Bu çalışma P01 A1078894 CAG Grant Ulusal Alerji Enstitüleri ve Enfeksiyon Hastalıkları tarafından desteklenen

<ol>
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O., et al. <a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&cmd=Search&doptcmdl=Citation&defaultField=Title+Word&term=Macrophage-Specific+TLR2+Signaling+Mediates+Pathogen-Induced+TNF-Dependent+Inflammatory+Oral+Bone+Loss.">Macrophage-Specific TLR2 Signaling Mediates Pathogen-Induced TNF-Dependent Inflammatory Oral Bone Loss.</a> The Journal of Immunology. , (2012).</li><li>Gibson, F. C., Hong , C., et al. <a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&cmd=Search&doptcmdl=Citation&defaultField=Title+Word&term=Innate+immune+recognition+of+invasive+bacteria+accelerates+atherosclerosis+in+apolipoprotein+E-deficient+mice.">Innate immune recognition of invasive bacteria accelerates atherosclerosis in apolipoprotein E-deficient mice.</a> Circulation. 109 (22), 2801-2806 (2004).</li><li>Miyamoto, T., Yumoto, H., Takahashi, Y., Davey, M., Gibson, F. C., Genco, C. A. <a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&cmd=Search&doptcmdl=Citation&defaultField=Title+Word&term=Pathogen-accelerated+atherosclerosis+occurs+early+after+exposure+and+can+be+prevented+via+immunization.">Pathogen-accelerated atherosclerosis occurs early after exposure and can be prevented via immunization.</a> Infection and Immunity. 74 (2), 1376-1380 (2006).</li><li>Baker, P. J., Dixon, M., Roopenian, D. C. <a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&cmd=Search&doptcmdl=Citation&defaultField=Title+Word&term=Genetic+control+of+susceptibility+to+Porphyromonas+gingivalis-induced+alveolar+bone+loss+in+mice.">Genetic control of susceptibility to Porphyromonas gingivalis-induced alveolar bone loss in mice.</a> Infection and Immunity. 68 (10), 5864-5868 (2000).</li><li>Baker, P. J., Dixon, M., Evans, R. T., Roopenian, D. C. <a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&cmd=Search&doptcmdl=Citation&defaultField=Title+Word&term=Heterogeneity+of+Porphyromonas+gingivalis+strains+in+the+induction+of+alveolar+bone+loss+in+mice.">Heterogeneity of Porphyromonas gingivalis strains in the induction of alveolar bone loss in mice.</a> Oral Microbiology and Immunology. 15 (1), 27-32 (2000).</li><li>Daugherty, A. <a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&cmd=Search&doptcmdl=Citation&defaultField=Title+Word&term=Mouse+models+of+atherosclerosis.">Mouse models of atherosclerosis.</a> The American Journal of the Medical Sciences. 323 (1), 3-10 (2002).</li><li>Weinreb, D. B., Aguinaldo, J. G. S., Feig, J. E., Fisher, E. A., Fayad, Z. A. <a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&cmd=Search&doptcmdl=Citation&defaultField=Title+Word&term=Non-invasive+MRI+of+mouse+models+of+atherosclerosis.">Non-invasive MRI of mouse models of atherosclerosis.</a> NMR in Biomedicine. 20 (3), 256-264 (2007).</li></ol>

Yazarlar hiçbir rakip mali çıkarlarının olmadığını beyan ederim.

S. gingivalis ağızdan enfeksiyon modeli lokal ve sistemik siteleri patojen kaynaklı kronik enflamasyon çalışma için değerli bir araç sağlar. Bu benzersiz model, kronik inflamasyon ve İmmünopatolojiye katkıda hem ev sahibi ve patojen spesifik mekanizmaların karakterizasyonu izin verir. Buna ek olarak, bağışıklık kazandırma ve model farmakolojik müdahale dahil, yeni tedavi stratejileri, taranması için de kullanılabilir. Bu protokolde belirtilen adımlar P. başlamasını, ilerleme...

Kronik inflamasyon patolojik doku hasarı ve insanlarda birçok kronik hastalıkların bir birleştirici özelliği önemli bir sürücüdür. Bu hastalıklar neoplastik, otoimmün ve kronik enflamatuar hastalıklar 1 içerir. Birçok kronik hastalığın etyolojisi bilinmemektedir ama genetik yatkınlık ve çevresel faktörlerin de tanışmasını içeren, karmaşık ve çok faktörlü olduğu anlaşılmaktadır. Enflamasyon ettiricileri zor olmaya devam ederken immün aktivasyon hücresel ve moleküler profilleri patojenlere karşı ev sahibi tepkilerin 2 gözlenen desenleri ile önemli ölçüde üst üste gelir. Montaj kanıt mikrobiyal gelişme patojenler ve kronik inflamasyon ilerlemesi ve onun çeşitli klinik belirtiler 2,3 ile enfeksiyon implicates. Patojenler neden ve kalıcı enfeksiyonlar konak bağışıklık sistemini yıkarak ve kurarak kronik enflamasyonu doğrudan sürdürmek <sup&gt; 4. Mikrobiyal kalıcılık yokluğunda, enfeksiyon, self-antijenlere moleküler taklidin tetiklenen oto-bağışıklık tepkilerinin, imünojenik hale getirmek, self-antijenlere ya da daha önce maskeli ana antijenleri açıklamaları zarar değişikliklerden kaynaklanan kronik enflamasyonu hızlandırabilir. Nadiren, ancak spesifik patojenler özel bir kronik hastalık evrensel nedeni olarak tanımlanmıştır. Aksine, mevcut verilerin çoğunluğu patojenler genetik olarak yatkın konak 3 klinik belirtileri ve hastalık sonuçları geniş bir yelpazede ile kronik inflamasyon ortaya çıkarmak için farklı mekanizmaları kullandığını iddia. Böylece, spesifik patojenler önemli bir halk sağlığı etkileri yanı sıra, pek çok kronik hastalıkların tedavisi ve önlenmesi olabilir kronik enflamasyona neden olan mekanizmaların ayrıntılı bir anlayış. Kronik inflamasyon indüksiyon ve bakım katkıda konak ve patojen spesifik mekanizmalar olmasına rağmenkötü patojen kaynaklı kronik inflamasyon modellemede gelişmeler bu süreçlerin anlayışımızı ilerletmek için başladı, anladım. S. gingivalis oral enfeksiyon modeli konak ve patojen lokal (oral kemik kaybı) kronik enflamasyon katkıda özgü mekanizmaları ve sistemik siteleri (ateroskleroz) 5,6 analizi izin verir patojen kaynaklı kronik inflamasyon eşsiz, iyi karakterize fare modelidir. S. gingivalis insan periodontal hastalık, doku 7 nolu destekleme dişin tahribatı ile karakterize edilen bir enfeksiyon kaynaklı kronik enflamatuar hastalıkta rol oynayan bir gram-negatif anaerob ağızdan patojendir. Enfeksiyonun başlangıç ​​yerinde patoloji ek olarak, artan kanıtlar P. implicates gingivalis aterosklerozun gelişiminde ve 5 dahil sistemik hastalıkların ilerlemesinde kronik inflamasyon -sebepli, bir hastalık kronik iltihabın özelliği, arter damar duvarının: n. P. olan spesifik patojensiz farelerde ağızdan enfeksiyonu gingivalis alveoler kemik 8 destek dişin tahribatıyla sonuçlanan bir inflamatuar yanıtı tetikler. P. gingivalis 42 gün Enfeksiyondan 8 ve farenin patogene-özgü serum antikor titrelerinin yüksek seviyelerini 9 geliştirmek için, enfekte edilmiş farelerin ağızlarından elde edilebilir. - / - Apo-E kullanılarak aterosklerozun yerleşmiş fare modelinde farenin (Apo - / -), P. ile ağızdan enfeksiyondan gingivalis aort sinüs 10 ve innominat arter 11 inflamatuar plak birikimini sürücüler kronik enflamasyona neden olur. P. innominat arter içinde ilerici inflamasyon gingivalis farenin in vivo MRG kullanılarak canlı hayvanlarda izlenebilir ğında. Histolojik olarak, P., arter lezyonlar gingivalis farenin lipidler accompa artmış birikimini sergilemek ğındavasküler endotel aktivasyonu, artmış bir immün hücre infiltrasyonu ve iltihap aracılarının 12 artmış ekspresyonu ile reddedilmiş. Nakavt farelerde, bu modelin kullanımı, ana sinyal parçalan ve iltihaplanma aracılan rolü, hem de hücre S. sürücü spesifik etkileşimler açıklamıştır 14 - gingivalis immünopatoloji 12 -kaynaklı. Buna ek olarak, tarif bakteriyel mutantlar kullanılarak deneyler önemli S. belirledik gingivalis lokal ve sistemik sitelerinde 15 kronik enflamasyon katkıda bulunan faktörleri virülansa. Bu makale P. değerlendirilmesi için yöntemler detayları gingivalis lokal ve sistemik sitelerinde kronik inflamasyon -kaynaklı. Bu Witt yazılımı kullanılarak mikroBT alveol kemiği kaybı analizi için ayrıntılı bir protokol sağlar. Ayrıca, biz ilerici değerlendirmesinde vivo, canlı hayvan MRG serial yararını tanımlamakinnominat arter içinde inflamasyon. Biz görselleştirme ve arteriyel lezyonlarda inflamatuar plak ölçümü için yöntemler içerir ve histolojik karakterizasyonu açıklar. Transgenik farelerden ve tanımlı bakteriyel mutantlarının kullanımı ana ve hastalığın başlaması, ilerlemesi ve sonuç olarak ilgili mikrobiyal faktörlerini tanımlamak için bu model özellikle uygun hale getirir. Buna ek olarak, model, aşı ve farmakolojik müdahale dahil, yeni tedavi stratejileri, taranması için de kullanılabilir.

<table><tbody><tr><td>Amira analysis software</td><td>Visualization Sciences Group</td><td></td><td></td></tr><tr><td>Anaerobic chamber DW Scientific Model MG500&amp;nbsp;</td><td>Microbiology International</td><td></td><td></td></tr><tr><td>BHI&amp;nbsp;</td><td>Becton-Dickinson&amp;nbsp;</td><td>211059</td><td></td></tr><tr><td>Hemin&amp;nbsp;</td><td>Sigma-Aldrich&amp;nbsp;</td><td>51280-5G</td><td></td></tr><tr><td>Menadione (Vitamin K)</td><td>Sigma-Aldrich&amp;nbsp;&amp;nbsp;</td><td>M5625-25G</td><td></td></tr><tr><td>Yeast Extract</td><td>Becton-Dickinson&amp;nbsp;</td><td>212750</td><td></td></tr><tr><td>Carboxymethyl cellulose (medium viscocity)&amp;nbsp;</td><td>Sigma-Aldrich&amp;nbsp;</td><td>C-4888</td><td></td></tr><tr><td>Sulfamethoxazole and trimethoprim oral suspension 200 mg/40 mg per 5 ml</td><td>Hi-Tech Pharmacal</td><td>NDC 50383-823-16</td><td></td></tr><tr><td>&amp;mu;CT 40&amp;nbsp;</td><td>Scanco</td><td></td><td></td></tr><tr><td>HistoChoice Tissue Fixative</td><td>Sigma-Aldrich&amp;nbsp;</td><td>H2904</td><td></td></tr><tr><td>Sudan IV</td><td>Sigma-Aldrich&amp;nbsp;</td><td>S4261-25G</td><td></td></tr><tr><td>Vertical-bore 11.7T Avance spectrometer&amp;nbsp;</td><td>Bruker</td><td></td><td></td></tr><tr><td>Paravision</td><td>Paravision</td><td></td><td></td></tr><tr><td>ImageJ</td><td>NIH</td><td></td><td></td></tr><tr><td>Rat anti-mouse F4/80</td><td>Serotec</td><td>MCA497R</td><td></td></tr><tr><td>Rat anti-mouse TLR2</td><td>eBioscience</td><td>13-9021-80</td><td></td></tr><tr><td>Leica S4 dissecting scope</td><td>Leica</td><td></td><td></td></tr><tr><td>Microm HM 550 cryostat</td><td>Microm</td><td></td><td></td></tr></tbody></table>

a mouse model for pathogen-induced chronic inflammation at local and systemic sites

Kronik inflamasyon patolojik doku hasarı ve neoplastik, otoimmün ve kronik iltihaplı hastalıklar, insanlarda pek çok kronik hastalıkların bir birleştirici özelliği önemli bir sürücüdür. Delil gelişen klinik belirtilerin çok çeşitli geliştirme ve kronik hastalıkların ilerlemesinde patojen kaynaklı kronik inflamasyon implicates. Kronik hastalığı karmaşık ve çok faktörlü etiyolojisi, nedensellik kanıtı ve mekanik bağlantıların kurulması için deney tasarlama insanlarda neredeyse imkansız. Hayvan modelleri kullanmanın bir avantajı özel bir hastalığın seyrini etkilediği, her ikisi de, genetik ve çevresel faktörler kontrol edilebilir olmasıdır. Böylece, enfeksiyon ilgili hayvan modelleri tasarlarken kronik inflamasyona katkıda konak ve patojen spesifik mekanizmaları belirlemede önemli bir adımı temsil etmektedir. Burada patojen kaynaklı kronik Serma bir fare modeli tarifOral patojen Porphyromonas gingivalis, çok insanlarda periodontal hastalık ile bağlantılı bir bakteri ile enfeksiyondan sonra, lokal ve sistemik sitelerde mmation. Özgül patojen içermeyen farelere ağızdan enfeksiyonu alveoler kemik, periodontal hastalık bir işaretidir destek dişin tahribatı ile sonuçlanan bir inflamatuar yanıtı tetikler. P. ile kurulmuş bir fare ateroskleroz modelinde, enfeksiyon gingivalis, vasküler endotel aktivasyonu, artmış bir immün hücre infiltrasyonu ve lezyonlarında iltihap aracılarının yükselen sentezlenmesi ile birlikte aort sinüs ve iliyak arteri içindeki inflamatuar plak birikimini hızlandırır. Biz lokal ve sistemik sitelerinde inflamasyon değerlendirilmesi için ayrıntılı metodolojiler. Transgenik farelerden ve tanımlı bakteriyel mutantlarının kullanımı ana ve hastalığın başlaması, ilerlemesi ve sonuç olarak ilgili mikrobiyal faktörlerini tanımlamak için bu model özellikle uygun hale getirir. Additionally modeli aşı ve farmakolojik müdahale dahil, yeni tedavi stratejileri, taranması için de kullanılabilir.

Uygun fare modeli ve oral enfeksiyon rejimi, S. kullanma gingivalis kronik inflamasyon ve Immunopathology yerel (oral kavite) seviyesinde ve sistemik the (atardamar) (Şekil 1) indükler. Farelerde, P. ile ağızdan enfeksiyondan gingivalis alveoler kemik 8 destek dişin yok edilmesini sağlayan bir inflamatuar yanıtı tetikler. P. gingivalis farenin ağırlıklı IgG izo 9 vardır, bu organizma için, serum...

Watch this Scientific Journal Video about A Mouse Model for Pathogen-induced Chronic Inflammation at Local and Systemic Sites at JoVE.com

A Mouse Model for Pathogen-induced Chronic Inflammation at Local and Systemic Sites

Hayvan modelleri kronik inflamasyon gelişimine katkıda konak ve patojen spesifik mekanizmaları tanımlarken paha biçilmez araçlardır olduğu kanıtlanmıştır. Burada, lokal ve sistemik inflamasyon bölgelerinde ilerlemesini değerlendirmek için insan patojeni Porphyromonas gingivalis ve detay metodolojileri ile ağızdan enfeksiyondan bir fare modeli tarif eder.

Lokal ve sistemik Yer de patojen kaynaklı kronik enflamasyon Fare Modeli

Chronic inflammation is a major driver of pathological tissue damage and a unifying characteristic of many chronic diseases in humans including ...

a-mouse-model-for-pathogen-induced-chronic-inflammation-at-local

Universidad de Cartagena UDEC

Research

JoVE Journal

Immunology and Infection

17.5K Görüntüleme.  Boston University School of Medicine.  Hayvan modelleri kronik inflamasyon gelişimine katkıda konak ve patojen spesifik mekanizmaları tanımlarken paha biçilmez araçlardır olduğu kanıtlanmıştır. Burada, lokal ve sistemik inflamasyon bölgelerinde ilerlemesini değerlendirmek için insan patojeni Porphyromonas gingivalis ve detay metodolojileri ile ağızdan enfeksiyondan bir fare modeli tarif eder. 

Video: A Mouse Model for Pathogen-induced Chronic Inflammation at Local and Systemic Sites

The Citrobacter rodentium Mouse Model: Studying Pathogen and Host Contributions to Infectious Colitis

This protocol outlines the steps required to produce a robust model of infectious disease and colitis, as well as the methods used to characterize Citrobacter rodentium infection in mice. C. rodentium is a gram negative, murine specific bacterial pathogen that is closely related to the clinically important human pathogens enteropathogenic E. coli and enterohemorrhagic E. coli. Upon infection with C. rodentium, immunocompetent mice suffer from modest and transient weight loss and diarrhea. Histologically, intestinal crypt elongation, immune cell infiltration, and goblet cell depletion are observed. Clearance of infection is achieved after 3 to 4 weeks. Measurement of intestinal epithelial barrier integrity, bacterial load, and histological damage at different time points after infection, allow the characterization of mouse strains susceptible to infection.
The virulence mechanisms by which bacterial pathogens colonize the intestinal tract of their hosts, as well as specific host responses that defend against such infections are poorly understood. Therefore the C. rodentium model of enteric bacterial infection serves as a valuable tool to aid in our understanding of these processes. Enteric bacteria have also been linked to Inflammatory Bowel Diseases (IBDs). It has been hypothesized that the maladaptive chronic inflammatory responses seen in IBD patients develop in genetically susceptible individuals following abnormal exposure of the intestinal mucosal immune system to enteric bacteria. Therefore, the study of models of infectious colitis offers significant potential for defining potentially pathogenic host responses to enteric bacteria. C. rodentium induced colitis is one such rare model that allows for the analysis of host responses to enteric bacteria, furthering our understanding of potential mechanisms of IBD pathogenesis; essential in the development of novel preventative and therapeutic treatments.

The Citrobacter rodentium Mouse Model: Studying Pathogen and Host Contributions to Infectious Colitis

Citrobacter rodentium infection provides a valuable model to study enteric bacterial infections as well as host immune responses and colitis in mice. This protocol outlines the measurement of barrier integrity, pathogen load and histological damage allowing for the thorough characterization of pathogen and host contributions to murine infectious colitis.

<em&gt; Citrobacter rodentium</em&gt; Mouse Model: Bulaşıcı Kolit için çalışılması Patojen ve Host Katılımlar

This protocol  outlines the steps required to produce a robust model of infectious disease and  colitis, as well as the methods used to characterize ...

İmmünoloji ve Enfeksiyon

Humanized Mouse Model to Study Bacterial Infections Targeting the Microvasculature

Neisseria meningitidis causes a severe, frequently fatal sepsis when it enters the human blood stream. Infection leads to extensive damage of the blood vessels resulting in vascular leak, the development of purpuric rashes and eventual tissue necrosis. Studying the pathogenesis of this infection was previously limited by the human specificity of the bacteria, which makes in vivo models difficult. In this protocol, we describe a humanized model for this infection in which human skin, containing dermal microvessels, is grafted onto immunocompromised mice. These vessels anastomose with the mouse circulation while maintaining their human characteristics. Once introduced into this model, N. meningitidis adhere exclusively to the human vessels, resulting in extensive vascular damage, inflammation and in some cases the development of purpuric rash. This protocol describes the grafting, infection and evaluation steps of this model in the context of N. meningitidis infection. The technique may be applied to numerous human specific pathogens that infect the blood stream.

Neisseria meningitidis is a human specific pathogen that infects blood vessels. In this protocol human microvessels are introduced into a mouse by grafting human skin onto immunocompromised mice. Bacteria adhere extensively to the human vessels, leading to vascular damage and development of the purpuric rash typically observed in human cases.

Insanlaşmış Fare Modeli mikrovaskülatürde Hedefleme Bakteriyel Enfeksiyonlar Eğitim için

Neisseria meningitidis causes a severe, frequently fatal sepsis when it enters the human blood stream. Infection leads to extensive damage of the blood ...

Chronic Salmonella Infected Mouse Model

The bacterial infected mouse model is a powerful model system for studying areas such as infection, inflammation, immunology, signal transduction, and tumorigenesis. Many researchers have taken advantage of the colitis induced by Salmonella typhimurium for the studies on the early phase of inflammation and infection. However, only few reports are on the chronic infection in vivo. Mice with Salmonella persistent existence in the gastrointestinal tract allow us to explore the long-term host-bacterial interaction, signal transduction, and tumorigenesis. We have established a chronic bacterial infected mouse model with Salmonella typhimurium colonization in the mouse intestine over 6 months. To use this system, it is necessary for the researcher to learn how to prepare the bacterial culture and gavage the animals. We detail a methodology for prepare bacterial culture and gavage mice. We also show how to detect the Salmonella persistence in the gastrointestinal tract. Overall, this protocol will aid researchers using the bacterial infected mouse model to address fundamentally important biological and microbiological questions.

Chronic Salmonella Infected Mouse Model

Establish a chronic bacterial infected mouse model with persistent Salmonella typhimurium colonization in intestine for 27 weeks.

Kronik Salmonella Infected Fare Modeli

The bacterial infected mouse model is a powerful model system for studying areas such as infection, inflammation, immunology, signal transduction, and ...

Biyoloji

Induction of Experimental Autoimmune Encephalomyelitis in Mice and Evaluation of the Disease-dependent Distribution of Immune Cells in Various Tissues

Multiple sclerosis is presumed to be an inflammatory autoimmune disease, which is characterized by lesion formation in the central nervous system (CNS) resulting in cognitive and motor impairment. Experimental autoimmune encephalomyelitis (EAE) is a useful animal model of MS, because it is also characterized by lesion formation in the CNS, motor impairment and is also driven by autoimmune and inflammatory reactions. One of the EAE models is induced with a peptide derived from the myelin oligodendrocyte protein (MOG)35-55 in mice. The EAE mice develop a progressive disease course. This course is divided into three phases: the preclinical phase (day 0 - 9), the disease onset (day 10 - 11) and the acute phase (day 12 - 14). MS and EAE are induced by autoreactive T cells that infiltrate the CNS. These T cells secrete chemokines and cytokines which lead to the recruitment of further immune cells. Therefore, the immune cell distribution in the spinal cord during the three disease phases was investigated. To highlight the time point of the disease at which the activation/proliferation/accumulation of T cells, B cells and monocytes starts, the immune cell distribution in lymph nodes, spleen and blood was also assessed. Furthermore, the levels of several cytokines (IL-1&#946;, IL-6, IL-23, TNF&#945;, IFN&#947;) in the three disease phases were determined, to gain insight into the inflammatory processes of the disease. In conclusion, the data provide an overview of the functional profile of immune cells during EAE pathology.

This manuscript describes the methods for induction and scoring of the experimental autoimmune encephalomyelitis (EAE) model, together with the assessment of immune cell distribution and mRNA cytokine levels in lymph nodes, spleen, blood and spinal cord using flow cytometry and quantitative PCR, respectively, at various disease phases.

Çeşitli Dokularda Bağışıklık Hücreleri Hastalık bağımlı Dağıtım Fareler ve Değerlendirilmesi Deneysel Otoimmün Ensefalomyelitli indüksiyon

Multiple sclerosis is presumed to be an inflammatory autoimmune disease, which is characterized by lesion formation in the central nervous system (CNS) ...

An IL-8 Transiently Transgenized Mouse Model for the In Vivo Long-term Monitoring of Inflammatory Responses

Airway inflammation is often associated with bacterial infections and represents a major determinant of lung disease. The in vivo determination of the pro-inflammatory capabilities of various factors is challenging and requires terminal procedures, such as bronchoalveolar lavage and the removal of lungs for in situ analysis, precluding longitudinal visualization in the same mouse. Here, lung inflammation is induced through the intratracheal instillation of Pseudomonas aeruginosa culture supernatant (SN) in transiently transgenized mice expressing the luciferase reporter gene under the control of a heterologous IL-8 bovine promoter. Luciferase expression in the lung is monitored by in vivo bioluminescent image (BLI) analysis over a 2.5- to 48-h timeframe following the instillation. The procedure can be repeated multiple times within 2 - 3 months, thus permitting the evaluation of the inflammatory response in the same mice without the need to terminate the animals. This approach permits the monitoring of pro- and anti-inflammatory factors acting in the lung in real time and appears suitable for functional and pharmacological studies.

An IL-8 Transiently Transgenized Mouse Model for the In Vivo Long-term Monitoring of Inflammatory Responses

The method described here allows for the visualization of IL-8 promoter-dependent inflammation activation in the lungs of mice through non-invasive bioluminescence imaging (BLI). The same animal can be subjected to BLI multiple times for up to two months from the time of delivery of the luciferase reporter construct.

Bir IL-8 Geçici Transgenize Edilmiş Fare Modeli<emIn vivo</em&gt; İnflamatuvar Yanıtların Uzun Vadeli İzlenmesi

Airway inflammation is often associated with bacterial infections and represents a major determinant of lung disease. The in vivo determination of the ...

The bm12 Inducible Model of Systemic Lupus Erythematosus (SLE) in C57BL/6 Mice

Systemic lupus erythematosus (SLE) is an autoimmune disease with diverse clinical and immunological manifestations. Several spontaneous and inducible animal models mirror common components of human disease, including the bm12 transfer model. Upon transfer of bm12 splenocytes or purified CD4 T cells, C57BL/6 mice rapidly develop large frequencies of T follicular helper cells (Tfh), germinal center (GC) B cells, and plasma cells followed by high levels of circulating anti-nuclear antibodies. Since this model utilizes mice on a pure C57BL/6 background, researchers can quickly and easily study disease progression in transgenic or knockout mouse strains in a relatively short period of time. Here we describe protocols for the induction of the model and the quantitation Tfh, GC B cells, and plasma cells by multi-color flow cytometry. Importantly, these protocols can also be used to characterize disease in most mouse models of SLE and identify Tfh, GC B cells, and plasma cells in other disease models.

The bm12 Inducible Model of Systemic Lupus Erythematosus SLE in C57BL/6 Mice

The transfer of bm12 lymphocytes into a C57BL/6 recipient is an established model of systemic lupus erythematosus. Here we describe how to initiate disease using this model and how to characterize T follicular helper cells, germinal center B cells and plasma cells by flow cytometry.

C57BL / 6 FARELERDE SLE bm12 İndüklenebilir Modeli (SLE)

Systemic lupus erythematosus (SLE) is an autoimmune disease with diverse clinical and immunological manifestations. Several spontaneous and inducible ...

Tıp

Bioluminescence and Near-infrared Imaging of Optic Neuritis and Brain Inflammation in the EAE Model of Multiple Sclerosis in Mice

Experimental autoimmune encephalomyelitis (EAE) in SJL/J mice is a model for relapsing-remitting multiple sclerosis (RRMS). Clinical EAE scores describing motor function deficits are basic readouts of the immune-mediated inflammation of the spinal cord. However, scores and body weight do not allow for an in vivo assessment of brain inflammation and optic neuritis. The latter is an early and frequent manifestation in about 2/3 of MS patients. Here, we show methods for bioluminescence and near-infrared live imaging to assess EAE evoked optic neuritis, brain inflammation, and blood-brain barrier (BBB) disruption in living mice using an in vivo imaging system. A bioluminescent substrate activated by oxidases primarily showed optic neuritis. The signal was specific and allowed the visualization of medication effects and disease time courses, which paralleled the clinical scores. Pegylated fluorescent nanoparticles that remained within the vasculature for extended periods of time were used to assess the BBB integrity. Near-infrared imaging revealed a BBB leak at the peak of the disease. The signal was the strongest around the eyes. A near-infrared substrate for matrix metalloproteinases was used to assess EAE-evoked inflammation. Auto-fluorescence interfered with the signal, requiring spectral unmixing for quantification. Overall, bioluminescence imaging was a reliable method to assess EAE-associated optic neuritis and medication effects and was superior to the near-infrared techniques in terms of signal specificity, robustness, ease of quantification, and cost.

We show a technique for in vivo live bioluminescence and near-infrared imaging of optic neuritis and encephalitis in the experimental autoimmune encephalomyelitis (EAE) model for multiple sclerosis in SJL/J mice.

Farelerde Multipl Skleroz EAE Modeli Optik Nörit ve Beyin Enflamasyon Biyoparlaklık ve Yakın-Kızılötesi Görüntüleme

Experimental autoimmune encephalomyelitis (EAE) in SJL/J mice is a model for relapsing-remitting multiple sclerosis (RRMS). Clinical EAE scores describing ...

A Mouse Model to Assess Innate Immune Response to Staphylococcus aureus Infection

Staphylococcus aureus (S. aureus)&#160;infections, including methicillin resistant stains, are an enormous burden on the healthcare system. With incidence rates of S. aureus infection climbing annually, there is a demand for additional research in its&#160;pathogenicity. Animal models of infectious disease advance our understanding of the host-pathogen response and lead to the development of effective therapeutics. Neutrophils play a primary role in the innate immune response that controls S. aureus infections by forming an abscess to wall off the infection and facilitate bacterial clearance; the number of neutrophils that infiltrate an S. aureus skin infection often correlates with disease outcome. LysM-EGFP mice, which possess the enhanced green fluorescent protein (EGFP) inserted in the Lysozyme M (LysM) promoter region (expressed primarily by neutrophils), when used in conjunction with in vivo whole animal fluorescence imaging (FLI) provide&#160;a means of quantifying neutrophil emigration noninvasively and longitudinally into wounded skin. When combined with a bioluminescent S. aureus strain and sequential in vivo whole animal bioluminescent imaging (BLI), it is possible to longitudinally monitor both the neutrophil recruitment dynamics and in vivo bacterial burden at the site of infection in anesthetized mice from onset of infection to resolution or death. Mice are more resistant to a number of virulence factors produced by S. aureus that facilitate effective colonization and infection in humans. Immunodeficient mice provide a more sensitive animal model to examine persistent S. aureus infections and the ability of therapeutics to boost innate immune responses. Herein, we characterize responses in LysM-EGFP mice that have been bred to MyD88-deficient mice (LysM-EGFP&#215;MyD88-/- mice) along with wild-type LysM-EGFP mice to investigate S. aureus skin wound infection. Multispectral simultaneous detection enabled study of neutrophil recruitment dynamics by using in vivo FLI, bacterial burden by using in vivo BLI, and wound healing longitudinally and noninvasively over time.

A Mouse Model to Assess Innate Immune Response to Staphylococcus aureus Infection

An approach is described for real-time detection of the innate immune response to cutaneous wounding and Staphylococcus aureus infection of mice. By comparing LysM-EGFP mice (which possess fluorescent neutrophils) with a LysM-EGFP crossbred immunodeficient mouse strain, we advance our understanding of infection and the development of approaches to combat infection.

Bir fare modeli için değerlendirmek doğuştan gelen bağışıklık yanıtı Staphylococcus aureus enfeksiyon

Staphylococcus aureus (S. aureus)&#160;infections, including methicillin resistant stains, are an enormous burden on the healthcare system. With incidence ...

Mouse Footpad Inoculation Model to Study Viral-Induced Neuroinflammatory Responses

This protocol describes a footpad inoculation model used to study the initiation and development of neuroinflammatory responses during alphaherpesvirus infection in mice. As alphaherpesviruses are main invaders of the peripheral nervous system (PNS), this model is suitable to characterize the kinetics of viral replication, its spread from the PNS to CNS, and associated neuroinflammatory responses. The footpad inoculation model allows virus particles to spread from a primary infection site in the footpad epidermis to sensory and sympathetic nerve fibers that innervate the epidermis, sweat glands, and dermis. The infection spreads via the sciatic nerve to the dorsal root ganglia (DRG) and ultimately through the spinal cord to the brain. Here, a mouse footpad is inoculated with pseudorabies virus (PRV), an alphaherpesvirus closely related to herpes simplex virus (HSV) and varicella-zoster virus (VZV). This model demonstrates that PRV infection induces severe inflammation, characterized by neutrophil infiltration in the footpad and DRG. High concentrations of inflammatory cytokines are subsequently detected in homogenized tissues by ELISA. In addition, a strong correlation is observed between PRV gene and protein expression (via qPCR and IF staining) in DRG and the production of pro-inflammatory cytokines. Therefore, the footpad inoculation model provides a better understanding of the processes underlying alphaherpesvirus-induced neuropathies and may lead to the development of innovative therapeutic strategies. In addition, the model can guide research on peripheral neuropathies, such as multiple sclerosis and associated viral-induced damage to the PNS. Ultimately, it can serve as a cost-effective in vivo tool for drug development.

The footpad inoculation model is a valuable tool for characterizing viral-induced neuroinflammatory responses in vivo. In particular, it provides a clear assessment of viral kinetics and associated immunopathological processes initiated in the peripheral nervous system.

Viral Kaynaklı Nöroinflamatuar Yanıtları İncelemek Için Fare Ayak Takımı Aşılama Modeli

This protocol describes a footpad inoculation model used to study the initiation and development of neuroinflammatory responses during alphaherpesvirus ...

A Mouse Model for the Transition of Streptococcus pneumoniae from Colonizer to Pathogen upon Viral Co-Infection Recapitulates Age-Exacerbated Illness

Streptococcus pneumoniae (pneumococcus) is an asymptomatic colonizer of the nasopharynx in most individuals but can progress to a pulmonary and systemic pathogen upon influenza A virus (IAV) infection. Advanced age enhances host susceptibility to secondary pneumococcal pneumonia and is associated with worsened disease outcomes. The host factors driving those processes are not well defined, in part due to a lack of animal models that reproduce the transition from asymptomatic colonization to severe clinical disease. 
This paper describes a novel mouse model that recreates the transition of pneumococci from asymptomatic carriage to disease upon viral infection. In this model, mice are first intranasally inoculated with biofilm-grown pneumococci to establish asymptomatic carriage, followed by IAV infection of both the nasopharynx and lungs. This results in bacterial dissemination to the lungs, pulmonary inflammation, and obvious signs of illness that can progress to lethality. The degree of disease is dependent on the bacterial strain and host factors. 
Importantly, this model reproduces the susceptibility of aging, because compared to young mice, old mice display more severe clinical illness and succumb to disease more frequently. By separating carriage and disease into distinct steps and providing the opportunity to analyze the genetic variants of both the pathogen and the host, this S. pneumoniae/IAV co-infection model permits the detailed examination of the interactions of an important pathobiont with the host at different phases of disease progression. This model can also serve as an important tool for identifying potential therapeutic targets against secondary pneumococcal pneumonia in susceptible hosts.

A Mouse Model for the Transition of Streptococcus pneumoniae from Colonizer to Pathogen upon Viral Co-Infection Recapitulates Age-Exacerbated Illness

This paper describes a novel mouse model for the transition of pneumococcus from an asymptomatic colonizer to a disease-causing pathogen during viral infection. This model can be readily adapted to study polymicrobial and host-pathogen interactions during the different phases of disease progression and across various hosts.

Streptococcus pneumoniae'nin Viral Ko-Enfeksiyon Üzerine Kolonizatörden Patojene Geçişi İçin Bir Fare Modeli, Yaşın Şiddetlendirdiği Hastalıkları Özetler

Streptococcus pneumoniae (pneumococcus) is an asymptomatic colonizer of the nasopharynx in most individuals but can progress to a pulmonary and systemic ...

Lokal ve sistemik Yer de patojen kaynaklı kronik enflamasyon Fare Modeli

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