vivo and in vitro. Conclusion Taken together, this study demonstrated that SM934 treatment could ameliorate the murine EAE disease, which might be mediated by inducing Treg differentiation and expansion.
Analysis of 128 Cases With Tuberculous Pleurisy  [PDF]
Levent Aky?ld?z,Tekin Y?ld?z,Güng?r Ate?,Baran Gündo?u?
Dicle Medical Journal , 2007,
Abstract: In our country, most common form of extrapulmonary tuberculosis is tuberculous pleurisy. The mean age of patients is increasing to older age in developed countries in last 50 years but tuberculosis is still the illness of early ages in developing countries. We aimed to evaluate retrospectively clinical, radiological and laboratory findings and diagnostic methods of 128 patients with tuberculous pleurisy who were diagnosed as tuberculosis, between 1999 and 2005 in this study. Seventy six patients of all (%59) were males and fifty two cases were females(41%) and mean age of all patients was 39±12 (15-74) year. Pleural adenosine deaminase level was evaluted in 19 patients and mean level of them was 62±23.7 IU/L. Most common symptoms were chest pain and cough. Tuberculosis pleurisy was unilateral in 97.6% of patients. Parenchymal infiltration on Chest X-ray was observed in 18 % of cases. Most common diagnostic method was (used) pleural biopsy in 82% of patients. In conclusion, tuberculosis pleurisy is usually the diseases of young adults. In almost all of the patients, pleural effusion was unilateral and closed pleural biopsy presented high rates of diagnosis in a short time.
1,25-Dihydroxyvitamin D3 Inhibits the Differentiation and Migration of TH17 Cells to Protect against Experimental Autoimmune Encephalomyelitis  [PDF]
Jae-Hoon Chang,Hye-Ran Cha,Dong-Sup Lee,Kyoung Yul Seo,Mi-Na Kweon
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0012925
Abstract: Vitamin D3, the most physiologically relevant form of vitamin D, is an essential organic compound that has been shown to have a crucial effect on the immune responses. Vitamin D3 ameliorates the onset of the experimental autoimmune encephalomyelitis (EAE); however, the direct effect of vitamin D3 on T cells is largely unknown.
Acute Disseminated Encephalomyelitis with Measles  [cached]
Ishrat Jahan,Shaheen Akter,Sharmin Akhtar Rupa
Journal of Enam Medical College , 2013, DOI: http://dx.doi.org/10.3329/jemc.v3i1.13875
Abstract: Acute disseminated encephalomyelitis is an inflammatory demyelinating illness usually associated with infections or antecedent immunization. Due to control of most vaccine preventable diseases in developed countries, most cases of acute disseminated encephalomyelitis occur in developing countries and are seen secondary to nonspecific upper respiratory tract infections. We report a case of acute disseminated encephalomyelitis associated with measles in a 2 -year-old male child despite having measles vaccination in infancy. The diagnosis was based on clinical findings and CT scan of brain. The patient was managed with high dose corticosteroids along with supportive measures. He recovered completely and follow-up for six months revealed no neurological deterioration.
Effects of methotrexate upon inflammatory parameters induced by carrageenan in the mouse model of pleurisy  [PDF]
Eduardo Monguilhott Dalmarco,Tania Silvia Fr de,Yara Santos Medeiros
Mediators of Inflammation , 2002, DOI: 10.1080/09629350210000015700
Abstract: Background: The model of pleurisy induced by carrageenan exhibits a biphasic response (4 and 48 h) and permits the quantification of exudate, cell migration and certain enzymes such as myeloperoxidase (MPO) and adenosine-deaminase (ADA) that are markers of activated leukocytes.
Acute Disseminated Encephalomyelitis
S.K. Gupta , Ajay Gupta, Annil Mahajan, Sourabh Verma, J.B. Singh
JK Science : Journal of Medical Education & Research , 2005,
Abstract: Acute disseminated encephalomyelitis is a multifocul inflammatory myelinopathy of the CNS whichis generally but not exclusively monophasic. Typically it follows after vaccination or some viralinfection. The diagnosis is difficult due to insensitivity of CT imaging and lack of pathognomic clinicaland laboratory features. We highlight the role of MRI in diagnosing an unusual case of ADEMpresenting to us with fever, seizures, hemiparesis and drowsiness who improved remarkably withmethyl prednisolone therapy.
Evaluation of Adenosine Deaminase (Ada) in Tuberculous Pleurisy
American Journal of Medicine and Medical Sciences , 2012, DOI: 10.5923/j.ajmms.20120201.01
Abstract: Tuberculosis is a global health problem whose morbidity and mortality is increasing, as one-third of the world population is estimated to be infected with Mycobacterium tuberculosis and eight million new active cases occur annually commonest being pulmonary tuberculosis and is often associated with effusion. Delay in diagnosis and treatment results in poor prognosis. Adenosine deaminase estimation was done by Blake-Berman method. The purpose of this study is to find out the role of ADA levels in differentiation of tuberculous and non-tuberculous exudative pleural effusions of different etiologies. Adenosine deaminase values were compared between tuberculous and non-tuberculous groups and difference in these values was statistically significant (*p<0.01 for ADA). Adenosine deaminase estimation in pleural fluid has long been taken as a marker for tuberculous pleurisy. ADA levels in non-tuberculous exudative pleural effusions rarely exceeded the cutoff; set for tuberculous disease. The pleural fluid ADA levels were significantly higher in tuberculous exudative pleural effusions when compared with non-tuberculous exudative pleural effusions.
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