Innate Immunity最新文献_第6页

From bats to pangolins: new insights into species differences in the structure and function of the immune system. 从蝙蝠到穿山甲:对免疫系统结构和功能的物种差异的新见解

IF 2.8 4区医学

Innate Immunity Pub Date : 2022-04-01 Epub Date: 2022-05-04 DOI: 10.1177/17534259221093120

Patrick J Haley

引用次数: 0

Differential susceptibility to lipopolysaccharide affects the activation of toll-like-receptor 4 signaling in THP-1 cells and PMA-differentiated THP-1 cells. 对脂多糖的不同敏感性影响THP-1细胞和pma分化的THP-1细胞中toll样受体4信号的激活。

IF 3.2 4区医学

Innate Immunity Pub Date : 2022-04-01 DOI: 10.1177/17534259221100170

Young Kyu Kim, Jeong Ho Hwang, Hoon Taek Lee

{"title":"Differential susceptibility to lipopolysaccharide affects the activation of toll-like-receptor 4 signaling in THP-1 cells and PMA-differentiated THP-1 cells.","authors":"Young Kyu Kim, Jeong Ho Hwang, Hoon Taek Lee","doi":"10.1177/17534259221100170","DOIUrl":"https://doi.org/10.1177/17534259221100170","url":null,"abstract":"Monocytes and macrophages that originate from common myeloid progenitors perform various crucial roles in the innate immune system. Stimulation with LPS combined with TLR4 drives the production of pro-inflammatory cytokines through MAPKs and NF-κB pathway in different cells. However, the difference in LPS susceptibility between monocytes and macrophages is poorly understood. In this study, we found that pro-inflammatory cytokines-IL-1β, IL-6 and TNFα showed greater induction in phorbol-12-myristate-13-acetate (PMA)-differentiated THP-1 cells than in THP-1 cells. To determine the difference in cytokine expression, the surface proteins such as TLR4-related proteins and intracellular adaptor proteins were more preserved in PMA-differentiated THP-1 cells than in THP-1 cells. MyD88 is a key molecule responsible for the difference in LPS susceptibility. Moreover, MAPKs and NF-κB pathway-related molecules showed higher levels of phosphorylation in PMA-differentiated THP-1 cells than in THP-1 cells. Upon MyD88 depletion, there was no difference in the phosphorylation of MAPK pathway-related molecules. Therefore, these results demonstrate that the difference in LPS susceptibility between THP-1 cells and PMA-differentiated THP-1 cells occur as a result of gap between the activated MAPKs and NF-κB pathways via changes in the expression of LPS-related receptors and MyD88.","PeriodicalId":13676,"journal":{"name":"Innate Immunity","volume":"28 3-4","pages":"122-129"},"PeriodicalIF":3.2,"publicationDate":"2022-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/0c/7a/10.1177_17534259221100170.PMC9136465.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10618404","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

The monocyte activation test detects potentiated cytokine release resulting from the synergistic effect of endotoxin and non-endotoxin pyrogens 单核细胞活化试验检测内毒素和非内毒素热原协同作用引起的细胞因子释放增强

IF 3.2 4区医学

Innate Immunity Pub Date : 2022-04-01 DOI: 10.1177/17534259221097948

S. Solati, Ting Zhang, S. Timman

{"title":"The monocyte activation test detects potentiated cytokine release resulting from the synergistic effect of endotoxin and non-endotoxin pyrogens","authors":"S. Solati, Ting Zhang, S. Timman","doi":"10.1177/17534259221097948","DOIUrl":"https://doi.org/10.1177/17534259221097948","url":null,"abstract":"Pyrogens are classified in two groups, endotoxin pyrogens and non-endotoxin pyrogens (NEPs). The presence of either in parenteral pharmaceuticals or medical devices can cause severe harm to subjects, and when occurring in combination, synergistic potentiation effects can occur. As the standard in vitro pyrogen test, the Limulus Amebocyte Lysate (LAL) assay can detect LPS only, an endotoxin, but not NEPs. We tested whether the Monocyte Activation Test (MAT) that measures IL-6 induction, is suited for detecting synergistic pyrogen effects. Here we show that MAT reliably detects the NEPs heat-killed Staphylococcus aureus, R848 and lipoteichoic acid, in addition to LPS. When combinations of these pyrogens were tested, a potentiation of IL-6 production was seen beyond an additive effect, apparently reflecting on in-vivo synergisms. The current study therefore demonstrates that MAT not only is a reliable and reproducible assay for the sensitive detection of both endotoxin and non-endotoxin pyrogens, but also for identifying synergistic effects when parenteral drugs are contaminated with multiple pyrogens.","PeriodicalId":13676,"journal":{"name":"Innate Immunity","volume":"28 1","pages":"130 - 137"},"PeriodicalIF":3.2,"publicationDate":"2022-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41509763","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 3

Silencing of circ_0000205 mitigates interleukin-1β-induced apoptosis and extracellular matrix degradation in chondrocytes via targeting miR-766-3p/ADAMTS5 axis circ_0000205的沉默通过靶向miR-766-3p/AADAMTS5轴减轻白细胞介素-1β诱导的软骨细胞凋亡和细胞外基质降解

IF 3.2 4区医学

Innate Immunity Pub Date : 2022-02-01 DOI: 10.1177/17534259221077078

Guowen Li, Heyuan Luo, Z. Ding, Haofeng Liang, Zhoupeng Lai, Shuzhen Chen, Yuliang Huang

{"title":"Silencing of circ_0000205 mitigates interleukin-1β-induced apoptosis and extracellular matrix degradation in chondrocytes via targeting miR-766-3p/ADAMTS5 axis","authors":"Guowen Li, Heyuan Luo, Z. Ding, Haofeng Liang, Zhoupeng Lai, Shuzhen Chen, Yuliang Huang","doi":"10.1177/17534259221077078","DOIUrl":"https://doi.org/10.1177/17534259221077078","url":null,"abstract":"The aim of this study was to explore the role of hsa_circRNA_0000205 (circ_0000205) in chondrocyte injury in osteoarthritis (OA) and the underlying mechanism. Expression of circ_0000205, microRNA (miR)-766-3p and a disintegrin and metalloproteinase with thrombospondin motif (ADAMTS)-5 was detected by quantitative real time (qRT)-polymerase chain reaction (PCR) and Western blot assays. Cell proliferation, apoptosis, and extracellular matrix (ECM) synthesis were examined by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide and 5-ethynyl-2-deoxyuridine assays, flow cytometry, and qRT-PCR and Western blot assays. The target relationship between miR-766-3p and circ_0000205 or ADAMTS5 was confirmed by luciferase reporter assay and RNA immunoprecipitation. IL-1β treatment could attenuate cell viability of primary chondrocytes and proliferating cell nuclear antigen (PCNA) and collagen II type alpha-1 (COL2A1) levels, and elevate apoptosis rate and cleaved caspase-3, ADAMTS5 and matrix metalloproteinase-13 (MMP13) levels, suggesting that IL-1β induced chondrocyte apoptosis and ECM degradation. Expression of circ_0000205 was up-regulated in OA tissues and IL-1β-induced primary chondrocytes, accompanied with miR-766-3p down-regulation and ADAMTS5 up-regulation. Knockdown of circ_0000205 could mitigate IL-1β-induced above effects and improve cell proliferation. Moreover, both depleting miR-766-3p and promoting ADAMTS5 could partially counteract circ_0000205 knockdown roles in IL-1β-cultured primary chondrocytes. Notably, circ_0000205 was verified as a sponge for miR-766-3p via targeting, and ADAMTS5 was a direct target for miR-766-3p. Silencing circ_0000205 could protect chondrocytes from IL-1β-induced proliferation reduction, apoptosis, and ECM degradation by targeting miR-766-3p/ADAMTS5 axis.","PeriodicalId":13676,"journal":{"name":"Innate Immunity","volume":"28 1","pages":"79 - 90"},"PeriodicalIF":3.2,"publicationDate":"2022-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"45681550","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 4

The effect of myeloperoxidase-oxidized LDL on THP-1 macrophage polarization and repolarization 髓过氧化物酶氧化LDL对THP-1巨噬细胞极化和复极的影响

IF 3.2 4区医学

Innate Immunity Pub Date : 2022-02-01 DOI: 10.1177/17534259221090679

Samer Bazzi, Christian Frangie, Eliana Azar, J. Daher

{"title":"The effect of myeloperoxidase-oxidized LDL on THP-1 macrophage polarization and repolarization","authors":"Samer Bazzi, Christian Frangie, Eliana Azar, J. Daher","doi":"10.1177/17534259221090679","DOIUrl":"https://doi.org/10.1177/17534259221090679","url":null,"abstract":"Macrophages (Mφs) play a crucial role in the development of atherosclerosis by engulfing modified LDL particles and forming foam cells, the hallmark of atherosclerosis. Many studies suggest that myeloperoxidase-oxidized LDL (Mox-LDL) is an important pathophysiological model for LDL modification in vivo. Classically (M1) and alternatively activated (M2) Mφs are both implicated in the process of atherogenesis. Mφs are highly plastic cells whereby they undergo repolarization from M1 to M2 and vice versa. Since little is known about the effects of Mox-LDL on Mφ polarization and repolarization, our study aimed at evaluating the in vitro effects of Mox-LDL at this level through making use of the well-established model of human THP-1-derived Mφs. Resting M0-Mφs were polarized toward M1- and M2-Mφs, then M0-, M1- and M2-Mφs were all treated with physiological concentrations of Mox-LDL to assess the effect of Mox-LDL treatment on Mφ polarization and repolarization. Treatment of M0-Mφs with a physiological concentration of Mox-LDL had no significant effects at the level of their polarization. However, treatment of M1-Mφs with Mox-LDL resulted in a significant reduction in their IL-10 cytokine secretion. Our results point to a potential role of Mox-LDL in increasing the pro-inflammatory state in Mφs through reducing the release of the anti-inflammatory cytokine, IL-10.","PeriodicalId":13676,"journal":{"name":"Innate Immunity","volume":"28 1","pages":"91 - 103"},"PeriodicalIF":3.2,"publicationDate":"2022-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"47863097","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 4

A novel antimicrobial peptide derived from human BPIFA1 protein protects against Candida albicans infection. 从人BPIFA1蛋白中提取的一种新型抗菌肽可预防白色念珠菌感染。

IF 3.2 4区医学

Innate Immunity Pub Date : 2022-02-01 DOI: 10.1177/17534259221080543

Nan Hu, Xi-Ming Mo, Shi-Na Xu, Hao-Neng Tang, Ying-Hui Zhou, Long Li, Hou-De Zhou

{"title":"A novel antimicrobial peptide derived from human BPIFA1 protein protects against Candida albicans infection.","authors":"Nan Hu, Xi-Ming Mo, Shi-Na Xu, Hao-Neng Tang, Ying-Hui Zhou, Long Li, Hou-De Zhou","doi":"10.1177/17534259221080543","DOIUrl":"https://doi.org/10.1177/17534259221080543","url":null,"abstract":"Bactericidal/permeability-increasing fold containing family A, member 1 (BPIFA1) is an innate immunity defense protein. Our previous studies proved its antibacterial and antiviral effects, but its role in fungi remains unknown. The study aimed to identify antifungal peptides (AFP) derived from BPIFA1, and three antimicrobial peptides (AMP1-3) were designed. The antifungal effects were proved by growth inhibition assay. AMP3 activity was confirmed by germ tube growth experiment and XTT assay. Its effects on cell wall and membrane of Candida albicans were assessed by tannic acid and Annexin V-FITC/PI double staining, respectively. Additionally, scanning electron microscope (SEM) and transmission electron microscopy (TEM) were used for morphological and ultrastructural observation. The expression of ALS1, EAP1, and SUN41 was tested by qPCR. Ultimately, three AMPs could fight against C. albicans in vitro, and AMP3 was highly effective. It functioned by destroying the integrity of cell wall and normal structure of cell membrane. It also inhibited biofilm formation of C. albicans. In addition, AMP3 down-regulated the expression of ALS1, EAP1, and SUN41, those are known to be involved in virulence of C. albicans. Altogether, the study reported successful development of a novel AFP, which could be used as a new strategy for antifungal therapy.","PeriodicalId":13676,"journal":{"name":"Innate Immunity","volume":"28 2","pages":"67-78"},"PeriodicalIF":3.2,"publicationDate":"2022-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/70/6d/10.1177_17534259221080543.PMC9058375.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10238633","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

Down-regulation of hsa_circ_0045474 induces macrophage autophagy in tuberculosis via miR-582-5p/TNKS2 axis. 下调hsa_circ_0045474通过miR-582-5p/TNKS2轴诱导结核中巨噬细胞自噬。

IF 3.2 4区医学

Innate Immunity Pub Date : 2022-01-01 Epub Date: 2021-12-03 DOI: 10.1177/17534259211064285

Min Wu, Zhibin Liu, Shaojun Zhang

{"title":"Down-regulation of hsa_circ_0045474 induces macrophage autophagy in tuberculosis via miR-582-5p/TNKS2 axis.","authors":"Min Wu, Zhibin Liu, Shaojun Zhang","doi":"10.1177/17534259211064285","DOIUrl":"https://doi.org/10.1177/17534259211064285","url":null,"abstract":"Macrophage autophagy plays a major role in the control and elimination of invading Mycobacterium tuberculosis. However, the function and mechanism of circRNA on macrophage autophagy in tuberculosis remain unclear. Therefore, this study aimed to explore the role of circRNA underlying macrophage autophagy in tuberculosis. Quantitative real-time polymerase chain reaction was used to detect the expression of hsa_circ_0045474, miR-582-5p and TNKS2. Autophagy was detected by LC3B immunofluorescence and transmission electron microscopy. Dual-luciferase reporter assays were used to detect the relationship of miR-582-5p and hsa_circ_0045474 or TNKS2. Western blot was used to detect the expression of LC3-І and LC3-ІІ. The results showed that hsa_circ_0045474 was down-regulated in monocytes from patients with tuberculosis and induced autophagy in macrophages. hsa_circ_0045474 sponged miR-582-5p and negatively regulated miR-582-5p expression. Overexpression of miR-582-5p affected by hsa_circ_0045474 induced autophagy in macrophages. TNKS2 served as a target of miR-582-5p and down-regulation of TNKS2 induced autophagy in macrophages regulated by miR-582-5p. In conclusion, our results demonstrated that hsa_circ_0045474 down-regulation induced macrophage autophagy in tuberculosis via miR-582-5p/ TNKS2 axis, implying a novel strategy to treat the occurrence of active pulmonary tuberculosis caused by immune escape of M. tuberculosis.","PeriodicalId":13676,"journal":{"name":"Innate Immunity","volume":"28 1","pages":"11-18"},"PeriodicalIF":3.2,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/a8/56/10.1177_17534259211064285.PMC8841633.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39957532","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

Circ_0026579 alleviates LPS-induced WI-38 cells inflammation injury in infantile pneumonia. Circ_0026579减轻lps诱导的婴儿肺炎WI-38细胞炎症损伤。

IF 3.2 4区医学

Innate Immunity Pub Date : 2022-01-01 DOI: 10.1177/17534259211069104

Yang Yu, Tingting Yang, Zhaozheng Ding, Yuan Cao

{"title":"Circ_0026579 alleviates LPS-induced WI-38 cells inflammation injury in infantile pneumonia.","authors":"Yang Yu, Tingting Yang, Zhaozheng Ding, Yuan Cao","doi":"10.1177/17534259211069104","DOIUrl":"https://doi.org/10.1177/17534259211069104","url":null,"abstract":"Circular RNA (circRNA) represents an important regulator in infantile pneumonia progression. To clarify the role of circ_0026579 in this disease, LPS was used to treat WI-38 cells to mimic inflammation injury. The levels of inflammatory factors were determined by ELISA assay. Cell proliferation and apoptosis were measured by MTT assay, EdU staining and flow cytometry. The protein levels of cyclinD1, cleaved-caspase-3 and insulin-like growth factor 2 (IGF2) were examined using Western blot analysis. Cell oxidative stress was assessed by detecting MDA level and SOD activity. The expression of circ_0026579, miR-24-3p and IGF2 were analyzed using quantitative real-time PCR, and the interaction between miR-24-3p and circ_0026579 or IGF2 was confirmed by dual-luciferase reporter assay and RIP assay. LPS induced inflammation in WI-38 cells. Circ_0026579 expression was promoted in LPS-induced WI-38 cells, and its knockdown alleviated LPS-induced WI-38 cells inflammation. MiR-24-3p was sponged by circ_0026579, and its expression was reduced by LPS. MiR-24-3p inhibitor reversed the regulation of circ_0026579 knockdown on LPS-induced WI-38 cells inflammation. IGF2 was targeted by miR-24-3p, and its expression could be enhanced by LPS. MiR-24-3p relieved the inflammation of WI-38 cells which could be abolished by IGF2 overexpression. Circ_0026579 positively regulated IGF2 expression through sponging miR-24-3p. Circ_0026579 knockdown alleviated LPS-induced WI-38 cells inflammation by miR-24-3p/IGF2 axis, suggesting that circ_0026579 might contribute to infantile pneumonia progression.","PeriodicalId":13676,"journal":{"name":"Innate Immunity","volume":"28 1","pages":"37-48"},"PeriodicalIF":3.2,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/f1/d6/10.1177_17534259211069104.PMC8841632.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39782420","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

Delayed inflammation decrease is associated with mortality in Tocilizumab-treated critically ill SARS-CoV-2 patients: A retrospective matched-cohort analysis. 托珠单抗治疗的重症SARS-CoV-2患者的延迟炎症减轻与死亡率相关:一项回顾性匹配队列分析

IF 3.2 4区医学

Innate Immunity Pub Date : 2022-01-01 Epub Date: 2022-01-28 DOI: 10.1177/17534259211064602

Tomas Urbina, Jean-Rémi Lavillegrand, Marc Garnier, Arsene Mekinian, Jerome Pacanowski, Nathalie Mario, Guillaume Dumas, Geoffroy Hariri, Antoine Pilon, Lucie Darrivère, Muriel Fartoukh, Bertrand Guidet, Eric Maury, Judith Leblanc, Yannick Chantran, Olivier Fain, Karine Lacombe, Guillaume Voiriot, Hafid Ait-Oufella

{"title":"Delayed inflammation decrease is associated with mortality in Tocilizumab-treated critically ill SARS-CoV-2 patients: A retrospective matched-cohort analysis.","authors":"Tomas Urbina, Jean-Rémi Lavillegrand, Marc Garnier, Arsene Mekinian, Jerome Pacanowski, Nathalie Mario, Guillaume Dumas, Geoffroy Hariri, Antoine Pilon, Lucie Darrivère, Muriel Fartoukh, Bertrand Guidet, Eric Maury, Judith Leblanc, Yannick Chantran, Olivier Fain, Karine Lacombe, Guillaume Voiriot, Hafid Ait-Oufella","doi":"10.1177/17534259211064602","DOIUrl":"https://doi.org/10.1177/17534259211064602","url":null,"abstract":"Little is known about the immuno-inflammatory response to Tocilizumab and its association with outcome in critically-ill SARS-CoV2 pneumonia. In this multicenter retrospective cohort of SARS-CoV-2 patients admitted to three intensive care units between March and April 2020, we matched on gender and SAPS II 21 Tocilizumab-treated patients to 42 non-treated patients. Need for mechanical ventilation was 76% versus 79%. IL-6, C-reactive protein, and fibrinogen had been collected within the first days of admission (T1), 3 d (T2) and 7 d (T3) later. Tocilizumab-treated patients had persistently higher IL-6 plasma levels and persistently lower C-Reactive protein and fibrinogen levels. Among Tocilizumab-treated patients, baseline levels of inflammatory biomarkers were not different according to outcome. Conversely, C-reactive protein and fibrinogen decrease was delayed in non-survivors. C-Reactive protein decreased at T1 in survivors (45 [30-98] vs 170 [69-204] mg/l, P < 0.001) but only at T2 in non-survivors (37 [13-74] vs 277 [235-288], P = 0.03). Fibrinogen decreased at T2 in survivors (4.11 [3.58-4.69] vs 614 [5.61-7.85] g/l, P = 0.005) but not in non-survivors (4.79 [4.12-7.58] vs 7.24 [6.22-9.24] g/l, P = 0.125). Tocilizumab treatment was thus associated with a persistent both increase in plasma IL-6, and decrease in C-reactive protein and fibrinogen. Among Tocilizumab-treated patients, the decrease in inflammatory biomarkers was delayed in non-survivors.","PeriodicalId":13676,"journal":{"name":"Innate Immunity","volume":"28 1","pages":"3-10"},"PeriodicalIF":3.2,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/d3/99/10.1177_17534259211064602.PMC8841634.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39743896","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

Early kinetics of calprotectin in plasma following inguinal hernia surgery. 腹股沟疝手术后血浆钙保护蛋白的早期动力学。

IF 3.2 4区医学

Innate Immunity Pub Date : 2022-01-01 Epub Date: 2022-02-01 DOI: 10.1177/17534259211069635

Kristina Sejersen, Aleksandra Havelka, Pearl Sanchez Salas, Anders Larsson

{"title":"Early kinetics of calprotectin in plasma following inguinal hernia surgery.","authors":"Kristina Sejersen, Aleksandra Havelka, Pearl Sanchez Salas, Anders Larsson","doi":"10.1177/17534259211069635","DOIUrl":"https://doi.org/10.1177/17534259211069635","url":null,"abstract":"Calprotectin is one of the most abundant proteins of neutrophil granulocytes. It is released upon neutrophil activation and is considered a sensitive and clinically useful marker for neutrophil-mediated inflammation, including bacterial infections. However, early kinetics of calprotectin activation following inflammatory activation has hitherto been unknown. The aim of the present study was to determine the early phase of the kinetics of calprotectin, in comparison with the inflammatory markers CRP, IL-6, TNF-α, and procalcitonin, in plasma following a standardized temporary mild inflammatory response, using uncomplicated inguinal hernia surgery as a model. The study cohort consisted of 17 adult patients (15 male and 2 female) undergoing elective surgery for hernia. Values of calprotectin increased significantly at 2 h following surgery, and continued to increase to reach the highest level at 24-36 h after surgery, values still not exceeding upper normal reference level. This contrasts to IL-6 and CRP, for which an elevation was found first later, 4 h and 24-36 h post-surgery, respectively, for IL-6, and CRP. No significant increase was seen for TNF-α, or procalcitonin. The data demonstrate a very rapid and significant but modest increase in calprotectin following induction of mild inflammation, supporting that calprotectin can be useful for early detection of inflammatory response.","PeriodicalId":13676,"journal":{"name":"Innate Immunity","volume":"28 1","pages":"49-54"},"PeriodicalIF":3.2,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8841635/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39739195","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: 2