Objectives:The purpose of this study was to examine the proportion of CD161 on CD56+Natural Killer(NK) cells in peripheral blood of primary Sjögren’s syndrome(pSS) and investigate its clinical relevance of pSS. Methods:The proportion of CD56+NK cells and CD161 on CD56+NK cells was detected by flow cytometry in 31 pSS patients and 29 healthy controls (HCs). The correlations between proportion of CD161+CD56+NK cells and clinical features and disease activity of pSS were further analysed. Meanwhile, we drew the receiver operating characteristic(ROC) curve to evaluate the diagnostic value of CD161+CD56+NK cells in pSS. Results: The proportion of CD56+ NK cells and CD161+CD56+NK cells decreased markly in pSS patients compared to HCs. The correlation analysis showed that proportion of CD161+CD56+NK cells negatively correlated with WBC,IgA,IgM,IgG,ESSRPI and ESSDAI,and positively correlated with complement C4.The proportion of CD161+CD56+NK cells in pSS patients with decayed tooth, fatigue, arthralgia, skin involvement, primary biliary cirrhosis(PBC),interstitial lung disease(ILD), anti-SSA/Ro60 positive, anti-SSB positive and high IgG was lower than that in negative patients. Furthermore, compared with innactive patients,the proportion of CD161+CD56+NK cells decreased obviously in active patients. The area under the curve(AUC)was 0.7375(P=0.0016),the results indicated that CD161+CD56+NK cells had certain diagnostic value for pSS. Conclusion: This study suggested that the proportion of CD56+NK cells and CD161+CD56+NK cells decreased significantly in pSS patients,and the proportion of CD161+CD56+NK cells negatively associated with the clinical features and disease activity of pSS patients. The CD161+CD56+NK cells may present as a potential target for therapy and a biomarker of disease activity in pSS .

Echinococcus multiloculasis is a zoonotic parasitic disease caused by Echinococcus multilocularis, which can cause liver injury, but the mechanism of liver injury is still unclear. Here, Echinococcus multilocularis was injected via the hepatic portal vein to establish a mouse model of infection, and high-throughput RNA sequencing was performed for detecting the expression of miRNAs in the liver of mice infected with 2000 Echinococcus multilocularis after 3 months infection, in order to understand the potential molecular mechanism of liver injury caused by Echinococcus multilocularis infection. Overall, 71 differentially expressed miRNAs were found in liver in comparison with control and a total of 36 mouse miRNAs with |FC|>0.585 were screened out, respectively. In addition, Targetscan (V5.0) and miRanda (v3.3a) software were used to predict differential miRNAs target genes and functional enrichment of target genes. Functional annotation showed that “cytokine-cytokine interaction”, “ positive regulation of cytokine production”, “ inflammatory respose”, “ leukocute activation” were enriched in the liver of Echinococcus multilocularis-infected mice. Moreover, the pathways “human cytomegalovirus infection”, “cysteine and methonine metabolism”, “Notch signaling pathway” and “ferroptosis” were involved in liver disease. Furthermore, 4 miRNAs (mmu-miR-30e-3p, mmu-miR-203-3p, mmu-miR-125b-5p and mmu-miR-30c-2-3p) related to liver injury were screened and verified. This study revealed that the expression profiling of miRNAs in the livers was changed after Echinococcus multilocularis infection, and improved our understanding of the transcriptomic landscape of hepatic echinococcosis in mice.

Background:Traumatic cartilage injury is an important cause of osteoarthritis (OA) and limb disability, and Toll-like receptors (TLRs) mediated innate immune response has been confirmed to play a crucial role in cartilage injury.In the previous study, we found that the activation of TLR8 molecules in injured articular cartilage was more obvious than other TLRs by establishing an animal model of knee impact injury in rabbits, and the changes of TLR8 molecules could significantly affect the process of articular cartilage injury and repair. Objective: To verify how mir-99a-5p regulates TLR8 receptor mediated innate immune response to treat traumatic cartilage injury. Methods: The impact of a heavy object on the medial condyle of the rabbit’s knee joint caused damage to the medial condylar cartilage. Through pathological and imaging analysis, it was demonstrated whether the establishment of an animal model of traumatic cartilage injury was successful. Establishing a cell model by virus transfection of chondrocytes to demonstrate the role of TLR8 in the innate immune response to impact cartilage injury. Through transcriptome sequencing, potential targets of TLR8, mir-99a-5p, were predicted, and basic experiments were conducted to demonstrate how they interact with innate immune responses to impact cartilage damage. Results:TLR8 is a receptor protein of the immune system, which is widely expressed in immune cells. In our study, we found that TLR8 expression is localized in lysosomes and endosomes.Mir-99a-5p can negatively regulate TLR8 to activate PI3K-AKT molecular pathway and aggravate cartilage damage.Inhibiting TLR8 expresson can effectively reduce the incidence of articular cartilage damage. Conclusion:Based on the results from this study, mir-99a-5p may be an effective molecular marker for predicting traumatic cartilage injury and targeting TLR8 is a novel and promising approach for the prevention or early treatment of cartilage damage.

The prospect of preventing HIV infection with broadly neutralising monoclonal antibodies (bNAbs) has generated unprecedented enthusiasm in the scientific community and hope among people living with HIV around the world. HIV bNAbs could be a game changer in the prevention of HIV acquisition. Some of these bNAbs are being tested in early phase clinical trials, and the debate is now about the priorities for strategic large-scale efficacy trials. The prevailing view is that only a fixed combination of at least three bNAbs could prevent HIV, regardless of target populations or routes of transmission. We propose an alternative strategy consisting of evaluating the tolerability and efficacy of one or two bNAbs cocktails tailored to different target populations and indications. The rationale for this alternative strategy is based on ethical, pathophysiological and practical facts and is illustrated by the possibility of preventing HIV transmission through breastfeeding in high incidence/prevalence areas such as southern Africa. There is a prospect of eliminating paediatric HIV acquisition through breastfeeding by using single/dual long-acting bNAb regimens.

Background: In addition to the elimination diet, dietary composition may influence disease severity in patients with Eosinophilic Esophagitis (EoE) through modulation of the immune response. Aim: To explore the immunomodulatory role of nutrition before and during elimination diet in adult EoE patients. Methods: Nutritional intake was assessed in 39 Dutch adult EoE patients participating in the Supplemental Elemental Trial (SET) using 3-day food diaries. In this randomized controlled trial, diagnosed patients received either a four-food elimination diet alone (FFED) or FFED with addition of an amino acid-based formula for six weeks. Multiple linear regression analyses were performed to assess associations between the intake of nutrients and food groups per 1000 kCal and peak eosinophil count/High Power Field (PEC), both at baseline and after six weeks. Results: At baseline, we found a statistically significant negative (thus favorable) relationship between the intake of protein, total fat, phosphorus, zinc, vitamin B12, folate and milk products and PEC (p<0.05), while calcium (p=0.058) and full fat cheese/curd (p=0.056) were borderline (favorably) significant. In contrast, total carbohydrates, prepacked fruit juice and white bread were significantly positively related to PEC (p<0.05) (unfavorable), while ultra-processed meals (p=0.059) were borderline (unfavorably) significant. After dietary intervention, coffee/tea were significantly negatively (favorably) related to PEC, hummus/legumes were significantly positively (unfavorably) related with PEC, while peanuts were borderline significantly positively related (p=0.058). Conclusion: Dietary composition may be related to inflammation in adult EoE patients. High quality and anti-inflammatory diets may be a promising adjuvant therapy in the dietary management of EoE.

Abstract Background: The purpose of this meta-analysis was to look at the relationship between hypernatremia and mortality in COVID-19 patients. Methods: We searched the PubMed, Web of science, Embase and Cochrane databases for articles published from the inception of the database until August 27, 2022. Three researchers reviewed the literature, retrieved data, and assessed the quality of the literature, respectively. A meta-analysis was performed using State 17 software to assess the value of the effect of hypernatremia on mortality in patients with new coronavirus pneumonia. Results: A total of 9 publications was finally included in this study, including a total of 11,801 patients with COVID-19, including 1,278 in the hypernatremia group and 10,523 in the normonatremia group. Meta-analysis showed that hypernatremia was associated with mortality in patients with COVID-19 [OR = 4.15, 95% CI (2.95-5.84), P = 0.002, I² = 66.7%] with a sensitivity of 0.36 [0.26, 0.48] and a specificity of 0.88 [ 0.83, 0.91]. The posterior probability of mortality was 42% in patients with COVID-19 hypernatremia and 15% in patients who did not have COVID-19 hypernatremia. Conclusion: According to available data, hypernatremia is associated with death in patients with COVID-19.

Idiopathic pulmonary fibrosis (IPF) is a progressive lung disease with unclear etiology. Clinical manifestations include dyspnea and nonproductive cough. Lung transplantation is the only cure, while Pirfenidone and Nintedanib are FDA-approved drugs for slowing disease progression. However, Saracatinib shows greater efficacy. This literature review assesses the safety and efficacy of IPF treatments, focusing on Pirfenidone and Nintedanib, which preserve lung function and reduce fibrosis and inflammation. We also evaluate emerging treatments such as saracatinib, pamrevlumab, pentraxin-2, BI 1015550, ziritaxestat, PBI-4050, bexotegrast, BMS-986020, TD 139, dasatinib, quercetin, and etanercept. Additional research is needed to explore the therapeutic potential and address gaps in IPF management, including exacerbation and associated pulmonary hypertension (PH). Immunosuppressive agents are used to manage IPF exacerbations, while PH is a recognized comorbidity. Clinical trials, PULSAR and SPECTRA, investigate Sotatercept as a potential PH treatment for IPF patients, showing promising results.

To determine distinct phenotype groups in patients with idiopathic inflammatory myopathy (IIM), and to identify the differences of clinical characteristics, laboratory findings, and the long-term outcomes in patients with antisynthetase syndrome (ASS) of different anti-aminoacyl-tRNA synthetase (ARS) antibodies. Methods: We enrolled retrospectively 280 patients with IIM, and the clinical characteristics and laboratory findings were collected. Additionally, multivariate COX regression analysis was performed to identify indicators of poor prognosis in patients with ASS. Results: 119 ASS and 161 non-ASS patients were identified in 280 patients with IIM, the occurrence rates of ILD, RP-ILD, pulmonary symptoms, arthritis, triad and mechanic’s hands with ASS group were more prevalent than non-ASS group ( p＜0.05). Among 119 patients with ASS, the highest incidence of RP-ILD occurred in the PL12 group (36.4%). There was clinical significance of statistical differences in arthritis, myositis, mechanic’s hands, triad, shawl sign, v sign, and Raynaud’s phenomenon among the 4 subgroups ( p＜0.05). At the same time, the individuals in the positive anti-Jo1 antibody group were more likely to exhibit arthritis, myositis, mechanic’s hands, triad and, v sign than the negative anti-Jo1 antibody group in patients with ASS, furthermore, statistically more prevalent ( p＜0.05). According to the multivariate COX regression analysis, mechanic’s hands, ANA, and ILD were independent risk factors for poor prognosis in patients with ASS ( p<0.001, p=0.026, and p<0.001, respectively). V sign was an independent protective factor for good prognosis in patients with ASS ( p=0.026). Conclusions: When clinical characteristics including pulmonary symptoms, arthritis, mechanic’s hands, ANA, along with ILD appear, clinicians should be on the alert for the occurrence of ASS in patients with IIM

Objective B cell activating factor (BAFF) is a key regulator of Primary Sjögren’s Syndrome (pSS), which is characterized by B lymphocyte hyperactivity. BAFF is also known as TNF ligand superfamily member 13B (TNFSF13B). This study aimed to explore whether five single nucleotide polymorphisms (SNPs) of the TNFSF13B gene (rs9514827, rs1041569, rs9514828, rs1224141, and rs12583006) are related to pSS susceptibility. Methods We searched Pubmed, Cochrane, Elsevier, Web of Science, CNKI, CQVIP, and WanFang databases (up to January 2023). In a population with pSS, the odds ratios (ORs) with 95% confidence intervals (CIs) of genotypes and each allele were provided to investigate relationships between the polymorphisms of the BAFF (TNFSF13B) gene and pSS. Results The meta-analysis in question contains three studies. In the group of pSS patients and randomly selected health controls (HCs), there was a statistically significant relationship between rs1041569 and rs12583006 and pSS susceptibility, respectively. In fixed models, there were statistical differences in pSS patients and randomly chosen HCs. Conclusions There were relationships of rs1041569 and rs12583006 in the pSS group and HC group. BAFF(TNFSF13B) genes, particularly rs1041569 and rs12583006, were related to pSS susceptibility in pSS patients.

ABSTRACT The current absence of gold-standard or all-aspect favorable therapies for COVID-19 renders a focus on multipotential drugs proposed to prevent or treat this infection or ameliorate its signs and symptoms vitally important. The present well-designed randomized controlled trial sought to evaluate the efficacy and safety of N-acetylcysteine as adjuvant therapy in hospitalized Iranian patients with COVID-19. Four different diets in 60 patients include; Kaletra (lopinavir/ritonavir) + hydroxychloroquine with/without N-acetylcysteine (600 mg TDS) and atazanavir/ritonavir + hydroxychloroquine with/without N-acetylcysteine (600 mg TDS), were administered in the study. At the end of the study, a further decrease in C-reactive protein was observed in groups with N-acetylcysteine (P =0.008), and no death occurred in the atazanavir/ritonavir + hydroxychloroquine + N-acetylcysteine group, showing that the combination of these drugs may reduce mortality. A significant rise in O2 saturation was observed in atazanavir/ritonavir+hydroxychloroquine+N-acetylcysteine group (P <0.05). Accordingly, oral or intravenous N-acetylcysteine, may enhance O2 saturation, blunt the inflammation trend (by reducing C-reactive protein), and reduce mortality in hospitalized patients with COVID-19. The N-acetylcysteine could be more effective as prophylactic or adjuvant therapy in stable and non-severe cases of COVID-19 with a particularly positive role in the augmentation of O2 saturation and faster reduction of the CRP level and inflammation.

Background: Type 2 diabetes mellitus (T2DM), which has a high incidence and several harmful consequences, poses a severe danger to human health. More research is being done on ferroptosis’ function in T2DM. This study uses a bioinformatics technique to look for new diagnostic T2DM biomarkers associated with ferroptosis. Methods: In order to identify ferroptosis-related genes (DEGs) that are differently expressed between T2DM patients and healthy individuals, we first obtained T2DM sequencing data and ferroptosis-related genes (FRGs) from the Gene Expression Omnibus (GEO) database and FerrDb database. Then, drug-gene interaction networks and ceRNA networks linked to the marker genes were built after marker genes were filtered by two machine learning algorithms (LASSO and SVM-RFE algorithms). Finally, to confirm the expression of marker genes, the GSE76895 dataset was utilized. The protein expression of some marker genes between T2DM and non-diabetic tissues was also examined by Western Blotting, Immunohistochemistry (IHC) and Immunofluorescence (IF), respectively. Results: We obtained 58 DEGs associated with ferroptosis. GO and KEGG enrichment analysis showed that these DGEs were significantly enriched in hypoxia and ferroptosis. Subsequently, eight marker genes (SCD, CD44, HIF1A, BCAT2, MTF1, HILPDA, NR1D2 and MYCN) were screened by LASSO and SVM- RFE machine learning algorithms, and a model was constructed based on these eight genes. These newly discovered marker genes may be linked to alterations in the immune microenvironment in T2DM patients. In addition, based on these 8 genes, we obtained 48 drugs and a complex ceRNA network map. Finally, Western Blotting, IHC and IF results of clinical samples further confirmed the results of public databases. Conclusions: The diagnosis and etiology of T2DM can be greatly aided by eight ferroptosis-related genes, opening up novel therapeutic avenues.

Paroxysmal nocturnal hemoglobinuria (PNH) is characterized by hemolytic anemia, bone marrow failure, thrombophilia. COVID-19, caused by a novel severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) with many variants including Omicron. This study depicted demographic and clinical characteristics of 20 PNH patients with SARS-Cov2 Omicron infection. All the patients hadn’t previously been administrated with complement inhibitors. They all were with high disease activity (HDA), and LDH level exceeded any documented since the diagnosis of PNH, and those reported in the literature for previously stable treatment with complement inhibitors. D-dimer level elevated in 10 patients. 2 patients developed mild pulmonary artery hypertension. Glomerular filtration rate (GFR) declined in 5 patients. 1 patient developed acute renal failure and underwent hemodialysis. Anemia and hemolysis were improved in 5 patients treated with eculizumab. Hemolytic exacerbation of PNH with COVID-19 is severe and eculizumab may be an effective treatment.

Background Gout is a chronic non-communicable disease that might lead to multiple systemic complications if it is left untreated. The knowledge and attitudes among patients towards the diagnosis and management of gout are important indicators in determining the prognosis and predicting sequelae of the disease. This cross-sectional survey aimed to assess the knowledge, perspectives, and attitudes of patients diagnosed with gout toward the disease pathology, diagnosis, and treatment. Methodology An observational cross-sectional study was conducted at university clinics and local health facilities in central Riyadh, Saudi Arabia. Two-hundred thirteen patients diagnosed with gout were selected by non-random, non-probability convenience sampling and invited to voluntarily participate in this survey. A structured questionnaire, which was written in Arabic and pre-tested in a previous pilot study, was distributed to and collected from the participants between April 2022 and August 2022. The data were entered into an Excel (version 2010) spreadsheet. Pearson chi- square analysis was used to determine associations between dependent variables. Statistical significance was defined as a P-value <0.05. Results The study included 109 patients (51.2%) ≥51 years of age with uncontrolled gout (more than two attacks), 38% of whom were males. The variation in body mass index was not statistically significant (P=0.384). The proportions of patients with diabetes mellitus, hypertension, dyslipidemia, and osteoarthritis were significantly different between patients with uncontrolled vs. controlled gout (P=0.041). There were significant differences between patients with uncontrolled vs. controlled gout in terms of age at diagnosis and the interval between symptom onset and rheumatologist consultation (P=0.043, P=0.043, and P=0.027, respectively). Conclusion Patients were adequately informed about gout and its treatment. Gout control was significantly associated with patients’ knowledge levels, patient age, and gout therapy. There were no associations between patients’ primary complaints and gout status at the time of diagnosis

Abstract Objectives: To evaluate patient activation in Rheumatoid Arthritis (RA) patients using the patient activation measure 13 (PAM-13) on a national level in Saudi Arabia. Method: A national survey was administered across multiple centres in Saudi Arabia. The survey assessed patient activation using the PAM-13. The Compliance Questionnaire for Rheumatology (CQR) and the RA Impact of Disease (RAID) tool, were assessed. The data from the survey were analysed, and the results were stratified based on activation level. All factors affecting patient activation were explored and reported. Results: A total of 1241 participants were included. Most of the patients were females (85%), the mean age was 47 (±14), and most patients lived in the central region (47%). The mean (±SD) patient activation score was 578.7 (±13.0). Patient activation was affected by multiple factors: demographic characteristics, such as education, with a beta value of 1.11 (95% CI 0.64 ̵̶ 1.58, p<0.001). Higher CQR scores were associated with higher activation level, with a beta value of 2.61 (95% CI 0.80 ̵̶ 4.44, p=0.005); and higher RAID scores were associated with lower activation levels, with a beta value of 3.13 (95% CI 1.36 ̵̶ 4.91, p=0.001). Conclusions: Patient activation was affected by several demographic characteristics and impact of RA. A higher activation may improve compliance. Future longitudinal studies are required to confirm these findings and should explore the underlying mechanism of these effects.

Background: As a polyphenolic compound originated from the food spice turmeric, curcumin (CUR) has various pharmacological effects, such as anti-inflammatory, anti-oxidation, anti-proliferative and anti-angiogenic activities. Psoriasis is centered on the overproduction of Th1- and Th2-related cytokines (e. g. IL-23, IL-17, TNF-α, IL-22), which is involved in the occurrence and development of its pathogenesis. However, whether CUR is involved in the treatment of psoriasis and its specific mechanisms are not fully understood. Methods: In this study, we detected the therapeutic effect of CUR (100mg/kg· d) on IMQ-induced dermatitis in mice, analyzed by PASI scores, ELISA, HE staining, immunofluorescence. Moreover, we further confirmed the alteration in the relative abundance of the gut microbiota through 16sRNA to explore whether CUR could regulate the gut microbiota of IMQ-induced mice. Result: Through intragastric administration, CUR can alleviate psoriasis-like lesions of mice by decreasing PASI scores, reducing the level of IL-6, IL-17A, IL-22, IL-23, TNF-α and TGF-β1, promoting the expression of IL-10. Moreover, 16 sRNA sequencing revealed that CUR could regulate the alteration in the abundance alteration of gut microbiota related to inflammation, such as Alistipes, Mucispirillum and Rikenella at genus level. The correlation analysis further confirmed the close association between important microflora and psoriasis-like inflammation indicators. Conclusions: CUR exerts the effect of alleviating dermatitis of psoriatic mice by regulating Th-17 related inflammatory factors. Moreover, the changes in gut microbiota via CUR may be another factor of relieving IMQ-induced lesions in mice. Therefore, CUR may be a highly promising candidate for the treatment of psoriasis.

The Marburg virus, which is a member of the same virus family as the Ebola virus called Filoviridae, causes the severe infectious disease known as Marburg Virus Disease (MVD). Previously, different outbreaks of MVD have appeared in different African countries, including Ghana, Guinea, Uganda, Angola, the Democratic Republic of the Congo, Kenya, and South Africa. For the first time, Equatorial Guinea and Tanzania are experiencing MVD outbreaks. A total of 15 laboratory-confirmed cases of MVD and 23 probable cases have been reported in Equatorial Guinea since the confirmation of the outbreak on 13 February 2023. The first MVD outbreak in the United Republic of Tanzania was formally confirmed by the Ministry of Health on March 21, 2023. As of 22 March, there were eight cases and five fatalities (case fatality ratio [CFR]: 62.5%). Due to the facts that Ebebiyin and Nsock Nsomo districts, the affected regions of Equatorial Guinea, borders Cameroon and Gabon, and Kagera region, the affected region of Tanzania, borders Uganda, Rwanda and Burundi, there is fear of cross-border spread of MVD due to cross-border migrations, and this can be a great crisis in West and East Africa. Although there are currently outbreaks of MVD in Equatorial Guinea and Tanzania, there is currently no proof of an epidemiological connection between the two outbreaks. The aim of this paper is to describe Marburg Virus Disease (MVD), describe its first outbreak in Equatorial Guinea and Tanzania, explain the efforts being used and the challenges being faced in MVD mitigation, and recommend different measures to be taken to cope with the outbreak of MVD in Equatorial Guinea and Tanzania.

Background: Kawasaki disease (KD) is a kind of vasculitis with an unidentified etiology. Cathelicidin (LL-37) may be involved in the development of the KD process; therefore, further research to investigate the molecular mechanism of LL-37 involvement in KD is warranted. Methods: Enzyme-linked immunosorbent assay (ELISA) was used to detect the levels of TNF-α, IL-1β, NLRP3, and LL-37 in the sera of healthy subjects, children with KD, and children with pneumonia. Subsequently, human recombinant LL-37 or/and TLR4-specific inhibitor TAK-242 stimulated HCAECs cells, CCK-8 was used to detect cell proliferation, flow cytometry to detect apoptosis, transmission electron microscopy to observe cytoskeletal changes, Transwell to measure cell migration ability, ELISA to detect inflammatory factor levels, Western blotting to analyze protein levels of TLR4 and NF-κB p-65, and qRT-PCR to determine LL-37, NLRP3 mRNA levels. Results: In this study, we found that the level of LL-37 was highly expressed in the serum of children with KD, and after LL-37 stimulation, apoptosis was significantly increased in HCAECs, and the expression levels of TLR4, NLRP3 and inflammatory factors in cells were significantly enhanced. Intervention with the TLR4-specific inhibitor TAK-242 significantly alleviated the LL-37 effects on cellular inflammation, TLR4, NLRP3 promotion effect. Conclusions: Our data suggest that LL-37 induces an inflammatory response in endothelial cells via TLR4-NF-κB, leading to coronary artery injury in KD, providing a potential target to treat KD.

Objective: Acute-on-chronic liver failure (ACLF) causes organ system failures and the high mortality, and there is currently a lack of effective means of prevention. The purpose of the study was to explore the therapeutic effects of Resolvin D1 (RvD1) on ACLF rats and its underlying mechanism. Methods: ACLF rat model was constructed by intraperitoneally injecting CCl4 and porcine serum for 6 weeks and then induced acute liver injury by treating with both LPS and D-Galn. The ACLF rats were pretreated with different doses of RvD1 (0.3 or 1 ug/kg) before the acute liver injury. Biochemical analysis, H&E and sirius red staining, flow cytometry assay and real-time PCR were used to assess rat liver histopathological injury, determine the Treg cell frequencies in spleen and the mRNA levels of transcription factors and immunologic cytokines in liver. Results: The necro-inflammatory scores and the serum levels of transaminase significantly increased in ACLF model rats compared to those in normal control rats, with the peak at 8 h. Low-dose of RvD1 could limit necrosis and inflammation and decrease the ALT level of ACLF rats. The degree of damage in ACLF rats was related to the increased mRNA levels of IL-17 and IL-6 in the ACLF rats’ liver and Treg cells reduction in the spleen. Low-dose of RvD1 could protect against liver injury in ACLF rats, as indicated by increasing Treg cell frequency in rats’ spleen and the mRNA levels of Foxp3/RORγ and decreasing the expression of both IL-6 and IL-17. Conclusion: Low-dose of RvD1 plays a protective role in ACLF rats by increasing the proportion of Treg cells. It is the first time to reveal the function of RvD1 in the treatment of ACLF. This work may help us clarify the pathogenesis of ACLF and find effective therapeutic drugs for ACLF.