Innate Immunity最新文献_第10页

The TNF-α (-238 G/A) polymorphism could protect against development of severe sepsis. TNF-α（-238 G/A）多态性可预防严重败血症的发生。

IF 2.8 4区医学

Innate Immunity Pub Date : 2021-07-01 DOI: 10.1177/17534259211036186

A Hugo Montes, Eulalia Valle-Garay, Guadalupe Martin, Julio Collazos, Victoria Alvarez, Alvaro Meana, Laura Pérez-Is, José A Carton, Francisco Taboada, Víctor Asensi

{"title":"The TNF-α (-238 G/A) polymorphism could protect against development of severe sepsis.","authors":"A Hugo Montes, Eulalia Valle-Garay, Guadalupe Martin, Julio Collazos, Victoria Alvarez, Alvaro Meana, Laura Pérez-Is, José A Carton, Francisco Taboada, Víctor Asensi","doi":"10.1177/17534259211036186","DOIUrl":"10.1177/17534259211036186","url":null,"abstract":"Primary responses in sepsis-mediated inflammation are regulated by pro-inflammatory cytokines. Variations in the cytokine genes might modify their transcription or expression, plasma cytokines levels and response to sepsis. Activation protein-1 (AP-1) and NF-κB regulate cytokines gene expression in sepsis. A total of 90 severely septic and 91 non-infected patients were prospectively studied. IL-1α (-889 C/T), IL-1β (+3954 C/T), IL-6 (-174 G/C), TNF-α (-238 G/A), TNF-α (-308G/A), IL-8 (-251A/T) and IL-10 (-1082 G/A) SNPs, plasma IL-1β, IL-4, IL-6, IL-8, IL-10, IL-13, IFN-γ, TNF-α and monocyte chemoattractant protein 1 (MCP-1) levels, and AP-1 and NF-κB gene expression by neutrophils were assessed. A allele carriers of TNF-α (-238 G/A) SNP were less frequent among septic patients. IL-6, IL-8, IL-10, TNF-α and MCP-1 levels were higher, and AP-1 and NF-κB gene expressions lower in septic patients. Sepsis was independently associated with higher fibrinogen, neutrophils counts and IL-8 levels, lower prothrombin, absence of the variant A allele of the TNF-α (-238 G/A) SNP, and haemodynamic failure. Death was independently associated with a higher APACHE II score, higher IL-8 levels, and the diagnosis of sepsis. TNF-a (-238 G/A) SNP could protect against sepsis development. Higher IL-8 levels are predictive of sepsis and mortality.","PeriodicalId":13676,"journal":{"name":"Innate Immunity","volume":"27 5","pages":"409-420"},"PeriodicalIF":2.8,"publicationDate":"2021-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/9e/06/10.1177_17534259211036186.PMC8419297.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39376818","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

miR-150 and SRPK1 regulate AKT3 expression to participate in LPS-induced inflammatory response. miR-150和SRPK1调节AKT3表达参与lps诱导的炎症反应。

IF 3.2 4区医学

Innate Immunity Pub Date : 2021-05-01 DOI: 10.1177/17534259211018800

Yanfen Yao, Hong Wang, Xueqin Xi, Wei Sun, Junke Ge, Pibao Li

{"title":"miR-150 and SRPK1 regulate AKT3 expression to participate in LPS-induced inflammatory response.","authors":"Yanfen Yao, Hong Wang, Xueqin Xi, Wei Sun, Junke Ge, Pibao Li","doi":"10.1177/17534259211018800","DOIUrl":"https://doi.org/10.1177/17534259211018800","url":null,"abstract":"miR-150 was found to target the 3'-untranslated regions of AKT3, and the AKT pathway was affected by SR protein kinase 1 (SRPK1). However, the expression and significance of miR-150, AKT3 and SRPK1 in acute lung injury (ALI) were not clear. Here, we found that the expression of miR-150 was significantly reduced, while the expression of AKT3 and SRPK1 were markedly increased in LPS-treated A549, THP-1 and RAW 264.7 cells. miR-150 significantly decreased levels of pro-inflammatory cytokines IL-1β, IL-6 and TNF-α, reduced the expression of AKT3, but had no impact on SRPK1 expression compared with the control group in LPS-treated A549, THP-1 and RAW 264.7 cells. AKT3 silencing only reduced the production of pro-inflammatory cytokines and showed no effect on miR-150 and SRPK1 expression. Finally, we observed that miR-150 mimics and/or silencing of SRPK1 decreased the expression of AKT3 mRNA. Besides, over-expression of miR-150 or silencing of SRPK1 also reduced the expression of AKT3 protein, which exhibited the lowest level in the miR-150 mimics plus si-SRPK1 group. However, si-SRPK1 had no effect on miR-150 level. In conclusion, miR-150 and SRPK1 separately and cooperatively participate into inflammatory responses in ALI through regulating AKT3 pathway. Increased miR-150 and silenced SRPK1 may be a novel potential factor for preventing and treating more inflammatory lung diseases.","PeriodicalId":13676,"journal":{"name":"Innate Immunity","volume":"27 4","pages":"343-350"},"PeriodicalIF":3.2,"publicationDate":"2021-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1177/17534259211018800","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38997301","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 5

Implication of Toll/IL-1 receptor domain containing adapters in Porphyromonas gingivalis-induced inflammation. Toll/IL-1受体结构域在牙龈卟啉单胞菌诱导炎症中的意义。

IF 3.2 4区医学

Innate Immunity Pub Date : 2021-05-01 Epub Date: 2021-05-21 DOI: 10.1177/17534259211013087

Isaac M Bugueno, Nadia Benkirane-Jessel, Olivier Huck

{"title":"Implication of Toll/IL-1 receptor domain containing adapters in Porphyromonas gingivalis-induced inflammation.","authors":"Isaac M Bugueno, Nadia Benkirane-Jessel, Olivier Huck","doi":"10.1177/17534259211013087","DOIUrl":"https://doi.org/10.1177/17534259211013087","url":null,"abstract":"Periodontitis is induced by periodontal dysbiosis characterized by the predominance of anaerobic species. TLRs constitute the classical pathway for cell activation by infection. Interestingly, the Toll/IL-1 receptor homology domain adapters initiate signaling events, leading to the activation of the expression of the genes involved in the host immune response. The aim of this study was to evaluate the effects of Porphyromonas gingivalis on the expression and protein-protein interactions among five TIR adapters (MAL, MyD88, TRIF, TRAM and SARM) in gingival epithelial cells and endothelial cells. It was observed that P. gingivalis is able to modulate the signaling cascades activated through its recognition by TLR4/2 in gingival epithelial cells and endothelial cells. Indeed, MAL-MyD88 protein-protein interactions associated with TLR4 was the main pathway activated by P. gingivalis infection. When transient siRNA inhibition was performed, cell viability, inflammation, and cell death induced by infection decreased and such deleterious effects were almost absent when MAL or TRAM were targeted. This study emphasizes the role of such TIR adapter proteins in P. gingivalis elicited inflammation and the precise evaluation of TIR adapter protein interactions may pave the way for future therapeutics in both periodontitis and systemic disease with a P. gingivalis involvement, such as atherothrombosis.","PeriodicalId":13676,"journal":{"name":"Innate Immunity","volume":"27 4","pages":"324-342"},"PeriodicalIF":3.2,"publicationDate":"2021-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1177/17534259211013087","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38923187","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 1

Baicalin attenuates LPS-induced alveolar type II epithelial cell A549 injury by attenuation of the FSTL1 signaling pathway via increasing miR-200b-3p expression. 黄芩苷通过增加miR-200b-3p表达，减弱FSTL1信号通路，从而减轻lps诱导的肺泡II型上皮细胞A549损伤。

IF 3.2 4区医学

Innate Immunity Pub Date : 2021-05-01 Epub Date: 2021-05-18 DOI: 10.1177/17534259211013887

Xin-Ya Duan, Yang Sun, Zhu-Feng Zhao, Yao-Qing Shi, Xun-Yan Ma, Li Tao, Ming-Wei Liu

{"title":"Baicalin attenuates LPS-induced alveolar type II epithelial cell A549 injury by attenuation of the FSTL1 signaling pathway via increasing miR-200b-3p expression.","authors":"Xin-Ya Duan, Yang Sun, Zhu-Feng Zhao, Yao-Qing Shi, Xun-Yan Ma, Li Tao, Ming-Wei Liu","doi":"10.1177/17534259211013887","DOIUrl":"https://doi.org/10.1177/17534259211013887","url":null,"abstract":"In China, baicalin is the main active component of Scutellaria baicalensis, which has been used in the treatment of inflammation-related diseases, such as inflammation-induced acute lung injury. However, its specific mechanism remains unclear. This study examined the protective effect of baicalin on LPS-induced inflammation injury of alveolar epithelial cell line A549 and explored its protective mechanism. Compared with the LPS-induced group, the proliferation inhibition rates of alveolar type II epithelial cell line A549 intervened by different concentrations of baicalin decreased significantly, as did the levels of inflammatory factors IL-6, IL-1β, prostaglandin 2 and TNF-α in the supernatant. The expression levels of inflammatory proteins inducible NO synthase (iNOS), NF-κB65, phosphorylated ERK (p-ERK1/2), and phosphorylated c-Jun N-terminal kinase (p-JNK1) significantly decreased, as did the protein expression of follistatin-like protein 1 (FSTL1). In contrast, expression of miR-200b-3p significantly increased in a dose-dependent manner. These results suggested that baicalin could significantly inhibit the expression of inflammation-related proteins and improve LPS-induced inflammatory injury in alveolar type II epithelial cells. The mechanism may be related to the inhibition of ERK/JNK inflammatory pathway activation by increasing the expression of miR-200b-3p. Thus, FSTL1 is the regulatory target of miR-200b-3p.","PeriodicalId":13676,"journal":{"name":"Innate Immunity","volume":"27 4","pages":"294-312"},"PeriodicalIF":3.2,"publicationDate":"2021-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1177/17534259211013887","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38992137","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 9

Anti-HMGB1 auto-Abs influence fatigue in patients with Crohn's disease. 抗hmgb1自身抗体对克罗恩病患者疲劳的影响

IF 3.2 4区医学

Innate Immunity Pub Date : 2021-05-01 Epub Date: 2021-05-03 DOI: 10.1177/17534259211014252

Ingeborg Kvivik, Tore Grimstad, Grete Jonsson, Jan T Kvaløy, Roald Omdal

{"title":"Anti-HMGB1 auto-Abs influence fatigue in patients with Crohn's disease.","authors":"Ingeborg Kvivik, Tore Grimstad, Grete Jonsson, Jan T Kvaløy, Roald Omdal","doi":"10.1177/17534259211014252","DOIUrl":"https://doi.org/10.1177/17534259211014252","url":null,"abstract":"Fatigue is common in all chronic inflammatory and autoimmune diseases. A conceptual model for understanding the biological basis of fatigue describes it as being a part of the sickness behaviour response generated by pro-inflammatory cytokines and other mediators. We hypothesised that the pro-inflammatory high mobility group box 1 (HMGB1) protein is a fatigue-inducing molecule and that auto-Abs against HMGB1 reduce fatigue. We measured Abs against disulphide (ds) HMGB1 and fully reduced (fr) HMGB1 in plasma from 57 patients with Crohn's disease. Fatigue was rated using the fatigue visual analogue scale (fVAS) and disease activity with faecal calprotectin, C-reactive protein and the Simple Endoscopic Score for Crohn's disease. Multivariable regression models identified anti-dsHMGB1 and anti-frHMGB1 Abs as the strongest contributing factors for fVAS scores (B = -29.10 (P = 0.01), R2 = 0.17, and B = -17.77 (P = 0.01), R2 = 0.17, respectively). Results indicate that anti-HMGB1 auto-Abs alleviate fatigue possibly by down-regulating HMGB1-induced sickness behaviour.","PeriodicalId":13676,"journal":{"name":"Innate Immunity","volume":"27 4","pages":"286-293"},"PeriodicalIF":3.2,"publicationDate":"2021-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1177/17534259211014252","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38864353","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 4

Protective effects of recombinant 53-kDa protein of Trichinella spiralis on acute lung injury in mice via alleviating lung pyroptosis by promoting M2 macrophage polarization. 旋毛虫重组53-kDa蛋白通过促进M2巨噬细胞极化减轻肺焦亡对小鼠急性肺损伤的保护作用。

IF 3.2 4区医学

Innate Immunity Pub Date : 2021-05-01 Epub Date: 2021-05-20 DOI: 10.1177/17534259211013397

Ling-Yu Wei, An-Qi Jiang, Ren Jiang, Si-Ying Duan, Xue Xu, Ze-da-Zhong Su, Jia Xu

{"title":"Protective effects of recombinant 53-kDa protein of Trichinella spiralis on acute lung injury in mice via alleviating lung pyroptosis by promoting M2 macrophage polarization.","authors":"Ling-Yu Wei, An-Qi Jiang, Ren Jiang, Si-Ying Duan, Xue Xu, Ze-da-Zhong Su, Jia Xu","doi":"10.1177/17534259211013397","DOIUrl":"https://doi.org/10.1177/17534259211013397","url":null,"abstract":"Trichinella spiralis represents an effective treatment for autoimmune and inflammatory diseases. The effects of recombinant T. spiralis (TS) 53-kDa protein (rTsP53) on acute lung injury (ALI) remain unclear. Here, mice were divided randomly into a control group, LPS group, and rTsP53 + LPS group. ALI was induced in BALB/c mice by LPS (10 mg/kg) injected via the tail vein. rTsP53 (200 µl; 0.4 μg/μl) was injected subcutaneously three times at an interval of 5 d before inducing ALI in the rTsP53+LPS group. Lung pathological score, the ratio and markers of classic activated macrophages (M1) and alternatively activated macrophages (M2), cytokine profiles in alveolar lavage fluid, and pyroptosis protein expression in lung tissue were investigated. RTsP53 decreased lung pathological score. Furthermore, rTsP53 suppressed inflammation by increasing IL-4, IL-10, and IL-13. There was an increase in alveolar M2 macrophage numbers, with an increase in CD206 and arginase-1-positive cells and a decrease in alveolar M1 markers such as CD197 and iNOS. In addition, the polarization of M2 macrophages induced by rTsP53 treatment could alleviate ALI by suppressing lung pyroptosis. RTsP53 was identified as a potential agent for treating LPS-induced ALI via alleviating lung pyroptosis by promoting M2 macrophage polarization.","PeriodicalId":13676,"journal":{"name":"Innate Immunity","volume":"27 4","pages":"313-323"},"PeriodicalIF":3.2,"publicationDate":"2021-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1177/17534259211013397","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38930803","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 8

A pilot study of an anti-endotoxin Ig-enriched bovine colostrum to prevent experimental sepsis. 富含抗内毒素 Ig 的牛初乳预防实验性败血症的试点研究。

IF 3.2 4区医学

Innate Immunity Pub Date : 2021-04-01 DOI: 10.1177/17534259211007538

Alan S Cross, Steven M Opal, John E Palardy, Surekha Shridhar, Scott M Baliban, Alison J Scott, Abdullah B Chahin, Robert K Ernst

{"title":"A pilot study of an anti-endotoxin Ig-enriched bovine colostrum to prevent experimental sepsis.","authors":"Alan S Cross, Steven M Opal, John E Palardy, Surekha Shridhar, Scott M Baliban, Alison J Scott, Abdullah B Chahin, Robert K Ernst","doi":"10.1177/17534259211007538","DOIUrl":"10.1177/17534259211007538","url":null,"abstract":"Despite the dramatic increase in antimicrobial resistance, there is a dearth of antibiotics in development and few pharmaceutical companies working in the field. Further, any new antibiotics are likely to have a short shelf life. Ab-based interventions offer alternatives that are not likely to be circumvented by the widely prevalent antibiotic resistance genes. Bovine colostrum (BC)-the first milk after parturition, rich in nutrients and immune components-promotes gut integrity and modulates the gut microbiome. We developed a hyperimmune BC (HBC) enriched in Abs to a highly conserved LOS core region of Gram-negative bacteria by immunizing pregnant cows with a vaccine comprised of detoxified LOS from Escherichia coli O111 Rc (J5) mutant non-covalently complexed to group B meningococcal outer membrane protein (J5dLOS/OMP). This vaccine generated robust levels of anti-J5 LOS Ab in the colostrum. When given orally to neutropenic rats challenged orally with Pseudomonas aeruginosa, administration of HBC improved survival compared to non-immune rats, while both BC preparations improved survival compared to PBS controls. Elevated circulating endotoxin levels correlated with mortality. HBC and to a lesser extent non-immune BC reduced bacterial burden from the liver, lung, and spleen. We conclude that HBC and to a lesser extent BC may be effective supplements that improve outcome from lethal gut-derived disseminated infection and may reduce transmission of Gram-negative bacilli from the gastrointestinal tract.","PeriodicalId":13676,"journal":{"name":"Innate Immunity","volume":"27 3","pages":"266-274"},"PeriodicalIF":3.2,"publicationDate":"2021-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/fa/a9/10.1177_17534259211007538.PMC8054147.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38797577","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Anti-nociceptive effect of Portulaca oleracea L. ethanol extracts attenuated zymosan-induced mouse joint inflammation via inhibition of Nrf2 expression. 马齿苋乙醇提取物通过抑制Nrf2的表达来减轻酵素诱导的小鼠关节炎症的抗伤害作用。

IF 3.2 4区医学

Innate Immunity Pub Date : 2021-04-01 Epub Date: 2021-02-20 DOI: 10.1177/1753425921994190

Yunwu He, Hui Long, Cong Zou, Wuzhou Yang, Liping Jiang, Zhenping Xiao, Qing Li, Shiyin Long

{"title":"Anti-nociceptive effect of Portulaca oleracea L. ethanol extracts attenuated zymosan-induced mouse joint inflammation via inhibition of Nrf2 expression.","authors":"Yunwu He, Hui Long, Cong Zou, Wuzhou Yang, Liping Jiang, Zhenping Xiao, Qing Li, Shiyin Long","doi":"10.1177/1753425921994190","DOIUrl":"https://doi.org/10.1177/1753425921994190","url":null,"abstract":"The aim of this study was to explore the effects of ethanol extracts from Portulaca oleracea L. (ePO) on joint inflammation and to explain the underlying mechanisms. A joint inflammation mouse model was constructed by injecting zymosan, and the Von Frey method was employed and the joint thickness measured. The numbers of leukocytes, neutrophils, and monocytes were counted in the joint cavity and the infiltration of inflammatory cells was assessed by joint histopathological analysis. The mRNA levels of inflammatory cytokines were determined by quantitative RT-PCR and their secretion levels were determined by specific ELISAs. Pre-treatment with ePO inhibited articular mechanical hyperalgesia and edema and ameliorated the recruitment of mononuclear neutrophils and leukocytes. In addition, pre-treatment with ePO improved pathological alternations in the joint tissues by reducing the number of inflammatory cells. Pre-treatment with ePO regulated the nuclear factor erythroid 2-related factor 2 (Nrf2)-related proteins and thereby inhibited oxidative stress. In addition, ePO inhibited NLR family pyrin domain containing 3 (NLRP3) inflammasome-related genes (NLRP3, ASC, pro-caspase-1 and pro-IL-1ß), modulated inflammatory cytokines and the activation of NF-κB. ePO attenuated zymosan-induced joint inflammation by regulating oxidative stress, NLRP3 inflammasome, and NF-κB.","PeriodicalId":13676,"journal":{"name":"Innate Immunity","volume":"27 3","pages":"230-239"},"PeriodicalIF":3.2,"publicationDate":"2021-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1177/1753425921994190","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"25389351","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 7

Circulating cell-free DNA, peripheral lymphocyte subsets alterations and neutrophil lymphocyte ratio in assessment of COVID-19 severity. 循环游离DNA、外周血淋巴细胞亚群改变和中性粒细胞比例在评估COVID-19严重程度中的作用。

IF 3.2 4区医学

Innate Immunity Pub Date : 2021-04-01 Epub Date: 2021-03-01 DOI: 10.1177/1753425921995577

Reham Hammad, Mona Abd El Rahman Eldosoky, Shaimaa Hani Fouad, Abdelaleem Elgendy, Amany M Tawfeik, Mohamed Alboraie, Mariam Fathy Abdelmaksoud

{"title":"Circulating cell-free DNA, peripheral lymphocyte subsets alterations and neutrophil lymphocyte ratio in assessment of COVID-19 severity.","authors":"Reham Hammad, Mona Abd El Rahman Eldosoky, Shaimaa Hani Fouad, Abdelaleem Elgendy, Amany M Tawfeik, Mohamed Alboraie, Mariam Fathy Abdelmaksoud","doi":"10.1177/1753425921995577","DOIUrl":"https://doi.org/10.1177/1753425921995577","url":null,"abstract":"Cell destruction results in plasma accumulation of cell-free DNA (cfDNA). Dynamic changes in circulating lymphocytes are features of COVID-19. We aimed to investigate if cfDNA level can serve in stratification of COVID-19 patients, and if cfDNA level is associated with alterations in lymphocyte subsets and neutrophil-to-lymphocyte ratio (NLR). This cross-sectional comparative study enrolled 64 SARS-CoV-2-positive patients. Patients were subdivided to severe and non-severe groups. Plasma cfDNA concentration was determined by real-time quantitative PCR. Lymphocyte subsets were assessed by flow cytometry. There was significant increase in cfDNA among severe cases when compared with non-severe cases. cfDNA showed positive correlation with NLR and inverse correlation with T cell percentage. cfDNA positively correlated with ferritin and C-reactive protein. The output data of performed ROC curves to differentiate severe from non-severe cases revealed that cfDNA at cut-off ≥17.31 ng/µl and AUC of 0.96 yielded (93%) sensitivity and (73%) specificity. In summary, excessive release of cfDNA can serve as sensitive COVID-19 severity predictor. There is an association between cfDNA up-regulation and NLR up-regulation and T cell percentage down-regulation. cfDNA level can be used in stratification and personalized monitoring strategies in COVID-19 patients.","PeriodicalId":13676,"journal":{"name":"Innate Immunity","volume":"27 3","pages":"240-250"},"PeriodicalIF":3.2,"publicationDate":"2021-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1177/1753425921995577","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"25417613","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 19

Haemophilus influenzae causes cellular trans-differentiation in human bronchial epithelia. 流感嗜血杆菌引起人支气管上皮细胞的转分化。

IF 3.2 4区医学

Innate Immunity Pub Date : 2021-04-01 Epub Date: 2021-03-01 DOI: 10.1177/1753425921994906

Michael Glöckner, Sebastian Marwitz, Kristina Rohmann, Henrik Watz, Dörte Nitschkowski, Jan Rupp, Klaus Dalhoff, Torsten Goldmann, Daniel Drömann

{"title":"Haemophilus influenzae causes cellular trans-differentiation in human bronchial epithelia.","authors":"Michael Glöckner, Sebastian Marwitz, Kristina Rohmann, Henrik Watz, Dörte Nitschkowski, Jan Rupp, Klaus Dalhoff, Torsten Goldmann, Daniel Drömann","doi":"10.1177/1753425921994906","DOIUrl":"https://doi.org/10.1177/1753425921994906","url":null,"abstract":"Non-typeable Haemophilus influenzae (NTHi) is the most common respiratory pathogen in patients with chronic obstructive disease. Limited data is available investigating the impact of NTHi infections on cellular re-differentiation processes in the bronchial mucosa. The aim of this study was to assess the effects of stimulation with NTHi on the bronchial epithelium regarding cellular re-differentiation processes using primary bronchial epithelial cells harvested from infection-free patients undergoing bronchoscopy. The cells were then cultivated using an air-liquid interface and stimulated with NTHi and TGF-β. Markers of epithelial and mesenchymal cells were analyzed using immunofluorescence, Western blot and qRT-PCR. Stimulation with both NTHi and TGF-ß led to a marked increase in the expression of the mesenchymal marker vimentin, while E-cadherin as an epithelial marker maintained a stable expression throughout the experiments. Furthermore, expression of collagen 4 and the matrix-metallopeptidases 2 and 9 were increased after stimulation, while the expression of tissue inhibitors of metallopeptidases was not affected by pathogen stimulation. In this study we show a direct pathogen-induced trans-differentiation of primary bronchial epithelial cells resulting in a co-localization of epithelial and mesenchymal markers and an up-regulation of extracellular matrix components.","PeriodicalId":13676,"journal":{"name":"Innate Immunity","volume":"27 3","pages":"251-259"},"PeriodicalIF":3.2,"publicationDate":"2021-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1177/1753425921994906","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"25423937","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 3