Human adenovirus type 55(HAdV-B55) is a re-emergent acute respiratory disease pathogen that causes adult communityacquired pneumonia(CAP). Previous studies have shown that the receptor of HAdV-B14, which genome is hig...Human adenovirus type 55(HAdV-B55) is a re-emergent acute respiratory disease pathogen that causes adult communityacquired pneumonia(CAP). Previous studies have shown that the receptor of HAdV-B14, which genome is highly similar with HAdV-B55, is human Desmoglein 2(DSG2). However, whether the receptor of HAdV-B55 is DSG2 is undetermined because there are three amino acid mutations in the fiber gene between HAdV-B14 and HAdV-B55. Here, firstly we found the 3T3 cells, a mouse embryo fibroblast rodent cell line which does not express human DSG2, were able to be infected by HAdV-B55 after transfected with pcDNA3.1-DSG2, while normal 3T3 cells were still unsusceptible to HAdV-B55 infection. Next, A549 cells with h DSG2 knock-down by siRNA were hard to be infected by HAdV-B3/-B14/-B55, while the control siRNA group was still able to be infected by all these types of HAdVs. Finally, immunofluorescence confocal microscopy indicated visually that Cy3-conjugated HAdV-B55 viruses entered A549 cells by binding to DSG2 protein.Therefore, DSG2 is a major receptor of HAdV-B55 causing adult CAP. Our finding is important for better understanding of interactions between adenoviruses and host cells and may shed light on the development of new drugs that can interfere with these processes as well as for the development of potent prophylactic vaccines.展开更多
Pemphigus is an autoimmune bullous disease observed with lesions in the skin and mucosa. Pemphigus is classified by antibodies against desmogleins, which is cadherin type intercellular adhesion factors involved in adh...Pemphigus is an autoimmune bullous disease observed with lesions in the skin and mucosa. Pemphigus is classified by antibodies against desmogleins, which is cadherin type intercellular adhesion factors involved in adhesion between epidermal cells. In this case, because erosion of the oral mucosa was the primary symptom, a relationship with membrane-dominant pemphigus vulgaris was strongly suspected. And in terms of histopathology, findings not conflicted with pemphigus vulgaris were observed, but given all these different findings, the results did not correspond with bullous pemphigoid in clinical findings, and with pemphigus foliaceus and pemphigus vulgaris in various testing results, leading us to believe this represented a very rare case. We started oral health care, and when application of steroid ointment to the entire surface of the mucosa was continued, symptoms disappeared within approximately 2 months. In this case, relapse has not yet occurred and periodic follow-up was continued.展开更多
To the Editor:Bullous pemphigoid(BP)is a rare autoimmune skin disorder characterized by significant mortality,with BP prevalence ranging from 1.46 to 47.99 cases per 100,000 people.[1]The pathogenic mechanism of BP is...To the Editor:Bullous pemphigoid(BP)is a rare autoimmune skin disorder characterized by significant mortality,with BP prevalence ranging from 1.46 to 47.99 cases per 100,000 people.[1]The pathogenic mechanism of BP is attributed to pathogenic autoantibodies targeting BP180 and BP230 antigens,resulting in the formation of subepidermal blisters.[1]Reports indicate that some BP patients also have circulating anti-desmoglein(Dsg)autoantibodies,which are pathogenic antibodies in pemphigus.[2]However,it remains uninvestigated whether the concomitant anti-Dsg antibodies in BP are pathogenic and thereby represent a coincidental occurrence or signify the coexistence of the two diseases.This knowledge gap introduces uncertainty in patient care management.Therefore,a comprehensive analysis was performed to explore the clinicohistopathological characteristics,human leukocyte antigen(HLA)genetic risk factors,and pathogenicity of anti-Dsg antibodies in BP patients with anti-Dsg antibodies compared to those without.展开更多
Objective: This paper aims at measurement enhanced effect of oxidized lipoprotien(a) [ox Lp(a)] on permeability of monolayer endothelial cells and relationship with reactive oxygen species(ROS) generation and desmogle...Objective: This paper aims at measurement enhanced effect of oxidized lipoprotien(a) [ox Lp(a)] on permeability of monolayer endothelial cells and relationship with reactive oxygen species(ROS) generation and desmogleins(DSGs) expression.Methods and Results: Transendothelial permeability was assayed by transwell and reactive oxygen species(ROS) was determined by DCFH-DA staining. RT-PCR was carried out to determine DSGl and DSC2 expression in m RNA, respectively.Transendothelial permeability was enhanced by ox LP(a) dose and time dependently. The most marked effect appeared at a concentration of 100 mg/L, Transendothelial permeability reached the maximum value after 2 h of FITC-dextran addition, and then gradually decreased after 4 h. ox Lp(a) induces the generation of cellular reactive oxygen species(ROS), and this effect could be inhibited by superoxide dismutase(SOD).Incubation of HUVECs with ox Lp(a) resulted in a dose and time-dependent down-regulation of DSGl and DSC2 expression at transcriptional level. Conclusion:Permeability of monolayer endothelial cells was enhanced by ox Lp(a) which is related to up-regulating ROS formation and down-regulating desmogleins expression.展开更多
Sudden unexplained death(SUD)remains a puzzle in forensic medicine.Desmoglein‑2(DSG2)has been linked to arrhythmogenic right ventricular cardiomyopathy which may cause life‑threatening ventricular arrhythmias and sudd...Sudden unexplained death(SUD)remains a puzzle in forensic medicine.Desmoglein‑2(DSG2)has been linked to arrhythmogenic right ventricular cardiomyopathy which may cause life‑threatening ventricular arrhythmias and sudden death.Fatal arrhythmias resulting in sudden death also occur in the absence of morphologic cardiac abnormalities at autopsy.We hypothesized that DSG2 mutations may be responsible for certain Chinese SUD cases.We sequenced all 15 exons of DSG2 in DNA extracted from postmortem heart tissues of 25 Chinese patients dying from SUD.The primers were designed using the Primer Express 3.0 software.Direct sequencing for both sense and antisense strands was performed with a BigDye Terminator DNA sequencing kit on a 3130 Xl Genetic Analyzer.Mutation damage prediction was made using Mutation Taster,PolyPhen,and SIFT software.In 2 of 25 cases of Chinese SUD samples,two DSG2 heterozygous mutations(p.P927 L and p.T1070M)were identified,and one is probably damaging.We concluded that DSG2 mutations may be related to the occurrence of part of SUD cases in the Chinese Han population.展开更多
基金This work was supported by grants from the National Key Research and Development Program of China(2018YFE0204503)Natural Science Foundation of Guangdong Province(2021A1515010788 and 2018B030312010)the Guangzhou Healthcare Collaborative Innovation Major Project(201803040004 and 201803040007)。
文摘Human adenovirus type 55(HAdV-B55) is a re-emergent acute respiratory disease pathogen that causes adult communityacquired pneumonia(CAP). Previous studies have shown that the receptor of HAdV-B14, which genome is highly similar with HAdV-B55, is human Desmoglein 2(DSG2). However, whether the receptor of HAdV-B55 is DSG2 is undetermined because there are three amino acid mutations in the fiber gene between HAdV-B14 and HAdV-B55. Here, firstly we found the 3T3 cells, a mouse embryo fibroblast rodent cell line which does not express human DSG2, were able to be infected by HAdV-B55 after transfected with pcDNA3.1-DSG2, while normal 3T3 cells were still unsusceptible to HAdV-B55 infection. Next, A549 cells with h DSG2 knock-down by siRNA were hard to be infected by HAdV-B3/-B14/-B55, while the control siRNA group was still able to be infected by all these types of HAdVs. Finally, immunofluorescence confocal microscopy indicated visually that Cy3-conjugated HAdV-B55 viruses entered A549 cells by binding to DSG2 protein.Therefore, DSG2 is a major receptor of HAdV-B55 causing adult CAP. Our finding is important for better understanding of interactions between adenoviruses and host cells and may shed light on the development of new drugs that can interfere with these processes as well as for the development of potent prophylactic vaccines.
文摘Pemphigus is an autoimmune bullous disease observed with lesions in the skin and mucosa. Pemphigus is classified by antibodies against desmogleins, which is cadherin type intercellular adhesion factors involved in adhesion between epidermal cells. In this case, because erosion of the oral mucosa was the primary symptom, a relationship with membrane-dominant pemphigus vulgaris was strongly suspected. And in terms of histopathology, findings not conflicted with pemphigus vulgaris were observed, but given all these different findings, the results did not correspond with bullous pemphigoid in clinical findings, and with pemphigus foliaceus and pemphigus vulgaris in various testing results, leading us to believe this represented a very rare case. We started oral health care, and when application of steroid ointment to the entire surface of the mucosa was continued, symptoms disappeared within approximately 2 months. In this case, relapse has not yet occurred and periodic follow-up was continued.
基金supported by grants from the Central Guidance for Local Scientific and Technological Development Projects of Shandong Province(No.YDZX2023058)the Shandong Province Taishan Scholar Project(No.tsqn201909141).
文摘To the Editor:Bullous pemphigoid(BP)is a rare autoimmune skin disorder characterized by significant mortality,with BP prevalence ranging from 1.46 to 47.99 cases per 100,000 people.[1]The pathogenic mechanism of BP is attributed to pathogenic autoantibodies targeting BP180 and BP230 antigens,resulting in the formation of subepidermal blisters.[1]Reports indicate that some BP patients also have circulating anti-desmoglein(Dsg)autoantibodies,which are pathogenic antibodies in pemphigus.[2]However,it remains uninvestigated whether the concomitant anti-Dsg antibodies in BP are pathogenic and thereby represent a coincidental occurrence or signify the coexistence of the two diseases.This knowledge gap introduces uncertainty in patient care management.Therefore,a comprehensive analysis was performed to explore the clinicohistopathological characteristics,human leukocyte antigen(HLA)genetic risk factors,and pathogenicity of anti-Dsg antibodies in BP patients with anti-Dsg antibodies compared to those without.
基金Science and Technology Innovative Research Team in Higher Educational Institutions of Hunan Province,National and Natural Science Foundation of Chinagrant number:81070221Visiting Scholar Foundation of Key Laboratory of Biorheological Science and Technology (Chongqing University) of Ministry of Education(2010)
文摘Objective: This paper aims at measurement enhanced effect of oxidized lipoprotien(a) [ox Lp(a)] on permeability of monolayer endothelial cells and relationship with reactive oxygen species(ROS) generation and desmogleins(DSGs) expression.Methods and Results: Transendothelial permeability was assayed by transwell and reactive oxygen species(ROS) was determined by DCFH-DA staining. RT-PCR was carried out to determine DSGl and DSC2 expression in m RNA, respectively.Transendothelial permeability was enhanced by ox LP(a) dose and time dependently. The most marked effect appeared at a concentration of 100 mg/L, Transendothelial permeability reached the maximum value after 2 h of FITC-dextran addition, and then gradually decreased after 4 h. ox Lp(a) induces the generation of cellular reactive oxygen species(ROS), and this effect could be inhibited by superoxide dismutase(SOD).Incubation of HUVECs with ox Lp(a) resulted in a dose and time-dependent down-regulation of DSGl and DSC2 expression at transcriptional level. Conclusion:Permeability of monolayer endothelial cells was enhanced by ox Lp(a) which is related to up-regulating ROS formation and down-regulating desmogleins expression.
基金This study was funded by the National Natural Science Foundation of China(NSFC fund:81501630)the Opening Project of Shanghai Key Laboratory of Crime Scene Evidence(No.2016XCWZK20)+1 种基金This study was funded by the National Natural Science Foundation of China(NSFC fund:81501630)the Opening Project of Shanghai Key Laboratory of Crime Scene Evidence(No.2016XCWZK20).
文摘Sudden unexplained death(SUD)remains a puzzle in forensic medicine.Desmoglein‑2(DSG2)has been linked to arrhythmogenic right ventricular cardiomyopathy which may cause life‑threatening ventricular arrhythmias and sudden death.Fatal arrhythmias resulting in sudden death also occur in the absence of morphologic cardiac abnormalities at autopsy.We hypothesized that DSG2 mutations may be responsible for certain Chinese SUD cases.We sequenced all 15 exons of DSG2 in DNA extracted from postmortem heart tissues of 25 Chinese patients dying from SUD.The primers were designed using the Primer Express 3.0 software.Direct sequencing for both sense and antisense strands was performed with a BigDye Terminator DNA sequencing kit on a 3130 Xl Genetic Analyzer.Mutation damage prediction was made using Mutation Taster,PolyPhen,and SIFT software.In 2 of 25 cases of Chinese SUD samples,two DSG2 heterozygous mutations(p.P927 L and p.T1070M)were identified,and one is probably damaging.We concluded that DSG2 mutations may be related to the occurrence of part of SUD cases in the Chinese Han population.
