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简介：ScientistsattheUniversityofPittsburghSchoolofMedicinehavediscoveredanewbiologicalpathwayofinnateimmunitythatrampsupinflammationandthenidentifiedagentsthatcanblockit,leadingtoincreasedsurvivalandimprovedlungfunctioninanimalmodelsofpneumonia.TheyreportedtheirfindingstodayinNatureImmunology.

简介：针刺关元,气海,三阴交,中极,水道,地机,足三里,肾俞,大肠俞和次髎穴,同时用清热解毒和活血化瘀中药进行保留灌肠,治疗了15例慢性盆腔炎患者,经过2个疗程治疗,13例痊愈,2例有效.

简介：AbstractCerebral amyloid angiopathy-related inflammation (CAA-RI) is a rare but increasingly recognized subtype of CAA. CAA-RI consists of two subtypes: inflammatory cerebral amyloid angiopathy and amyloid β (Aβ)-related angiitis. Acute or subacute onset of cognitive decline or behavioral changes is the most common symptom of CAA-RI. Rapid progressive dementia, headache, seizures, or focal neurological deficits, with patchy or confluent hyperintensity on T2 or fluid-attenuated inversion recovery sequences and evidence of strictly lobar microbleeds or cortical superficial siderosis on susceptibility-weighted imaging imply CAA-RI. The gold standard for diagnosis is autopsy or brain biopsy. However, biopsy is invasive; consequently, most clinically diagnosed cases have been based on clinical and radiological data. Other diagnostic indexes include the apolipoprotein E ε4 allele, Aβ and anti-Aβ antibodies in cerebral spinal fluid and amyloid positron emission tomography. Many diseases with similar clinical manifestations should be carefully ruled out. Immunosuppressive therapy is effective both during initial presentation and in relapses. The use of glucocorticoids and immunosuppressants improves prognosis. This article reviews the pathology and pathogenesis, clinical and imaging manifestations, diagnostic criteria, treatment, and prognosis of CAA-RI, and highlights unsolved problems in the existing research.

简介：AbstractType 2 inflammation is a complex immune response and primary mechanism for several common allergic diseases including allergic rhinitis, allergic asthma, atopic dermatitis, and chronic rhinosinusitis with nasal polyps. It is the predominant type of immune response against helminths to prevent their tissue infiltration and induce their expulsion. Recent studies suggest that epithelial barrier dysfunction contributes to the development of type 2 inflammation in asthma, which may partly explain the increasing prevalence of asthma in China and around the globe. The epithelial barrier hypothesis has recently been proposed and has received great interest from the scientific community. The development of leaky epithelial barriers leads to microbial dysbiosis and the translocation of bacteria to inter- and sub-epithelial areas and the development of epithelial tissue inflammation. Accordingly, preventing the impairment and promoting the restoration of a deteriorated airway epithelial barrier represents a promising strategy for the treatment of asthma. This review introduces the interaction between type 2 inflammation and the airway epithelial barrier in asthma, the structure and molecular composition of the airway epithelial barrier, and the assessment of epithelial barrier integrity. The role of airway epithelial barrier disruption in the pathogenesis of asthma will be discussed. In addition, the possible mechanisms underlying the airway epithelial barrier dysfunction induced by allergens and environmental pollutants, and current treatments to restore the airway epithelial barrier are reviewed.

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简介：Objective:Tostudytheeffectofdecoy-oligodeoxynucleotides(decoy-ODNs)indumbbellshapewiththeoligodeoxynucleotidesequencesimilartonuclearfactorkappaB(NF-κB)cis-elementsonexpressionofinflammationmediatorsinpMΦcellsfromrats.Methods:Withcarriersofcationicliposomes,decoy-ODNsweretransfectedintopMΦcellsofrats.Thentheinhibitingeffectsofthedecoy-ODNsontumornecrosisfactorα(TNFα),interleukin-6(IL-6)andIL-10wereanalyzed.Results:Decoy-ODNscoulddecreasetheexpressionofTNFαandIL-6indose-dependentfashionbuthadweakerinhibitingeffectonIL-10.Conclusions:Decoy-ODNstargetingNF-κBcandecreasetheexpressionofinflammatorymediatorsinpMΦcellsfromrats.

简介：AbstractAspirin-exacerbated respiratory disease (AERD) is characterized by the triad of chronic rhinosinusitis with nasal polyposis, adult-onset asthma and non-IgE mediated reactions to aspirin and other cyclooxygenase-1 (COX-1) inhibitors. Patients with AERD are dependent on COX-1 activity to maintain production of prostaglandin (PG) species, such as PGE2, which maintain physiologic levels of inflammation and limit the production of pro-inflammatory cysteinyl leukotrienes. The endogenous cannabinoid system is a family of immunomodulatory lipids and their innate g-protein coupled receptors that are closely related to arachidonic acid and may modulate inflammation via several pathways, including the direct production of metabolically active prostaglandin glycerol-esters. A recent pilot study has identified the significant up-regulation of the peripherally expressed, type-2 cannabinoid receptor (CB2) in AERD nasal polyps versus control tissues from patients with either allergic fungal rhinosinusitis or no history of chronic sinonasal inflammation. These early findings suggest the involvement of increased endogenous cannabinoid activity in prostaglandin deficient states such as AERD. Future study is needed to explore the significance of these findings, with specific investigation of the impact of CB2 activation on markers of airway inflammation, as well as the potential to measure CB2 expression as a screening biomarker for the evaluation of unrecognized disease.

简介：有编码Dermatophagoidespteronyssinus组2的DNA的种痘(Derp2)变应原以前在Derp上显示出它immunologic保护的效果在老鼠的2导致变应原的过敏航线发炎。在现在的学习，我们调查了是否2能施加的DNA疫苗编码Derp在老鼠模型的导致变应原的过敏航线发炎上的治疗学的角色并且在气喘探索了DNA种痘的机制特定变应原的免疫疗法。在由Derp敏化并且质问以后2，BALB/c老鼠与DNA被使免疫疫苗。细胞的渗入的度被获得。在浆液的IgE层次和在BALF的IL-4/lL-13层次被ELISA决定。肺纸巾被组织学的考试估计。在肺的STAT6和NF-B的表情被染色的immunohistochemistry决定。有DNA疫苗的老鼠的种痘禁止了航线发炎和变应原导致的粘蛋白的生产的发展，并且减少了Derp2-specificIgE水平的水平。eosinophii渗入的重要减小和在BALF的IL-4andIL-13的层次在种痘以后被观察。进一步更，DNA种痘在Derp2-immunized老鼠在肺织物禁止了STAT6和NF-Bexpression。这些结果显示DNA疫苗编码Derp2allergen能在我们的老鼠模型被用于导致变应原的过敏航线发炎的治疗。

简介：Directionalmigrationofleukocytesisindispensabletoinnateimmunityforhostdefense.However,recruitmentofleukocytestoasiteoftissueinjuryalsoconstitutesaleadingcauseforinflammatoryresponses.Mechanistically,itinvolvesacascadeofcellulareventspreciselyregulatedbytemporalandspatialpresentationofarepertoireofmoleculesinthemigratingleukocytesandtheirsurroundings(microenvironments).HereIwillsummarizetheemergingevidencethathasshedlightsontheunderlyingmolecularmechanismfordirectionalmigrationofleukocytes,whichhasguidedthetherapeuticaldevelopmentforinnovativeanti-inflammatorymedicines.

简介：AbstractImportance:The impact of long-term burden of excessive body weight, beginning in childhood, on inflammatory status in adulthood has been poorly described.Objective:To characterize the longitudinal body mass index (BMI) trajectory from childhood and examine its relationship with inflammatory status in adulthood.Methods:We included 1285 adults who had 4-15 repeat measurements of BMI from childhood to adulthood. The area under the curve (AUC) of growth curves was calculated to characterize long-term burden (total AUC) and trends (incremental AUC) of BMI.Results:After adjusting for covariates, higher values of BMI in terms of childhood and adulthood, as well as total and incremental AUC, were strongly associated with elevated levels of adult C-reactive protein (CRP) in the four race-sex groups. There were significant differences in linear and nonlinear curve parameters between the normal and high CRP groups for all race-sex groups (P < 0.01). Compared with participants who had consistently low BMI in both childhood and adulthood, participants with high BMI in adulthood had higher CRP levels (P < 0.001), irrespective of their childhood BMI status; participants with high BMI in childhood but low BMI in adulthood had similar adult CRP levels.Interpretation:The impact of excessive body weight on inflammation is cumulative and exacerbated over time. The influence of childhood overweight/obesity on inflammatory status in adulthood can be alleviated by reducing adiposity in adulthood.

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简介：作为一个内部应用的反煽动性的代理人，Escin广泛地在从损伤或操作导致诊所的发炎和浮肿的治疗被使用了。然而，它皮肤的发炎和浮肿上的外部使用的效果仍然保持未经勘探。在现在的学习，反煽动性并且escin的外部使用的anti-edematous效果在老鼠，在老鼠胀大的导致paraxylene的耳朵，和棉花在导致carrageenan的爪浮肿和导致组织安的毛状的渗透被学习在老鼠的导致小团的granuloma。前列腺素E2(PGE2)上的escin胶化的外部使用的效果，肿瘤坏死因素--(TNF-)，并且interleukin-1(IL-1)被ELISA决定。反煽动性的机制被与西方的弄污和实时PCR分析检测glucocorticoid受体(GR)的表示探索，与原子factor-B(NF-B)的进一步的探索，p38激活mitogen的蛋白质kinase(P38MAPK)和使活跃之物protein-1(AP-1)表情。我们证明escin的外部使用证明在不同动物模型的尖锐、长期的发炎上的重要反煽动性的效果和它的反煽动性的效果可能与PGE2，TNF-，和IL-1的下面规定有关。结果也证明escin由支持GR的表示施加了它的反煽动性的效果，与是的可能的机制象NF-B和AP-1那样的GR相关的发信号的分子的表情的抑制。

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简介：到真菌的促进感受性经常导致是特别地困难的临床上设法的气喘的一种严重形式，导致在这些病人的增加的病态和住院。尽管B淋巴细胞可能通过IgE的生产加重气喘症状，这些房间可能也在对吸入的真菌的保护的反应是重要的。通过cytokine版本和T房间相互作用，这些淋巴细胞可能也影响航线墙纤维变性的发展和维护。JH−/−老鼠为抗体的重链部件缺乏JH基因，它为B房间功能和幸存是批评的。这些动物在很多有免疫力的回答便于B淋巴细胞的角色的说明；然而，JH−/−老鼠没被用来学习真菌的过敏症。在这研究，我们用曲霉属菌fumigatus检验了B淋巴细胞的角色模仿被环境真菌的暴露触发的人的航线疾病的鼠科的真菌的高空过敏症模型。我们在敏化的野类型的BALB/c和J暴露于的H−/−老鼠重复了真菌的暴露并且没在大航线附近在航线hyperresponsiveness，全面肺的发炎或骨胶原免职发现差别。然而，Th2类型cytokinesIL-4和IL-13的层次显著地在J相对BALB/c控制的H−/−鼠标。由对比，煽动性的cytokinesIL-17A和IL-6的层次显著地在JH−/−动物，并且有显著地更柔韧的航线嗜曙红血球过多和neutrophilia比在控制动物。一起拿，这些调查结果表明淋巴细胞帮助在肺的分隔空间调整granulocytic回答到真菌的暴露的那B。

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简介：BackgroundHypertensionassociatedwithhyperhomocysteinemia(HHcy)isdefinedasH-typehypertension.HypertensionandHHcyhasastrongsynergythatcouldleadtotheriskofvasculardisease,suchascarotidremodeling.However,therelationofinflammatoryfactorsandadhesionmoleculewithcarotidremodelinginH-typehypertensionisunknown.MethodsFifty-sixpatientswithH-typehypertensionand52withouthyperhomocysteinemiahypertensionwereenrolledinthisstudy,with42healthyvolunteersasthecontrolgroup.AllthesubjectsunderwentcolorDopplerultrasoundexaminationofcarotidartery.TheexpressionofICAM-1inperipheralbloodmonocyteswasmeasuredbydirectimmunofluorescencetechniqueincombinationwithflowcytometry.ThelevelsofhighsensitivityC-reactiveprotein(hs-CRP),Monocytechemoattractantprotein-1(MCP-1)andsICAM-1weremeasured.Thecorrelationsbetweencarotidvascularremodelingandthesebiomarkerswereanalyzed.ResultsTheintima-mediathickness(IMT),circulatinglevelsofhs-CRPandMCP-1,andmonocyteICAM-1weresignificantlyincreasedinH-typehypertensiongroup(P<0.05).Therewerenosignificantdifferenceinthosemeasurementsbetweenthesimplehypertensiongroupandthecontrolgroup(P>0.05).ThelevelsofsICAM-1showednosignificanceamongthethreegroups(P>0.05).Correlationanalysesrevealedapositivecorrelationofcarotidplaqueindexwithhomocysteine,hs-CRPandMCP-1,andtheexpressionofICAM-1inthemonocytesintheH-typehypertensiongroup.MultivariatelogisticregressionanalysisrevealedthatHcyandhs-CRPweretheindependentriskfactorsofIMTintheH-typehypertensiongroup.ConclusionThepatientswithH-typehypertensionaremorelikelytohavecarotidvascularremodelingwithhigherlevelsofinflammationandadhesionmoleculeswhichmightleadtothedevelopmentofatherosclerosis.

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简介：AbstractBackground:Psoriasis is a common chronic inflammatory skin disease with 2% to 3% prevalence worldwide and a heavy social-psychological burden for patients and their families. As the exact pathogenesis of psoriasis is still unknown, the current treatment is far from satisfactory. Thus, there is an urgent need to find a more effective therapy for this disease. Keratin 17 (K17), a type I intermediate filament, is overexpressed in the psoriatic epidermis and plays a critical pathogenic role by stimulating T cells in psoriasis. Therefore, we hypothesized that inhibiting K17 may be a potential therapeutic approach for psoriasis. This study aimed to investigate the therapeutic effect of K17-specific small interfering RNA (siRNA) on mice with imiquimod (IMQ)-induced psoriasis-like dermatitis.Methods:Eight-week-old female BALB/c mice were administered a 5% IMQ cream on both ears to produce psoriatic dermatitis. On day 3, K17 siRNA was mixed with an emulsion matrix and applied topically to the left ears of the mice after IMQ application every day for 7 days. The right ears of the mice were treated in parallel with negative control (NC) siRNA. Inflammation was evaluated by gross ear thickness, histopathology, the infiltration of inflammatory cells (CD3+ T cells and neutrophils) using immunofluorescence, and the expression of cytokine production using real-time quantitative polymerase chain reaction. The obtained data were statistically evaluated by unpaired t-tests and a one-way analysis of variance.Results:The severity of IMQ-induced dermatitis on K17 siRNA-treated mice ears was significantly lower than that on NC siRNA-treated mice ears, as evidenced by the alleviated ear inflammation phenotype, including decreased ear thickness, infiltration of inflammatory cells (CD3+ T cells and neutrophils), and inflammatory cytokine/chemokine expression levels (interleukin 17 [IL-17], IL-22, IL-23, C-X-C motif chemokine ligand 1, and C-C motif chemokine ligand 20) (P < 0.05 vs. the Blank or NC siRNA groups). Compared to the NC siRNA treatment, the K17 siRNA treatment resulted in increased K1 and K10 expression, which are characteristic of keratinocyte differentiation (vs. NC siRNA, K17 siRNA1 group: K1, t= 4.782, P= 0.0050; K10, t= 3.365, P= 0.0120; K17 siRNA2 group: K1, t= 4.104, P= 0.0093; K10, t= 4.168, P= 0.0042; siRNA Mix group: K1, t= 3.065, P = 0.0221; K10, t = 10.83, P < 0.0001), and decreased K16 expression, which is characteristic of keratinocyte proliferation (vs. NC siRNA, K17 siRNA1 group: t= 4.156, P= 0.0043; K17 siRNA2 group: t= 2.834, P= 0.0253; siRNA Mix group: t= 2.734, P = 0.0250).Conclusions:Inhibition of K17 expression by its specific siRNA significantly alleviated inflammation in mice with IMQ-induced psoriasis-like dermatitis. Thus, gene therapy targeting K17 may be a potential treatment approach for psoriasis.