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Hydatidiform moles are gestational trophoblastic disease. They are abnormal proliferations of trophoblast cells that have the potential to become cancerous. miR‐miR30a‐5p is a tumour suppressor that participates in the development of numerous diseases. However, the role of miR‐30a in hydatidiform moles and the mechanisms underlying its effects are presently unclear. This study explored the levels of miR‐30a and B3GNT5 expression in human hydatidiform mole tissue. The results showed that miR‐30a and B3GNT5 were differentially expressed in normal placenta and hydatidiform mole, and miR‐30a decreased cell proliferation, invasion and migration in trophoblast cell lines. Upon further examination, it was confirmed that miR‐30a directly targeted the 3’untranslated region of B3GNT5 using a dual‐luciferase assay. The results of the present study also revealed that miR‐30a reduced the proliferation, invasion and migration ability in JAR and BeWo cells by regulating B3GNT5, which may inactivate the ERK and AKT signalling pathways. This study demonstrated that miR‐30a was a novel target B3GNT5 that serves an important role in the development of hydatidiform moles, suggesting that miR‐30a may serve as a novel potential biomarker or useful diagnostic and therapeutic tool for hydatidiform moles in clinical settings.

Background: Pyruvate dehydrogenase protein X (PDHX) is a non-catalytic subunit of the pyruvate dehydrogenase (PDH) complex. It is located in the center of mitochondrial energy metabolism and is an essential component to maintain the biological activity of PDH complex. The purpose of this study was to explore its expression level in gastric cancer and its relationship with immune infiltration. Methods: Through immunohistochemical analysis of 80 pairs of gastric cancer tissue samples and open database analys such as Kaplan-Meier Plotter, TIMER2.0,GEPIA,String and DAVID database.Results: We found that the expression of PDHX in paracancerous tissues was significantly higher than that in gastric cancer tissues. Database analysis showed that the expression of PDHX was low in gastric cancer tissues, and the total survival time (OS) of relatively high expression in gastric cancer patients was higher. In N1~N3 and M stages, the P values of OS and PFS with high expression of PDHX were less than 0.05. It is suggested that the overexpression of PDHX may affect the prognosis of gastric cancer patients with lymph node and distant metastasis. Conclusions: Therefore, we concluded that the expression of PDHX is suppressed in gastric cancer and has a longer overall survival time of 5 years in patients with relatively high expression, and that the increased expression of PDHX may improve the prognosis of patients with lymph node and distant metastasis of gastric cancer.

The physiological chirality of extracellular environments is substantially affected by pathological diseases. However, how this stereochemical variation drives host immunity remains poorly understood. Here, it is reported that pathology-mimetic M-nanofibrils-but not physiology-mimetic P-nanofibrils-act as a defense mechanism that helps to restore tissue homeostasis by manipulating immunological response. Quantitative multi-omics in vivo and in vitro shows that M-nanofibrils significantly inhibit inflammation and promote tissue regeneration by upregulating M2 macrophage polarization and downstream immune signaling compared with P-nanofibrils. Molecular analysis and theoretical simulation demonstrate that M-chirality displays higher stereo-affinity to cellular binding, which induces higher cellular contractile stress and activates mechanosensitive ion channel PIEZOl to conduct Ca2+ influx. In turn, the nuclear transfer of STAT is biased by Ca2+ influx to promote M2 polarization. These findings underscore the structural mechanisms of disease, providing design basis for immunotherapy with bionic functional materials.

Introduction: N6-methyladenosine (m6A) is the most abundant form of methylation modification in eukaryotic cell mRNA. However, the role of m6A in gastric cancer is unclear, which is one of the most common gastrointestinal malignancies. The m6A-relevant mRNA signatures and risk scores are determined to predict the prognosis of gastric cancer in this study.Methods: The expression profiles and clinical information of 367 patients were downloaded from the Cancer Genome. Cluster analysis and univariate Cox analysis were used to identify the regulatory factors of RNA methylation associated with gastric cancer prognosis. The co-expression network was constructed by the WGCNA package in R. Then, the correlations between module eigengenes and clinical traits were calculated to identify the relevant modules. We used univariate Cox analysis to screen for genes that were significantly associated with prognosis in the module (P < 0.01 was considered significant). We identified hub genes by LASSO and multivariate analysis, and developed a Cox prognostic model. Finally, the hub gene expression values weighted by the coefficients from the LASSO regression generated a risk score for each patient, receiver operating characteristic (ROC) and Kaplan-Meier curves were used to assess the prognostic capacity of the risk scores.Results: HNRNPC was shown as P1 in the TCGA gastric cancer data set, which might be a pathogenic factor affecting the prognosis of gastric cancer. The results indicated that AARD, ASPN, SLAMF9, MIR3117 and DUSP1 were hub genes affecting the prognosis of gastric cancer patients, and the m6A methylation of these mRNAs might be regulated by HNRNPC. The risk score = − (0.166195281×AARD + 0.016850602×ASPN + 0.591607997×SLAMF9 + 0.591607997×MIR3117 + 0.00276337×DUSP1), and our results indicated a bad performance of the five-gene signature for survival prediction (P < 0.05).Conclusion: HNRNPC (a m6A RNA methylation regulator) can participate in the serious progression of gastric cancer by regulating the m6A of AARD, ASPN, SLAMF9, MIR3117 and DUSP1, which may be used for prognosis stratification and treatment strategy formulation.

Repairing tooth defects with dental resin composites is currently the most commonly used method due to their tooth-colored esthetics and photocuring properties. However, the higher than desirable failure rate and moderate service life are the biggest challenges the composites currently face. Secondary caries is one of the most common reasons leading to repair failure. Therefore, many attempts have been carried out on the development of a new generation of antimicrobial and therapeutic dental polymer composite materials to inhibit dental caries and prolong the lifespan of restorations. These new antimicrobial materials can inhibit the formation of biofilms, reduce acid production from bacteria and the occurrence of secondary caries. These results are encouraging and open the doors to future clinical studies on the therapeutic value of antimicrobial dental resin-based restoratives. However, antimicrobial resins still face challenges such as biocompatibility, drug resistance and uncontrolled release of antimicrobial agents. In the future, we should focus on the development of more efficient, durable and smart antimicrobial dental resins. This article focuses on the most recent 5 years of research, reviews the current antimicrobial strategies of composite resins, and introduces representative antimicrobial agents and their antimicrobial mechanisms.

Dihydroartemisinin (DHA) is a semi-synthetic derivative and the main active metabolite of artemisinin. The purpose of this study was to investigate the effect of DHA on the ulcerative colitis (UC) in both in vivo and in vitro models. Weight, survival rate, colon length, and Disease Activity Index score were used to evaluate the severity of colitis. Reverse transcription quantitative polymerase chain reaction and enzyme-linked immunosorbent assay were used to detect the expressions of cytokines interleukin (IL)-1, IL-1β, IL-4, IL-6, IL-10, IL-12, and tumor necrosis factor-α (TNF-α). The expressions of Janus kinase 2 (JAK2) and signal transducer and activator of transcription 3 (STAT3), and the phosphorylation of JAK2 (p-JAK2) and STAT3 (p-STAT3), were measured by western blot analysis. Western blot analysis and immunohistochemistry were used to detect the expressions of tight junction proteins. We found that the weights and colon lengths of mice in dextran sodium sulfate (DSS)+DHA group were significantly lower and longer than those in the DSS group, respectively. Compared with those in the DSS group, the expressions of IL-1β, IL-6, IL-17, and TNF-α in the DSS+DHA and DSS+5-aminosalicylic acid (5-ASA) groups were decreased, while the expressions of IL-4 and IL-10 were significantly upregulated. DHA largely increased the expressions of zonula occludens-1 and occludin. Western blot analysis and/or immunohistochemical staining analysis showed that the expressions of JAK2, STAT3, p-JAK2, and p-STAT3 in DSS+DHA and DSS+5-ASA groups were significantly lower than those in DSS group. DHA has a specific therapeutic effect on UC. The anti-inflammatory mechanism of DHA is related to the blockage of the JAK2/STAT3 signaling pathway. These findings provide evidence that DHA may be a useful drug and is expected to become a promising new treatment for human UC.

The oral cavity harbors complex microbial communities, which leads to biomaterial-associated infections (BAI) during dental and orthopedic treatments. Conventional antibiotic treatments have met great challenges recently due to the increasing emergency of drug-resistant bacteria. To tackle this clinical issue, antibacterial surface treatments, containing surface modification and coatings, of dental and orthopedic materials have become an area of intensive interest now. Among various antibacterial agents used in surface treatments, metallic agents possess unique properties, mainly including broad-spectrum antibacterial properties, low potential to develop bacterial resistance, relative biocompatibility, and chemical stability. Therefore, this review mainly focuses on underlying antibacterial applications and the mechanisms of metallic agents in dentistry and orthopedics. An overview of the present review indicates that much work remains to be done to deepen the understanding of antibacterial mechanisms and potential side-effects of metallic agents.

This study presents a retrospective study aimed to analyze the facial features at each stage of surgical-orthodontic treatment for skeletal class III malocclusion, and predict the changes in the lips after treatment. There were 49 skeletal class III malocclusion patients treated with bimaxillary surgery and orthodontic treatment enrolled in this study. Lateral cephalograms were obtained before treatment (T0), 1 month before surgery (T1), 1 month after surgery (T2), and after debonding (T3) for cephalometric measurements. After the measurement of the required variables, paired t-test, Pearson’s correlation analysis, and multiple linear regression were performed using SPSS 19.0. The main factors associated with changes in the upper lip included ΔUIE-V, ΔA-V, ΔU1A-V, and ΔL1A-V, and those associated with changes in the lower lip included ΔLIE-V, ΔL1A-V, ΔB-V, ΔPog-V, and Δfacial angle. The predicted regression equation for the horizontal change in the upper lip was represented as ΔUL-vertical reference line (VRL) = 9.430 + 0.779 (ΔUIE-VRL) − 0.542(VULT) (P < 0.05) with a mean error of 1.04 mm; the corresponding equation for the lower lip was ΔLL-VRL = −1.670 + 0.530 (ΔB-VRL) + 0.360 (Ls-E) + 0.393 (ΔLIE-VRL) (P < 0.05), with a mean error of 1.51 mm. This study explored the relationship between orthognathic surgery and changes in the lips and obtained the predictive equations of lip position after treatment by using multiple linear regression, which likely offers a reference for prediction of soft tissue changes before surgical-orthodontic treatment in patients with skeletal class III malocclusion. The findings can help dentists to rapidly predict the lip changes after surgical-orthodontic treatment in patients with skeletal class III malocclusion. The study has been registered with the Chinese Clinical Trial Registration (No: ChiCTR1800017694).

Backgroud To analyze the morphological changes of the anterior alveolar bone after the retraction of incisors in premolar extraction cases and the relationship between incisor retraction and remodeling of the alveolar base represented by points A and B displacements. Methods Pre- (T0) and post-treatment (T1) lateral cephalograms of 308 subjects in the maxilla and 154 subjects in the mandible who underwent the orthodontic treatment with extraction of 2 premolars in upper or lower arches were included. Alveolar bone width and height in both the maxillary and mandible incisor area were measured at T0 and T1 respectively. By superimposing the T0 and T1 cephalometric tracings, changes of points A and B, and the movement of the incisors were also measured. Then the correlation between incisor movement and the displacements of points A and B was analyzed. Results The alveolar bone width (ABW) showed a significant decrease in both maxilla and mandible (P P > 0.05). The alveolar bone height (ABH) showed a significant increase in the labial side of maxilla and a significant decrease in the lingual side of maxilla and mandible. A strong positive correlation was verified between incisor movement and position changes of points A and B in both horizontal and vertical directions. Conclusions Anterior alveolar bone width and height generally decreased after orthodontic treatment. Incisor retraction led to significant position changes of points A and B. The decrease of anterior alveolar bone due to significant incisor retraction should be taken into account in treatment planning.

STUDY QUESTION How does aquaporin-3 (AQP3) affect endometrial receptivity? SUMMARY ANSWER AQP3, which is regulated by the combination and estrogen (E2) and progesterone (P4), induces epithelial–mesenchymal transition (EMT) of endometrial epithelial cells. WHAT IS KNOWN ALREADY Embryo implantation is an extremely complex process, and endometrial receptivity is essential for successful embryo implantation. Estrogen and progesterone regulate endometrial receptivity. AQP3, which is regulated by estrogen (E2), increases cell migration and invasion ability by regulating the expression of EMT-related factors and influencing the reorganization of the actin cytoskeleton. STUDY DESIGN, SIZE, DURATION This study investigated the pathophysiological significance of AQP3 in human endometrial function during different phases of the menstrual cycle. PARTICIPANTS/MATERIALS, SETTING, METHODS AQP3 expression levels during different phases of the menstrual cycle were measured using immunohistochemical assays. In cells of different receptivity (high-receptive RL95-2 cells and low-receptive HEC-1A cells), the expression of AQP3 was measured using western blotting, qRT-PCR and immunofluorescence assays. Activities of AQP3, and its regulation by E2 and P4, were studied through in-vitro experiments using RL95-2 cells. MAIN RESULTS AND THE ROLE OF CHANCE AQP3 expression in the mid- and late-secretory phases of the human endometrium is significantly higher than in other phases. Since AQP3 expression levels were higher in RL95-2 cells than in HEC-1A cells, mechanisms of AQP3 regulation by E2 and P4 were studied using RL95-2 cells. We provided the first report that P4 up-regulates AQP3 by directly targeting the promoter of the AQP3 gene. The up-regulation of AQP3 expression by a combination of E2 and P4 is significantly higher than that caused by either E2 or P4 alone. Together E2 and P4 promote RL95-2 cell migration and invasion by inducing EMT through AQP3. We also found that AQP3 co-localizes with ezrin and affects the formation of filopodia and lamellipodia during the E2 and P4-induced EMT process but has no effect on the expression of ezrin and F-actin. LARGE SCALE DATA N/A. LIMITATIONS, REASONS FOR CAUTION It is still unclear whether AQP3 is a main regulator of endometrial receptivity or one of several factors influencing the process. WIDER IMPLICATIONS OF THE FINDINGS Further investigation on AQP3 may contribute to a greater understanding of endometrial receptivity. STUDY FUNDING/COMPETING INTEREST(S) This work was supported by the National Natural Scientific Grants of China (No. 31570798), the Program for Liaoning Excellent Talents in University (LR2017042), the Doctoral Scientific Research Foundation of Liaoning province (201601236), and the Liaoning Provincial Program for Top Discipline of Basic Medical Sciences. There are no conflicts of interest.

Objective: The present case-control study sought to explore at-risk riding behaviors associated with e-bike related traffic crashes among e-bike riders in China. Methods: Cases were recruited from residents aged 16 years and over in communities which stated “selected e-bikes as travel tools and experienced traffic crashes in the last year”. Two controls for each case were randomly selected from a population of e-bike riders who had not experienced a traffic crash in the past year. The cases and controls were matched by gender, age (within 5 years) and school education level. Data were collected using questionnaires and face-to-face interviews from July 2015 to September 2015 in China. After conducting univariate logistic analysis on study variables, a conditional logistic regression model based on the 1:2 matched case-control study design was developed. Results: Multiple-factor conditional logistic regression analysis of e-bike related traffic crashes showed that running red lights (always vs. never, AOR = 3.094, 95% CI, 1.077-8.891, P < .05), riding after drinking (yes vs. no, AOR = 1.578, 95% CI, 1.102-2.259, P < .05), carrying adults while riding (always vs. never, AOR = 2.140, 95% CI, 1.273-3.595, P < .05), turning without signaling (sometimes vs. never, AOR = 1.446, 95% CI, 1.805-1.928, P < .05), riding in the motor vehicle lane (always vs. never, AOR = 2.413, 95% CI, 1.576-3.695, P < .01), prior crash history (yes vs. no, AOR = 1.670, 95% CI, 1.257-2.220, P < .05), and type of e-bikes (scooter-style e-bikes vs. bicycle-style e-bikes, AOR = 1.471, 95% CI, 1.068-2.026, P < .05) were identified as possible risk factors for e-bike traffic crashes. Conclusion: The findings of this research provide evidence about specific risky behaviors related to road traffic crashes involving e-bikes and indicated that behavioral intervention and education need to be strengthened to reduce dangerous riding behaviors. These results will be helpful for design of e-bike road risk prevention programs.

// Xiangzhen Wang 1, 2 , Nana Ma 3 , Qiannan Sun 4 , Chenlingzi Huang 1 , Yanmei Liu 5 , Xin Luo 1 1 The First Affiliated Hospital of Jinan University, Guangzhou, Guangdong, China, 510630 2 Nanshan Maternity and Child Healthcare Hospital of Shenzhen, Shenzhen, Guangdong, China, 518052 3 The First Affiliated Hospital of Xinxiang medical college of Henan, Xinxiang, Henan, China, 453100 4 Changzhi City People’s Hospital of Shanxin Medical University Affiliated Hospital, Changzhi, Shanxi, China, 046000 5 Huadu District, Guangzhou City People’s Hospital, Guangzhou, Guangdong, China, 510630 Correspondence to: Xiangzhen Wang, email: 1093456531@qq.com Xin Luo, email: tluox@126.com Keywords: NF-κB, Asherman syndrome, intrauterine adhesion, pregnancy, uterine disease Received: October 09, 2016 Accepted: January 09, 2017 Published: January 27, 2017 ABSTRACT Asherman syndrome (intrauterine adhesion) is often associated with menstrual abnormalities, infertility and recurrent miscarriage in female. Currently the molecular mechanism regulating the pathogenesis of Asherman syndrome is not known. Here we revealed that the inflammatory factor NF-κB expression is significantly elevated in the endometrial samples of Asherman syndrome patients. To further study the molecular mechanisms, we established an Asherman syndrome rat model and confirmed the important role of NF-κB in the pathogenesis of Asherman syndrome. In addition, our rat model provided direct evidence that intrauterine adhesion results in impaired pregnancy, supporting the clinical association between intrauterine adhesion and mis-regulated pregnancy. Our result identified NF-κB as a novel pathogenesis factor of Asherman syndrome and provided new insights for the prevention and treatment of intrauterine adhesions in Asherman syndrome patients.

Bone defects, massive bone defects in particular, is still an issue clinically. Acetylsalicylic acid (ASA), also known as aspirin, has been proven to be conducive for mesenchymal stem cells osteogenic differentiation, which may be benefited for bone regeneration. In order to achieve a more appealing prognosis of bone defect, here we develop a well-defined tetra-PEG hydrogel sealant with rapid gelation speed, strong tissue adhesion, and high mechanical strength. After in-situ encapsulation of aspirin, this drug-loaded tetra-PEG hydrogel possessed a sustained release, anti-inflammation, and osteoinductive properties. In vitro experiments showed that the cell proliferation was slightly facilitated, and the osteogenic differentiation was notably augmented when periodontal ligament stem cells (PDLSCs) were co-incubating with the hydrogel materials. Moreover, in vivo study manifested that the aspirin sustained release system significantly facilitated the PDLSCs mediated bone defect regeneration. Overall, tetra-PEG hydrogel-based aspirin sustained release system is applicable not only for enhancing the osteogenesis capacity of PDLSC but also providing a new thought of bone regenerative therapy.

Background: We aimed to investigate the expression and clinical significance of interleukin 17 (IL-17) in patients with primary biliary cirrhosis (PBC). Methods: PBC patients (n=127), patients without PBC (n=100) were selected from January 2015 to December 2015.The measure of IL-17 level was performed by cytometric beads array (CBA), immunohistochemistry and real-time PCR (QRT-PCR). Results: The expression levels of serum IL-17, IL-6, IFN-γ, TNF-α and IL-10 in PBC groups were significantly higher than control group, a positively correlation between IL-17 and ALT, ALP, GGT, CIV was observed in PBC patients (r=0.35, P=0.013; r=0.373, P=0.008; r=0.337, P=0.017; r=0.349, P=0.021). In addition, IL-17 mRNA expression level in PBC group was higher than control group. Immunohistochemical results suggest that positive cells did not appear in normal tissues, while they appeared in the PBC liver tissue, mainly in the bile duct. Conclusions: This study shows that IL-17 over expressed in PBC patients, it played a pro-inflammatory effect in the pathogenesis of PBC, most probably as a targeting drug research.

Surgical excision is the main choice for tongue cancer treatment. However, the physiological functions of oral and maxillofacial regions might be severely impaired and high risk of tongue tumor recurrence cannot be avoided. It is thus becoming urgently important to develop alternative strategies for tongue cancer therapy. In this regard, a new class of near-infrared (NIR) light-responsive and peritumoral injectable hydrogel is fabricated with extraordinary photothermal therapy (PTT) for in situ tongue tumors. The as-prepared soft material exhibits good biocompatibility and ultra-strong photothermal effect due to the formed network by negatively charged proteins, chitosan molecules, and Ag3 AuS2 nanoparticles (NPs). In a well-constructed in situ tongue tumor model, tumors can be efficiently eradicated by one-time PTT treatment. Importantly, there are no side effects on surrounding normal tissues and potential tumor recurrence is inhibited. In stark contrast to traditional surgical excision, such biomaterials hold great potential for clinical treatment of oral cancers.

A novel photothermal hydrogel is fabricated, which can transform into a mechanically strong network by in situ gelation with Ca2+ in tissues. With the properties of good biocompatibility, long residential time, outstanding photothermal conversion efficiency, and high toughness, the hydrogel can be used as an ideal platform to realize a significant tumor photothermal therapy effect and bone defects repair simultaneously.

Staphylococcus aureus employs an arsenal of secreted virulence factors to evade host immune responses, such as inducing host cell death pathways or hiding within phagocytes. A previous study indicated that the transcription regulator SA1804 is a novel virulence repressor of S. aureus, and is regulated by SaeRS. However, the function of this regulator in S. aureus pathogenesis remains unclear. In this study, we created a SA1804 homologue, SAUSA300_1968, deletion mutant in the S. aureus USA300 strain LAC, and found that culture supernatant proteins of the mutant exhibit higher cytotoxicity and greater ability to induce the expression of inflammatory cytokines in mouse primary peritoneal macrophages as compared with that of its parent strain. Comparative proteome analysis of secreted protein expression profiles between the two strains was determined through tandem mass tags (TMT). Among the 18 well-known extracellular virulence-related factors that showed significantly different expressions, 17 proteins were up-regulated in the SAUSA300_1968 deletion mutant, including various pore-forming toxins and extracellular proteases. Accordingly, we also found that inactivation of SAUSA300_1968 enhanced S. aureus survival in mouse macrophages. Our data provide novel insights into the role of the SAUSA300_1968 regulator in host immune evasion and S. aureus pathogenesis.

MicroRNAs (miRNAs) are a class of small non-coding RNAs that are closely associated with carcinogenesis. Accumulating data indicate that miR-196b participates in the development of various types of cancers. However, the role of miR-196b in the formation of hydatidiform mole (HM) is still unclear. Our previous studies have demonstrated that miR-196b levels were decreased in JAR and BeWo cells and in HM tissue samples, as demonstrated by RT-PCR analysis. Furthermore, we discovered that overexpression of miR-196b in JAR and BeWo cells inhibited cellular proliferation, migration and invasion, as shown by Cell counting kit-8 (CCK-8) and transwell assays, respectively. Subsequently, we explored the interaction of miR-196b with its target gene in human choriocarcinoma cell lines. MAP3K1 is a target gene predicted by bioinformatic analysis that was previously shown to exhibit reduced expression levels following treatment with miR-196b in JAR and BeWo cells. We demonstrated that MAP3K1 was a direct target of miR-196b using the dual-luciferase reporter assay in Hela cells. In summary, the present study demonstrated that miR-196b suppressed proliferation, migration and invasion of human choriocarcinoma cells by inhibiting its transcriptional target MAP3K1. miR-196b and MAP3K1 may be considered potential targets for the clinical treatment of HM.

Sepsis is a major cause of death for hospitalized patients and is characterized by massive overreaction of immune responses to invading pathogens which is mediated by cytokines. For decades, there has been no effective treatment for sepsis. Sialic acid-binding, Ig-like lectin-9 (Siglec-9), is an immunomodulatory receptor expressed primarily on hematopoietic cells which is involved in various aspects of inflammatory responses and is a potential target for treatment of sepsis. The aim of the present study was to develop a human anti-Siglec-9 Fab fragment, which was named hS9-Fab03 and investigate its immune activity in human macrophages. We began by constructing the hS9-Fab03 prokaryotic expression vector from human antibody library and phage display. Then, we utilized a multitude of assays, including SDS-PAGE, Western blotting, ELISA, affinity, and kinetics assay to evaluate the binding affinity and specificity of hS9-Fab03. Results demonstrated that hS9-Fab03 specifically bind to Siglec-9 antigen with high affinity, and pretreatment with hS9-Fab03 could attenuate lipopolysaccharide (LPS)-induced TNF-α, IL-6, IL-1β, IL-8, and IFN-β production in human PBMC-derived macrophages, but slightly increased IL-10 production in an early time point. We also observed similar results in human THP-1-differentiated macrophages. Collectively, we prepared the hS9-Fab03 with efficient activity for blocking LPS-induced pro-inflammatory cytokines production in human macrophages. These results indicated that ligation of Siglec-9 with hS9-Fab03 might be a novel anti-inflammatory therapeutic strategy for sepsis.