The interaction between T cell and osteoclasts is important in osteoimmunology.T-helper cells,which produce interleukin-17,induce the expression of receptor activator of nuclear factor κB ligand in synovial cells.Companied by with inflammatory cytokines,they stimulate the differentiation and activation of osteoclasts.Osteoimmunology helps us understand how antirheumatic drugs work,as well as developing new therapeutic strategies for rheumatic diseases.

Peroxidsome proliferator-activated rreceptor γ(PPARγ) has characteristics of regulation of adipocyte differentiation and lipid metabolism.In recent years,more and more evidences suggest that PPARγ plays an important role in the regulation of immune and inflammatory response.The PPARγ expression increased in airway of asthma patients, and PPARγ was involved in airway inflammation and airway hyperresponsiveneas. Recent studies have shown that PPARγ ligands may have a role in the treatment of asthma.

Objective To study the effect of Jade -Screen Powder (JSP)on regulating expression of 5 microRNAs associated with helper T cells in asthmatic mouse model.Methods Forty Balb /c mice were randomly di-vided into 4 groups,1 0 mice for each group,namely normal control,asthma model,JSP treatment and Dexamethasone treatment.The mouse models of allergic inflammation on both upper and lower airways were established by ovalbumin sensitization and challenge.Interleukin(IL)-1 3 and IL -1 7 expressions were detected from lung homogenates by ELISA.Hematoxylin and eosin staining was also performed to observe the pathological changes in the lung tissue.The expressions of miR -1 46a,miR -1 46b,miR -21 0,miR -1 26 and miR -21 a were detected by quantitative real time PCR from splenocytes.Results The lower levels of IL -1 3 [(6.382 ±1 .690)μg/L]and IL -1 7 [(24.21 2 ± 1 .250)μg/L]were found in JSP treatment group compared with those in the asthma model group [(20.1 54 ±7.960)μg/L;(50.31 2 ±5.770)μg/L,rseparately],there was significant difference in IL -1 3 between JSP group and the asthma model group,as well as IL -1 7 (t =3.785,P =0.005;t =9.891 ,P =0.000).Same findings were found in Dexamethasone treated group as well [IL -1 3:(9.366 ±3.460)μg/L,IL -1 7:(29.1 32 ±4.960)μg/L;t =2.779, P =0.024;t =6.225,P =0.000].However,upregulation of miR -21 0 was observed in JSP treatment group (2.052 ± 0.871 )compared with that in the asthma model group (4.034 ±1 .379)(3.95 folds,t =2.71 8,P =0.026).Mean-time,the expression of miR -1 26 in JSP group (4.920 ±0.924)and Dexamethasone group (3.862 ±1 .51 0)in-creased compared with asthma model group (6.024 ±0.447)(2.1 5 folds,t =2.405,P =0.043,and 4.48 folds,t =-3.069,P =0.01 5).Conclusions Th2 and Th1 7 T cells participate in the pathogenesis of asthma and the asthmatic process can be inhibited by JSP.JSP may affect the helper T cells by regulating miR -21 0 and miR -1 26.

AIM: To study the effect of Yupingfeng Powder(YPFP) on rat's allergic rhinitis induced by stimulating ovalbumin.and reveal the influence on Th1,Th2 and Th1/Th2 proportion. METHODS: 8-week-old BALB/c mice were sensitized by means of intranasal and systemic intraperitoneal injection application of OVA,6 subjects were administered including 2,500 mg/kg extracts of YPFP for 7 days in early stage(interference group);6 mice were administered YPFP in after challenge(therapy group);the placebo group were given saline.After 7 days,Th1 and Th2 in splenocyte were detected by flow cytometry(FCM) and nasobuccal mucosa pathology were observed. RESULTS: When compared with Th2 of animal model group(9.86?1.40),there was a significant decrease expressing Th2 after PFP treatment(3.41?0.72,P

Congenital abnormalities of the neonatal lung structure can easily cause childhood lung diseases and increase the susceptibility to chronic lung diseases in adulthood.Fibroblast growth factor 10(FGF10) regulates structu-ral morphology, cellular differentiation, and damage response at multiple stages of lung development.FGF10 deficiency in the formation stage of bronchial branches will lead to neonatal lung disease.In other words, congenital airway abnorma-lities caused by gene mutations in the fgf10 cause increase the risk of developing chronic lung diseases in adulthood.FGF10 also maintains lung precursor cell lines and promotes proliferation and differentiation of alveolar typeⅡ cells after lung injury.In this article, the cellular and molecular mechanisms of FGF10 associated with various lung diseases were reviewed, including bronchopulmonary dysplasia in extremely premature infants, cystic lung fibrosis in children, and chronic lung diseases in adults, so as to offer help for the development of new therapeutic strategies for respiratory diseases.

Objective:To assess the changes in profiles of microRNAs (miRNAs) in peripheral blood of neonatal Sprague-Dawley (SD) rats with hypoxia-ischemia(HI) injury with self-resuscitation.Methods:Neonatal rats of 3 pregnant rats were divided into 3 groups according to their nests, in which group A was the blank control group, group B was the HI group, and group C was the alternative group.The expression profiles of miRNAs in periphe-ral blood of neonatal rats in group A and B by high-throughput sequencing was compared.Bioinformatics analysis was applied to investigate these differentially expressed miRNAs.Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses were performed to screen out enriched signaling pathways and functions.Target genes of miRNAs and those correlated with hypoxia-ischemia brain damage were predicted using miRBaseData (miRBD) software.HE staining was performed to observe the pathological changes of rat brain tissues.Results:A total of 1 049 mature reliable miRNAs in peripheral blood of neonatal rats were identified, including 525 miRNAs in group A, and 524 in group B. There were 27 differentially expressed miRNAs between group A and B, and their types were highly correlated.A total of 38 dysregulated miRNAs were screened out in group B, involving 21 upregulated miRNAs and 17 downregulated ones.GO and KEGG analyses showed that the identified differentially expressed miRNAs were mainly enriched in the glutamatergic synapse pathway, myelin lipid metabolism, neural activity ligand-receptor interaction and the vascular epithelial growth factor (VEGF) signaling pathway, all of them were significantly correlated with HIBD and over-activated.Cortex and subcallosal white matter lesions, enlarged ventricles, disordered arrangement of gray matter neurons, and obvious apoptosis in rat brain tissues of group A and B were not observed in HE staining.Conclusions:Differential expression of miRNAs in peripheral blood of HI self-resuscitated rats suggests that miRNAs has a positive response to hypoxia and ischemia.Differentially expressed miRNAs, including miR-200, miR-471, miR-429, miR-216 and miR-871 families, in peripheral blood of neonatal rat with HI showed their active response after HIBD.They are related to the molecular mechanisms of the nervous system damage, and are expected to become novel diagnostic markers for HIBD or HI.Differentially expressed miRNAs are conductive to the development of therapeutic targets of HI.

2019-novel coronavirus (2019-nCoV) is a highly pathogenic human CoV that first emerged in Wuhan in 2019.2019-nCoV has a zoonotic origin and poses a major threat to public health.However, little is known about the viral factors contributing to the high virulence of 2019-nCoV.Many animal viruses, including CoVs, encode proteins that interfere with host gene expression, including those involved in antiviral immune responses, and these viral proteins are often major virulence factors.Human coronaviruses (HCoVs) are known respiratory pathogens associated with a range of respiratory infection.In the past 17 years, the onset of 2019-nCoV, severe acute respiratory syndrome coronavirus (SARS-CoV) and Middle East respiratory syndrome coronavirus (MERS-CoV) have thrust HCoVs into spotlight of the research community due to their high pathogenicity in humans.The recent study of HCoVs-host interactions has contributed extensively to our understanding of infection pathogenesis of 2019-nCoV.This review discuss various host physiopathologic mechanism, such as apoptosis, innate immunity, endoplasmic reticulum (ER) stress response, mitogen-activated protein kinase (MAPK) pathway and nuclear factor kappa B (NF-κB) pathway that may be modulated by HCoVs and provides evidence for the intensive investigate of 2019-nCoV infection.