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| 1 | NETosis,complement,and coagulation:a triangular relationship显示文摘NETosis is a regulated form of neutrophil cell death that contributes to the host defense against pathogens and was linked to various diseases soon after its first description in 2004.During NETosis,neutrophils release neutrophil extracellular traps(NETs),which can capture and kill bacteria and other pathogens to prevent them from spreading.Although substantial progress has been made in our understanding of NETosis,the precise mechanism underlying NETosis is still a matter of debate.Research continues to elucidate the molecular pathways involved in NETosis.In recent years,interactions with the complement and coagulation systems have become increasingly apparent.Activated complement proteins can stimulate NET formation,and NETs,in turn,can serve as a platform for complement activation.In addition,NETs can act as a scaffold for thrombus formation during coagulation.While crosstalk between the coagulation and complement systems has been previously described,NETosis appears to be a third important player in this consortium to protect the host against pathogens.This review summarizes our current knowledge on the mutual interactions between NETosis,the complement system and the coagulation system,with an emerging description of their complex triangular relationship. | Cynthia M.de Bont Wilbert C.Boelens Ger J.M.Pruijn | 2019 | Cellular & Molecular Immunology2019，16，1： | 22 |
| 2 | TREM-1 multimerization is essential for its activation on monocytes and neutrophils显示文摘The triggering receptor expressed on myeloid cells-1(TREM-1)is a receptor expressed on innate immune cells.By promoting the amplification of inflammatory signals that are initially triggered by Toll-like receptors(TLRs),TREM-1 has been characterized as a major player in the pathophysiology of acute and chronic inflammatory diseases,such as septic shock,myocardial infarction,atherosclerosis,and inflammatory bowel diseases.However,the molecular events leading to the activation of TREM-1 in innate immune cells remain unknown.Here,we show that TREM-1 is activated by multimerization and that the levels of intracellular Ca 2+release,reactive oxygen species,and cytokine production correlate with the degree of TREM-1 aggregation.TREM-1 activation on primary human monocytes by LPS required a two-step process consisting of upregulation followed by clustering of TREM-1 at the cell surface,in contrast to primary human neutrophils,where LPS induced a rapid cell membrane reorganization of TREM-1,which confirmed that TREM-1 is regulated differently in primary human neutrophils and monocytes.In addition,we show that the ectodomain of TREM-1 is able to homooligomerize in a concentration-dependent manner,which suggests that the clustering of TREM-1 on the membrane promotes its oligomerization.We further show that the adapter protein DAP12 stabilizes TREM-1 surface expression and multimerization.TREM-1 multimerization at the cell surface is also mediated by its endogenous ligand,a conclusion supported by the ability of the TREM-1 inhibitor LR12 to limit TREM-1 multimerization.These results provide evidence for ligand-induced,receptor-mediated dimerization of TREM-1.Collectively,our findings uncover the mechanisms necessary for TREM-1 activation in monocytes and neutrophils. | Kevin Carrasco Amir Boufenzer Lucie Jolly Helene Le Cordier Guanbo Wang Albert JR Heck Adelheid Cerwenka Emilie Vinolo Alexis Nazabal Alexandre Kriznik Pierre Launay Sebastien Gibot Marc Derive | 2019 | Cellular & Molecular Immunology2019，16，5： | 13 |
| 3 | Development and validation of a prediction model for microvascular invasion in hepatocellular carcinoma显示文摘BACKGROUND Microvascular invasion(MVI)is an important prognostic factor affecting early recurrence and overall survival in hepatocellular carcinoma(HCC)patients after hepatectomy and liver transplantation,but it can be determined only in surgical specimens.Accurate preoperative prediction of MVI is conducive to clinical decisions.AIM To develop and validate a preoperative prediction model for MVI in patients with HCC.METHODS Data from 454 patients with HCC who underwent hepatectomy at the First Affiliated Hospital of Nanjing Medical University between May 2016 and October 2019 were retrospectively collected.Then,the patients were nonrandomly split into a training cohort and a validation cohort.Logistic regression analysis was used to identify variables significantly associated with MVI that were then included in the nomogram.We evaluated the discrimination and calibration ability of the nomogram by using R software.RESULTS MVI was confirmed in 209(46.0%)patients by a pathological examination.Multivariate logistic regression analysis identified four risk factors independently associated with MVI:Tumor size[odds ratio(OR)=1.195;95%confidence interval(CI):1.107–1.290;P<0.001],number of tumors(OR=4.441;95%CI:2.112–9.341;P<0.001),neutrophils(OR=1.714;95%CI:1.036–2.836;P=0.036),and serumα-fetoprotein(20–400 ng/mL,OR=1.955;95%CI:1.055–3.624;P=0.033;>400 ng/mL,OR=3.476;95%CI:1.950–6.195;P<0.001).The concordance index was 0.79(95%CI:0.74–0.84)and 0.81(95%CI:0.74–0.89)in the training and validation cohorts,respectively.The calibration curves showed good agreement between the predicted risk by the nomogram and real outcomes.CONCLUSION We have developed and validated a preoperative prediction model for MVI in patients with HCC.The model could aid physicians in clinical treatment decision making. | Lin Wang Yue-Xinzi Jin Ya-Zhou Ji Yuan Mu Shi-Chang Zhang Shi-Yang Pan | 2020 | World Journal of Gastroenterology2020，26，14： | 12 |
| 4 | Characterization and allergic role of IL-33-induced neutrophil polarization显示文摘Neutrophils are involved in the pathogenesis of allergy.However,the contribution of the different functionally polarized neutrophils in allergy needs to be clarified.We sought to define the characteristics of interleukin(IL)-33-induced neutrophils and the involvement of this subset of polarized neutrophils in allergic pathogenesis.Freshly isolated neutrophils were treated with different cytokines and the cytokine expression levels were detected by realtime PCR.The gene expression profile of IL-33-induced neutrophils was determined by microarray assay.Adoptive transfer assay was used to investigate the function of IL-33-induced neutrophils in an ovalbumin(OVA)-induced allergic asthma model.IL-33-treated neutrophils selectively produced IL-4,IL-5,IL-9 and IL-13(referred as to N(IL-33)cells)and displayed a distinctive gene expression profile in sharp contrast to resting and lipopolysaccharide(LPS)-treated neutrophils.IL-33-induced neutrophils expressed high Levels of IL-1R2 on cell surface,whereas resting and LPS-treated neutrophils did not,indicating IL-1R2 might be used as a biomarker for N(IL-33)cells.Importantly,N(IL-33)neutrophils exist in the lungs of OVA-induced allergic asthma mice.Adoptive transfer of N(IL-33)neutrophils significantly promotes the severity of the lung pathogenesis in this model.IL-33 induces neutrophil polarization through c-Jun N-terminal kinase-and nuclear factor-κB-dependent pathways.A previously unappreciated neutrophil polarization driven by IL-33 with unique cell surface markers and cytokine/chemokineproducing gene profile was defined.The newly identified N(IL-33)subpopulation may have significant contribution to IL-33-related pathogenesis. | Bo Sun Linnan Zhu Yaling Tao Hai-Xi Sun Yang Li Peng Wang Yuzhu Hou Yang Zhao Xiaodong Zhang Lianfeng Zhang Ning Na Yong Zhao | 2018 | Cellular & Molecular Immunology2018，15，8： | 9 |
| 5 | Pathobiology of the neutrophil-intestinal epithelial cell interaction:Role in carcinogenesis显示文摘The role of chronic inflammation,acting as an independent factor,on the onset of gastrointestinal carcinogenesis is now well accepted.However,even if there is an increase in the number of elements directly involving polymorphonuclear leukocytes (PMNL),as a major actor in digestive carcinogenesis,the different cellular and molecular events occurring in this process are still not completely understood.The transepithelial migration of PMNL,which is the ultimate step of the afflux of PMNL into the digestive mucosa,is a complex phenomenon involving sequential interaction of molecules expressed both on PMNL and on digestive epithelial cells.Chronic inflammatory areas rich in PMNL [so-called (chronic active inflammation)] and iterative transepithelial migration of PMNL certainly evoke intracellular signals,which lead toward progressive transformation of epithelia.Among these different signals,the mutagenic effect of reactive oxygen species and nitrates,the activation of the nuclear factor-κB pathway,and the modulation of expression of certain microRNA are key actors.Following the initiation of carcinogenesis,PMNL are involved in the progression and invasion of digestive carcinomas,with which they interact.It is noteworthy that different subpopulations of PMNL,which can have some opposite effects on tumor growth,in association with different levels of transforming growth factor-β and with the number of CD8 positive T lymphocytes,could be present during the development of digestive carcinoma.Other factors that involve PMNL,such as massive elastase release,and the production of angiogenic factors,can participate in the progression of neoplastic cells through tissues.PMNL may play a major role in the onset of metastases,since they allow the tumor cells to cross the endothelial barrier and to migrate into the blood stream.Finally,PMNL play a role,alone or in association with other cell parameters,in the initiation,promotion,progression and dissemination of digestive carcinomas.This review focuses on the main currently accepted cellular and molecular mechanisms that involve PMNL as key actors in digestive carcinogenesis. | Paul M Hofman | 2010 | World Journal of Gastroenterology2010，16，46： | 9 |
| 6 | Neutrophil chemoattractant receptors in health and disease: double-edged swords显示文摘Neutrophils are frontline cells of the innate immune system.These effector leukocytes are equipped with intriguing antimicrobial machinery and consequently display high cytotoxic potential.Accurate neutrophil recruitment is essential to combat microbes and to restore homeostasis,for inflammation modulation and resolution,wound healing and tissue repair.After fulfilling the appropriate effector functions,however,dampening neutrophil activation and infiltration is crucial to prevent damage to the host.In humans,chemoattractant molecules can be categorized into four biochemical families,i.e.,chemotactic lipids,formyl peptides,complement anaphylatoxins and chemokines.They are critically involved in the tight regulation of neutrophil bone marrow storage and egress and in spatial and temporal neutrophil trafficking between organs.Chemoattractants function by activating dedicated heptahelical G protein-coupled receptors(GPCRs).In addition,emerging evidence suggests an important role for atypical chemoattractant receptors(ACKRs)that do not couple to G proteins in fine-tuning neutrophil migratory and functional responses.The expression levels of chemoattractant receptors are dependent on the level of neutrophil maturation and state of activation,with a pivotal modulatory role for the(inflammatory)environment.Here,we provide an overview of chemoattractant receptors expressed by neutrophils in health and disease.Depending on the(patho)physiological context,specific chemoattractant receptors may be up-or downregulated on distinct neutrophil subsets with beneficial or detrimental consequences,thus opening new windows for the identification of disease biomarkers and potential drug targets. | Mieke Metzemaekers Mieke Gouwy Paul Proost | 2020 | Cellular & Molecular Immunology2020，17，5： | 8 |
| 7 | Immunology of tuberculosis显示文摘Various T cells and macrophages as well as cytokines are involved in the immunopathogenesis of tuberculosis(TB). A better understanding of immunology of TB can not only lead to the discovery of new immunodiagnostic tools, accelerate and facilitate the assessment of new therapeutic methods, but also find new treatment regimens. In this highlight topic we cover the latest developments in the role of T cells, macrophages, Natural killer(NK) cells, invariant NK T(iN KT) cells and γδ T cells with TB infection. Histologically, TB displays exudative inflammation, proliferative inflammation and productive inflammation depending on the time course. T cells first recognize antigen within the mycobacterially-infected lung, and then activate, differentiate, but the first T cell activation occurs in the draining lymph nodes of the lung. When protective T cells reach sufficient numbers, they can stop bacterial growth. Except for T cells, neutrophils also participate actively in defense against early-phase TB. NK cells are innate lymphocytes which are a first line of defense against mycobacterial infection. Human NK cells use the NKp46, NCRs and NKG2 D receptors to lyse Mycobacterium TB-infected monocytes and alveolar macrophages. NK cells produce not only interferon-γ, but also interleukin(IL)-22, which is induced by IL-15 and DAP-10. iN KT cells show different phenotypes and functions. Many iN KT cells are CD4+,few iN KT cells are CD8+, while an additional fraction of iN KT cells are negative for both CD4 and CD8. γδ T cells represent an early innate defense in antimycobacterial immunity. Studies done in humans and animal models have demonstrated complex patterns of γδ T cell immune responses during chronic TB. Human alveolar macrophages and monocytes can serve as antigen presentation cells for γδ T cells. Furthermore, the predominance of Vγ9Vδ2 T cells in TB has been confirmed. | Qing Zhang Isamu Sugawara | 2012 | World Journal of Experimental Medicine2012，2，4： | 8 |
| 8 | Interleukin-1 and estrogen protect against disseminating dentoalveolar infections显示文摘Dentoalveolar bacterial infections cause localized tissue and bone destruction, but usually remain well-localized within teeth in immunocompetent hosts. However, in certain cases these infections may invade head and neck tissues, resulting in orofacial abscesses, cellulitis and sepsis, with resultant high morbidity and even mortality. In the present studies, we developed a novel model of spreading dentoalveolar infections in mice by treatment with neutralizing antibodies against both interleukin-1α(IL-1α)and IL-1β. Surprisingly male but not female mice given anti-IL-1 antibodies developed orofacial abscesses, weight loss,splenomegaly and sepsis. Female mice developed abscesses and sepsis comparable to males following ovariectomy(OVX), which was reversed by estrogen supplementation. Anti-IL-1 blockade inhibited IL-12, interferon γ(IFNγ) and IL-6 but not IL-10 expression in infrabony lesions, suggestive of a local anti-inflammatory response. There was greater infiltration of neutrophils and other inflammatory cells into lesions in anti-IL-1-treated animals; however, blood leukocytes had reduced bacterial phagocytic and killing activity ex vivo. Estrogen directly stimulated IL-1 production by macrophages, suggesting that the resistance of females to disseminating dentoalveolar infections may be due to their heightened pro-inflammatory responses following bacterial challenge, leading to enhanced localization of these infections. | hesham youssef philip stashenko | 2017 | International Journal of Oral Science2017，9，1： | 7 |
| 9 | IL-33 induces immunosuppressive neutrophils via a type 2 innate lymphoid cell/IL-13/STAT6 axis and protects the liver against injury in LCMV infection-induced viral hepatitis显示文摘Viral hepatitis is still a public health problem affecting several million people around the world.Neutrophils are polymorphonuclear cells that have a critical role in antibacterial infection.However,the role of neutrophils in viral infection is not fully understood.By using a mouse model of lymphocytic choriomeningitis virus infection-induced viral hepatitis,we observed increased neutrophil recruitment in the liver accompanied by enhanced CD8+T-cell responses.Liver neutrophils expressed high levels of immunomodulatory cytokines,such as C-X-C chemokine ligand 2,arginase-1,inducible nitric oxide synthase and interleukin(IL)-10,demonstrating immunosuppressive properties.Depletion of neutrophils in vivo by a neutralizing antibody resulted in the exacerbation of liver injury and the promotion of T-cell responses at the immune contraction stage.IL-33 significantly induced neutrophil recruitment in the liver and attenuated liver injury by limiting effector T-cell accumulation.Mechanistically,we found that IL-33 promoted the expression of arginase-1 in neutrophils through the type 2 innate lymphoid cell(ILC2)-derived IL-13.Additionally,IL-13 increased the inhibitory effect of neutrophils on CD8+T-cell proliferation in vitro,partially through arginase-1.Finally,we found that IL-13 induced arginase-1 expression,depending on signal transducer and activator of transcription factor 6(STAT6)signaling.Therefore,IL-33 induced immunosuppressive neutrophils via an ILC2/IL-13/STAT6 axis.Collectively,our findings shed new light on the mechanisms associated with IL-33-triggered neutrophils in the liver and suggest potential targets for therapeutic investigation in viral hepatitis. | Yuejin Liang Panpan Yi Denley Ming Kee Yuan Zuliang Jie Zakari Kwota Lynn Soong Yingzi Cong Jiaren Sun | 2019 | Cellular & Molecular Immunology2019，16，2： | 7 |
| 10 | The increase in surface CXCR4 expression on lung extravascular neutrophils and its effects on neutrophils during endotoxin-induced lung injury显示文摘Inflammatory stimuli,such as a microbes or lipopolysaccharides,induce a rapid release of neutrophils from the bone marrow and promote neutrophil migration into inflamed sites to promote host defense.However,an excess accumulation and retention of neutrophils in inflamed tissue can cause severe tissue injuries in the later stages of inflammation.Recent studies have reported that both CXCL12 levels in injured lungs and its receptor,CXCR4,on accumulated neutrophils in injured lungs,increased;furthermore,these studies showed that the CXCL12/CXCR4 signaling pathway participated in neutrophil accumulation in the later stages of lipopolysaccharide(LPS)-induced lung injury.However,the mechanisms underlying this increase in surface CXCR4 expression in neutrophils remain unclear.In this study,we found that surface CXCR4 expression increased in extravascular,but not intravascular,neutrophils in the lungs of LPS-induced lung injury model mice.Furthermore,ex vivo studies revealed that CXCL12 acted not only as a chemoattractant,but also as a suppressor of cell death for the lung neutrophils expressing CXCR4.Sulfatide,one of the native ligands for L-selectin,induced the increase of surface CXCR4 expression on isolated circulating neutrophils,suggesting that the activation of L-selectin may be involved in the increase in surface CXCR4.Our findings show that surface CXCR4 levels on neutrophils increase after extravasation into injured lungs,possibly through the activation of L-selectin.The CXCL12/CXCR4 signaling pathway plays an important role in the modulation of neutrophil activity during acute lung injury,not only by promoting chemotaxis but also by suppressing cell death. | Mitsuhiro Yamada Hiroshi Kubo Seiichi Kobayashi Kota Ishizawa Mei He Takaya Suzuki Naoya Fujino Hiroyuki Kunishima Masamitsu Hatta Katsushi Nishimaki Tetsuji Aoyagi Kouichi Tokuda Miho Kitagawa Hisakazu Yano Hirokazu Tamamura Nobutaka Fujii Mitsuo Kaku | 2011 | Cellular & Molecular Immunology2011，8，4： | 6 |
| 11 | Characteristics, phenotypes, mechanisms and management of severe asthma显示文摘Severe asthma is 'asthma which requires treatment with high dose inhaled corticosteroids (ICS) plus a second controller (and/or systemic corticosteroids) to prevent it from becoming ’’uncontrolled’ or which remains ’’uncontrolled’ despite this therapy.' The state of control was defined by symptoms, exacerbations and the degree of airflow obstruction. Therefore, for the diagnosis of severe asthma, it is important to have evidence for a diagnosis of asthma with an assessment of its severity, followed by a review of comorbidities, risk factors, triggers and an assessment of whether treatment is commensurate with severity, whether the prescribed treatments have been adhered to and whether inhaled therapy has been properly administered. Phenotyping of severe asthma has been introduced with the definition of a severe eosinophilic asthma phenotype characterized by recurrent exacerbations despite being on high dose ICS and sometimes oral corticosteroids, with a high blood eosinophil count and a raised level of nitric oxide in exhaled breath. This phenotype has been associated with a Type-2 (T2) inflammatory profile with expression of interleukin (IL)-4, IL-5, and IL-13. Molecular phenotyping has also revealed non-T2 inflammatory phenotypes such as Type-1 or Type-17 driven phenotypes. Antibody treatments targeted at the T2 targets such as anti-IL5, anti-IL5Rα, and anti-IL4Rα antibodies are now available for treating severe eosinophilic asthma, in addition to anti-immunoglobulin E antibody for severe allergic asthma. No targeted treatments are currently available for non-T2 inflammatory phenotypes. Long-term azithromycin and bronchial thermoplasty may be considered. The future lies with molecular phenotyping of the airway inflammatory process to refine asthma endotypes for precision medicine. | Kian Fan Chung Piers Dixey Hisham Abubakar-Waziri Pankaj Bhavsari Pujan H.Patel Sujuan Guo Yang Ji | 2022 | Chinese Medical Journal2022，，10： | 6 |
| 12 | Sialic acid-binding immunoglobulin-like lectin 9 as a potential therapeutic target for chronic obstructive pulmonary disease显示文摘Chronic obstructive pulmonary disease(COPD)has become the third-leading cause of death worldwide,which is a severe economic burden to the healthcare system.Chronic bronchitis is the most common condition that contributes to COPD,both locally and systemically.Neutrophilic inflammation predominates in the COPD airway wall and lumen.Logically,repression of neutrophilia is an essential fashion to COPD treatment.However,currently available anti-neutrophilic therapies provide little benefit in COPD patients and may have serious side effects.Thus,there is an urgent need to explore an effective and safe anti-neutrophilic approach that might delay progression of the disease.Sialic acid-binding immunoglobulin-like lectin(Siglec)-9 is a member of the Siglec cell surface immunoglobulin family.It is noteworthy that Siglec-9 is highly expressed on human neutrophils and monocytes.Ligation of Siglec-9 by chemical compounds or synthetic ligands induced apoptosis and autophagic-like cell death in human neutrophils.Furthermore,administration of antibody to Siglec-E,mouse functional ortholog of Siglec-9,restrained recruitment and activation of neutrophils in mouse models of airway inflammation in vivo.Given the critical role that neutrophils play in chronic bronchitis and emphysema,targeting Siglec-9 could be beneficial for the treatment of COPD,asthma,fibrosis,and related chronic inflammatory lung diseases. | Zi Chen Shuang-Lan Xu Lin-Yang Ge Jin Zhu Tao Zheng Zhou Zhu Linfu Zhou | 2021 | Chinese Medical Journal2021，，7： | 5 |
| 13 | Simple hematological predictors of AF recurrence in patients undergoing atrial fibrillation ablation显示文摘Backgound Red cell distribution width(RDW) and neutrophil-to-lymphocyte ratio(NLR) are simple hematologic indices that have been used to predict adverse outcomes in different clinical settings. The aim of our study is to determine whether RDW and NLR can predict atrial fibrillation(AF) recurrence in patients undergoing AF ablation. Methods Consecutive patients, without known hematological disorders, who underwent AF catheter ablation between January 2014 and April 2017 were enrolled into this study. Blood samples were taken one day before and five hours after the ablation procedure. Results A total of 346 patients(224 males(65%), mean age: 59 ± 11 years old) were included. After a mean follow up of 26.2 ± 12.1 months, 80(23.1%) patients experienced late AF recurrence(defined as any recurrence after the blanking period of three months), while 97(28%) patients experienced early AF recurrence during the blanking period. Univariate analysis showed that early arrhythmia recurrence, type of AF and NLR after the procedure were significantly associated with late AF recurrence, while early arrhythmia recurrence and NLR remained significant in multivariate analysis. RDW was not associated with late AF recurrence. None of the parameters above predicted early arrhythmia recurrence. Conclusions Simple and inexpensive hematological indices such as NLR should be evaluated for their ability to predict AF recurrence in patients undergoing catheter ablation in larger prospective studies. | George Bazoukis Konstantinos P Letsas Konstantinos Vlachos Athanasios Saplaouras Dimitrios Asvestas Konstantinos Tyrovolas Aikaterini Rokiza Eirini Pagkalidou Gary Tse Stavros Stavrakis Antonios Sideris Michael Efremidis | 2019 | Journal of Geriatric Cardiology2019，16，9： | 4 |
| 14 | Surface modification of PGP for a neutrophil–nanoparticle co-vehicle to enhance the anti-depressant effect of baicalein显示文摘Exploiting cells as vehicles combined with nanoparticles combined with therapy has attracted increasing attention in the world recently. Red blood cells, leukocytes and stem cells have been used for tumor immunotherapy, tissue regeneration and inflammatory disorders, and it is known that neutrophils can accumulate in brain lesions in many brain diseases including depression. N-Acetyl Pro–Gly–Pro(PGP) peptide shows high specific binding affinity to neutrophils through the CXCR2 receptor. In this study, PGP was used to modify baicalein-loaded solid lipid nanoparticles(PGP-SLNs) to facilitate binding to neutrophils in vivo. Brain-targeted delivery to the basolateral amygdala(BLA) was demonstrated by enhanced concentration of baicalein in the BLA. An enhanced anti-depressant effect was observed in vitro and in vivo. The mechanism involved inhibition of apoptosis and a decrease in lactate dehydrogenase release. Behavioral evaluation carried out with rats demonstrated that anti-depression outcomes were achieved. The results indicate that PGP-SLNs decrease immobility time, increase swimming time and climbing time and attenuate locomotion in olfactory-bulbectomized(OB) rats. In conclusion, PGP modification is a strategy for targeting the brain with a cell–nanoparticle delivery system for depression therapy. | Baoyu Chen Man Luo Jianming Liang Chun Zhang Caifang Gao Jue Wang Jianxin Wang Yongji Li Desheng Xu Lina Liu Ning Zhang Huijun Chen Jing Qin | 2018 | Acta Pharmaceutica Sinica B2018，8，1： | 4 |
| 15 | Differential diagnoses of magnetic resonance imaging for suspected acute appendicitis in pregnant patients显示文摘BACKGROUND: Accurate and timely diagnosis of acute surgical disease in pregnant patient is chal enging. Although magnetic resonance imaging(MRI) is the most accurate modality to diagnose acute appendicitis in pregnant patients, it is often used as a last resort because of high cost and long scan time. We performed this study to analyze differential diagnoses of appendix MRI and to investigate if there are any blood tests that can predict surgical condition in pregnant patients.METHODS: A retrospective, cross-sectional study was conducted on 46 pregnant patients who underwent non-enhanced appendix MRI in suspicion of acute appendicitis from 2010 to 2016. Differential diagnoses of appendix MRI were analyzed and blood tests were compared between those who had surgical and non-surgical disease.RESULTS: Appendix MRI differentiated two surgical disease; acute appendicitis and ovarian torsion; and various non-surgical conditions such as uterine myoma, hydronephrosis, ureterolithiasis and diverticulitis among clinically suspected acute appendicitis in pregnancy. The diagnostic accuracy of MRI for acute appendicitis in this study was 93.5%. Patients who had surgical disease showed significantly higher WBC count(≥11,000/mm^3), proportion of neutrophils in the WBC(≥79.9%), neutrophil-to-lymphocyte ratio(NLR≥6.4), levels of C-reactive protein(CRP≥1.82 mg/dL) and bilirubin(≥0.66 mg/dL) than those who had non-surgical disease.CONCLUSION: MRI can reliably differentiate surgical conditions and several blood tests(WBC, proportion of neutrophils in the WBC, NLR, CRP, bilirubin) can help anticipate acute surgical condition among pregnant patients suspected to have acute appendicitis. | Ji Yong Jung Ji Ung Na Sang Kuk Han Pil Cho Choi Jang Hee LEE Dong Hyuk Shin | 2018 | World Journal of Emergency Medicine2018，9，1： | 4 |
| 16 | Neutrophil programming dynamics and its disease relevance显示文摘Neutrophils are traditionally considered as first responders to infection and provide antimicrobial host defense. However, recent advances indicate that neutrophils are also critically involved in the modulation of host immune environments by dynamically adopting distinct functional states. Functionally diverse neutrophil subsets are increasingly recognized as critical components mediating host pathophysiology. Despite its emerging significance, molecular mechanisms as well as functional relevance of dynamically programmed neutrophils remain to be better defined. The increasing complexity of neutrophil functions may require integrative studies that address programming dynamics of neutrophils and their pathophysiological relevance. This review aims to provide an update on the emerging topics of neutrophil programming dynamics as well as their functional relevance in diseases. | Taojing Ran Shuo Geng Liwu Li | 2017 | Science China(Life Sciences)2017，60，11： | 3 |
| 17 | The role of LOX-1 on innate immunity against Aspergillus keratitis in mice显示文摘AIM:To explore the effects of lectin-like ox-LDL receptor(LOX-1) on innate immunity against Aspergillus fumigatus(A.fumigatus) in mice cornea.METHODS:The mRNA levels of LOX-1 were tested in normal and A.fumigatus infected corneas of C57BL/6and BALB/c mice.The expression of LOX-1,pro-inflammatory cytokines TNF-α,CXCL1 and IL-6,antiinflammatory cytokines IL-10,and matrix metalloproteinase 9(MMP9) were tested with treatment with LOX-1 neutralizing antibody or control IgG in A.fum/gatus infected corneas of C57BL/6.Macrophages and neutrophils were extracted from susceptible C57BL/6mice,and pretreated with LOX-1 neutralizing antibody or IgG,then stimulated with A.fum/gatus.The mRNA levels of LOX-1,TNF-α,CXCL1,IL-6,IL-10 and MMP9 were evaluated by polymerase chain reaction.RESULTS:The expression of LOX-1 was significantly increased in C57BL/6 mice corneas after A.fum/gatus infection compared with BABL/c mice.After treatment with LOX-1 neutralizing antibody,the expression of LOX-1,TNF-α,CXCL1,IL-6,MMP9 and IL-10 in C57BL/6corneas were significantly decreased compared with treatment with control IgG;the expression of LOX-1,CXCL1,IL-6 and IL-10 were significantly decreased in macrophages,while TNF-α and MMP9 expressions had no change;LOX-1,TNF-α,CXCL1,IL-6,MMP9 and IL-10 expressions were significantly decreased in neutrophils.CONCLUSION:The expression of LOX-1 can affect the expression of pro-inflammatory and anti-inflammatory cytokines in fungal infected corneas,macrophages and neutrophils of C57BL/6.LOX-1 inhibition rebalances the inflammatory response of fungal keratitis in mice. | Kun He Li-Hui Yue Gui-Qiu Zhao Cui Li Jing Lin Nan Jiang Qian Wang Qiang Xu Xu-Dong Peng Li-Ting Hu Jie Zhang | 2016 | International Journal of Ophthalmology(English edition)2016，9，9： | 3 |
| 18 | Role of the CXCR4-SDF1-HMGB1 pathway in the directional migration of cells and regeneration of affected organs显示文摘In recent years,several studies have reported positive outcomes of cell-based therapies despite insufficient engraftment of transplanted cells.These findings have created a huge interest in the regenerative potential of paracrine factors released from transplanted stem or progenitor cells.Interestingly,this notion has also led scientists to question the role of proteins in the secretome produced by cells,tissues or organisms under certain conditions or at a particular time of regenerative therapy.Further studies have revealed that the secretomes derived from different cell types contain paracrine factors that could help to prevent apoptosis and induce proliferation of cells residing within the tissues of affected organs.This could also facilitate the migration of immune,progenitor and stem cells within the body to the site of inflammation.Of these different paracrine factors present within the secretome,researchers have given proper consideration to stromal cell-derived factor-1(SDF1)that plays a vital role in tissue-specific migration of the cells needed for regeneration.Recently researchers recognized that SDF1 could facilitate site-specific migration of cells by regulating SDF1-CXCR4 and/or HMGB1-SDF1-CXCR4 pathways which is vital for tissue regeneration.Hence in this study,we have attempted to describe the role of different types of cells within the body in facilitating regeneration while emphasizing the HMGB1-SDF1-CXCR4 pathway that orchestrates the migration of cells to the site where regeneration is needed. | Nazmul Haque Ismail M Fareez Liew Fong Fong Chanchal Mandal Noor Hayaty Abu Kasim Kranthi RajaKacharaju Pratiwi Soesilawati | 2020 | World Journal of Stem Cells2020，12，9： | 3 |
| 19 | Characterization and biological significance of IL-23-induced neutrophil polarization显示文摘Neutrophils are heterogeneous with distinct subsets,and can switch phenotypes to exert regulatory functions on immunity.We herein demonstrate that IL-23-treated neutrophils selectively produce IL-17A,IL-17F and IL-22,and display a distinct gene expression profile in contrast to resting and lipopolysaccharide-treated neutrophils.IL-17+neutrophils are present in the colons of mice with dextran sulfate sodium-induced colitis.Adoptive transfer of IL-23-treated neutrophils significantly promotes pathogenesis in this model.IL-23 induces neutrophil polarization through STAT3-dependent RORγt and BATF pathways.Thus,IL-23-induced neutrophil polarization expresses a unique cytokine-producing profile,which may contribute to IL-23-mediated inflammatory diseases. | Yang Li Linnan Zhu Zhulang Chu Tao Yang Hai-Xi Sun Fan Yang Wei Wang Yuzhu Hou Peng Wang Qingjie Zhao Yaling Tao Lianfeng Zhang Xiaodong Zhang Yong Zhao | 2018 | Cellular & Molecular Immunology2018，15，5： | 3 |
| 20 | Contribution of neutrophils in the pathogenesis of rheumatoid arthritis显示文摘Neutrophils are major innate immune effector cells for host defense and have been a topic of active research for their participation in the pathogenesis of autoimmune inflammatory diseases including rheumatoid arthritis(RA)due to recently discovered neutrophil extracellular trap(NET) formation. NET formation and other mechanisms leading to the release of neutrophil nuclear and cytoplasmic contents are implicated as a source of citrullinated antigens in RA. Further investigations are required to delineate what factors diverge neutrophils from host defense to autoimmune response in RA. | Lingshu Zhang Yi Yuan Qiang Xu Zhengyu Jiang Cong-Qiu Chu | 2020 | The Journal of Biomedical Research2020，34，2： | 3 |
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