Nasal mucosal fibroblasts produce IL-4 to induce Th2 response.

Th2 polarization is essential for the pathogenesis of allergic rhinitis (AR). Th2 polarization's mechanism requires further understanding. IL-4 is the primary cytokine involved in Th2 response. Fibroblasts play a role in immune regulation. This study aims to elucidate the role of nasal mucosal fibroblast-derived IL-4 in the induction of Th2 responses. Nasal mucosal tissues were obtained from surgically removed samples from patients with nasal polyps, whether with or without AR. Fibroblasts were isolated from the tissues by flow cytometry cell sorting, and analyzed by RNA sequencing (RNAseq). The data from RNAseq showed that nasal fibroblasts expressed genes of GATA3, CD80, CD83, CD86, STAT6, IL2, IL4, IL5, IL6, IL13 and costimulatory factor. The data were verified by RT-qPCR. The level of gene activity was positively correlated with those of AR-related cytokines present in nasal secretions. Nasal fibroblasts release IL-4 upon activation. Nasal fibroblasts had the ability to transform naive CD4+ T cells into Th2 cells, which can be eliminated by inhibiting IL-4 receptor or CD28 in CD4+ T cells. To sum up, nasal mucosal fibroblasts produce IL-4, which can induce Th2 cell development. The data implicate that nasal fibroblasts are involved in the pathogenesis of nasal allergy.

Gastrodin regulates the expression of renin-angiotensin system-SIRT3 and proinflammatory mediators in reactive astrocytes via activated microglia.

Gastrodin, an anti-inflammatory herbal agent, is known to suppress microglia activation. Here, we investigated whether it would exert a similar effect in reactive astrocytes and whether it might act through the renin-angiotensin system (RAS) and sirtuin 3 (SIRT3). Angiotensinogen (ATO), angiotensin-converting enzyme (ACE), angiotensin II type 1 (AT1) and type 2 (AT2) receptor and SIRT3 expression was detected in TNC-1 astrocytes treated with BV-2 microglia conditioned medium (CM) with or without gastrodin and lipopolysaccharide (LPS) pre-treatment by RT-PCR, immunofluorescence and western blotting analysis. Expression of C3 (A1 astrocyte marker), S100A10 (A2 astrocyte marker), proinflammatory cytokines and neurotrophic factors was then evaluated. The results showed a significant increase of ATO, ACE, AT1, SIRT3, C3, proinflammatory cytokines and neurotrophic factors expression in TNC-1 astrocytes incubated in CM + LPS when compared with cells incubated in the CM, but AT2 and S100A10 expression was reduced. TNC-1 astrocytes responded vigorously to BV-2 CM treated with gastrodin + LPS as compared with the control. This was evident by the decreased expression of the abovementioned protein markers, except for AT2 and S100A10. Interestingly, SIRT3, IGF-1 and BDNF expression was enhanced, suggesting that gastrodin inhibited the expression of RAS and proinflammatory mediators but promoted the expression of neurotrophic factors. And gastrodin regulated the phenotypic changes of astrocytes through AT1. Additionally, azilsartan (a specific inhibitor of AT1) inhibited the expression of C3 and S100A10, which remained unaffected in gastrodin and azilsartan combination treatment. These findings provide evidence that gastrodin may have a therapeutic effect via regulating RAS-SIRT3.

Proline inhibits postharvest physiological deterioration of cassava by improving antioxidant capacity.

Cassava (Manihot esculenta Crantz), a crucial global tuber crop, encounters significant economic losses attributed to postharvest physiological deterioration (PPD). The PPD phenomenon in cassava is closely related to the accumulation of reactive oxygen species (ROS), and amino acids play a pivotal role in regulating signaling pathways and eliminating ROS. In this study, the storage performance of eight cassava varieties were conducted. Cassava cultivar SC5 showed the best storage performance among the eight cassava varieties, but the edible cassava cultivar SC9 performed much worse. Comparative analysis of free amino acids was conducted in eight cassava varieties, revealing changes in proline, aspartic acid, histidine, glutamic acid, threonine, and serine. Exogenous supplementation of these six amino acids was performed to inhibit PPD of SC9. Proline was confirmed as the key amino acid for inhibiting PPD. Treatment with optimal exogenous proline of 5 g/L resulted in a 17.9% decrease in the deterioration rate compared to untreated cassava. Accompanied by a decrease in H2O2 content and an increase in catalase, superoxide dismutase and ascorbate peroxidase activity. Proline treatment proved to be an effective approach to alleviate cell oxidative damage, inhibit PPD in cassava, and prolong shelf life.

Supramolecular 3 in 1: A Lubrication and Co-Delivery System for Synergistic Advanced Osteoarthritis Therapy.

The complexity, heterogeneity, and drug resistance of diseases necessitate a shift in therapeutic paradigms from monotherapy to combination therapy, which could augment treatment efficiency. Effective treatment of advanced osteoarthritis (OA) requires addressing three key factors contributing to its deterioration: chronic joint inflammation, lubrication dysfunction, and cartilage-tissue degradation. Herein, we present a supramolecular nanomedicine of multifunctionality via molecular recognition and self-assembly. The employed macrocyclic carrier, zwitterion-modified cavitand (CV-2), not only accurately loads various drugs but also functions as a therapeutic agent with lubricating properties for the treatment of OA. Kartogenin (KGN), a drug for articular cartilage regeneration and protection, and flurbiprofen (FP), an anti-inflammatory agent, were coloaded onto CV-2 assembly, forming a supramolecular nanomedicine KGN&FP@CV-2. The three-in-one combination therapy of KGN&FP@CV-2 addresses the three pathological features for treating OA collectively, and thus provides long-term therapeutic benefits for OA through sustained drug release and intrinsic lubrication in vivo. The multifunctional integration of macrocyclic delivery and therapeutics provides a simple, flexible, and universal platform for the synergistic treatment of diseases involving multiple drugs.

The Role of Left Ventricular Pressure-strain Loop in Evaluating Myocardial Work in Patients with Type 2 Diabetes.

Objective: To quantitatively analyze the myocardial work of patients with type 2 diabetes (T2D) by use of the pressure-strain loop and to investigate the clinical factors that affect myocardial work in the left ventricle. Methods: We analyzed data from 50 control patients and 180 case patients, with 70 cases in group A (T2D only), 40 cases in group B (T2D + high blood pressure), 33 cases in group C (T2D + coronary heart disease), and 37 cases in group D (T2D + high blood pressure + coronary heart disease). Each patient received conventional ultrasonography and 2-dimensional speckle-tracking echocardiography, and the pressure-strain loop technique was applied to measure the left ventricular myocardial work parameters to compare the control and case groups. Results: Systolic blood pressure was dramatically higher in groups B and D than in the control group and in groups A and C. N-terminal pro-brain natriuretic peptide was markedly higher in group D than in the control group, and the disease duration was markedly higher in groups C and D than in group A. The left ventricular global longitudinal strain of the epicardium (LVGLSepi) was substantially lower in groups B, C, and D than in the control group. The LVGLSepi of groups C and D was significantly lower than group A, and the LVGLSepi of group D was significantly lower than group B. The LVGLS, LVGLS of the endocardium, global work index, and global constructive work progressively reduced among the control and case groups. LVGLS strongly correlated with global work index (r = -0.886; P < .001) and global constructive work (r = -0.880; P < .001). Body mass index, duration of diabetes, and glycated hemoglobin A1c independently associated with global work index (Body mass index: P = .04; duration of diabetes: P < .001; glycated hemoglobin A1c: P = .02) . In addition to the above three indicators, systolic blood pressure independently associated with global constructive work (systolic blood pressure: P = .04). Conclusion: Pressure-strain loop technology can quantitatively, accurately, and sensitively monitor the variations in left ventricular myocardial contractile function of patients with T2D and detect subclinical cardiac injury at an early disease stage.

Alleviating Recombinant Tissue Plasminogen Activator-induced Hemorrhagic Transformation in Ischemic Stroke via Targeted Delivery of a Ferroptosis Inhibitor.

Intravenous thrombolysis with recombinant tissue plasminogen activator (rtPA) is the primary treatment for ischemic stroke. However, rtPA treatment can substantially increase blood-brain barrier (BBB) permeability and susceptibility to hemorrhagic transformation. Herein, the mechanism underlying the side effects of rtPA treatment is investigated and demonstrated that ferroptosis plays an important role. The ferroptosis inhibitor, liproxstatin-1 (Lip) is proposed to alleviate the side effects. A well-designed macrocyclic carrier, glucose-modified azocalix[4]arene (GluAC4A), is prepared to deliver Lip to the ischemic site. GluAC4A bound tightly to Lip and markedly improved its solubility. Glucose, modified at the upper rim of GluAC4A, imparts BBB targeting to the drug delivery system owing to the presence of glucose transporter 1 on the BBB surface. The responsiveness of GluAC4A to hypoxia due to the presence of azo groups enabled the targeted release of Lip at the ischemic site. GluAC4A successfully improved drug accumulation in the brain, and Lip@GluAC4A significantly reduced ferroptosis, BBB leakage, and neurological deficits induced by rtPA in vivo. These findings deepen the understanding of the side effects of rtPA treatment and provide a novel strategy for their effective mitigation, which is of great significance for the treatment and prognosis of patients with ischemic stroke.

Crosstalk between metabolism and cell death in tumorigenesis.

It is generally recognized that tumor cells proliferate more rapidly than normal cells. Due to such an abnormally rapid proliferation rate, cancer cells constantly encounter the limits of insufficient oxygen and nutrient supplies. To satisfy their growth needs and resist adverse environmental events, tumor cells modify the metabolic pathways to produce both extra energies and substances required for rapid growth. Realizing the metabolic characters special for tumor cells will be helpful for eliminating them during therapy. Cell death is a hot topic of long-term study and targeting cell death is one of the most effective ways to repress tumor growth. Many studies have successfully demonstrated that metabolism is inextricably linked to cell death of cancer cells. Here we summarize the recently identified metabolic characters that specifically impact on different types of cell deaths and discuss their roles in tumorigenesis.

DPP3 promotes breast cancer tumorigenesis by stabilizing FASN and promoting lipid synthesis.

DPP3, a dipeptidyl peptidase, participates in a variety of pathophysiological processes. DPP3 is upregulated in cancer and might serve as a key factor in the tumorigenesis and progression of various malignancies. However, its specific role and molecular mechanism are still unknown. In this study, the expression of DPP3 in breast cancer tissues is analyzed using TCGA database. Kaplan-Meier survival analysis is performed to estimate the effect of DPP3 on the survival outcomes. To explore the biological function and mechanisms of DPP3 in breast cancer, biochemical and cell biology assays are conducted in vitro. DPP3 expresses at a higher level in breast cancer tissues than that in adjacent tissues in both TCGA database and clinical samples. Patients with high expression of DPP3 have poor survival outcomes. The proliferation and migration abilities of tumor cells with stable DPP3 knockout in breast cancer cell lines are significantly inhibited, and apoptosis is increased in vitro. GSEA analysis shows that DPP3 can affect lipid metabolism and fatty acid synthesis in tumors. Subsequent experiments show that DPP3 could stabilize FASN expression and thus promote fatty acid synthesis in tumor cells. The results of the metabolomic analysis also confirm that DPP3 can affect the content of free fatty acids. This study demonstrates that DPP3 plays a role in the reprogramming of fatty acid metabolism in tumors and is associated with poor prognosis in breast cancer patients. These findings will provide a new therapeutic target for the treatment of breast cancer.

Lumbar puncture increases Alzheimer's disease biomarker levels in cerebrospinal fluid of rhesus monkeys.

Cerebrospinal fluid (CSF) samples are commonly collected via lumbar puncture (LP) in both clinical and research settings for measurement of biomarkers of Alzheimer's disease (AD). To determine the effects of LP on CSF AD biomarkers, we collected CSF samples at seven different time points after an LP in rhesus monkeys. We find that amyloid-beta (Aß) and Tau levels increased significantly on day 1, peaked on day 3, and returned to baseline on day 10 after LP. The NFL levels increased significantly on day 5, peaked on day 10, and returned to baseline after day 30. The increased AD biomarker levels were mainly due to CSF outflow and deep intrathecal invasion during LP. Therefore, if LPs are repeated within a short period of time, prior LP can affect Aß and Tau levels within 10 days and NFL levels within 30 days, which may lead to clinical misdiagnosis or incorrect scientific conclusions.

[Research progress of haematopoietic stem cells to generate immune cells and its application].

Hematopoietic stem cells (HSCs) posses the potential for highly self-renewal, proliferation and multi-lineage differentiation. HSC transplantation has long been the primary method for treating hematologic disorders and autoimmune diseases, and the ability to rebuild the immune system after transplantation is a key indicator of success. To enhance the reconstruction ability of the immune system after transplantation, current research focuses on genetic engineering and the use of HSCs modified by clustered regularly interspaced short palindromic repeats (CRISPR) gene editing technology as a source of transplant cells. This article summaries the biological characteristics, regulatory mechanism, ability to differentiate into immune cells, as well as the application and advance in the treatment of blood disorders, immune deficiencies, cancers and other related diseases, aiming to provide references for the research on relevant diseases.

Genome-Wide Identification and Co-Expression Networks of WOX Gene Family in Nelumbo nucifera.

WUSCHEL-related homeobox (WOX) genes are a class of plant-specific transcription factors, regulating the development of multiple tissues. However, the genomic characterizations and expression patterns of WOX genes have not been analyzed in lotus. In this study, 15 NnWOX genes were identified based on the well-annotated reference genome of lotus. According to the phylogenetic analysis, the NnWOX genes were clustered into three clades, i.e., ancient clade, intermediate clade, and WUS clade. Except for the conserved homeobox motif, we further found specific motifs of NnWOX genes in different clades and divergence gene structures, suggesting their distinct functions. In addition, two NnWOX genes in the ancient clade have conserved expression patterns and other NnWOX genes exhibit different expression patterns in lotus tissues, suggesting a low level of functional redundancy in lotus WOX genes. Furthermore, we constructed the gene co-expression networks for each NnWOX gene. Based on weighted gene co-expression network analysis (WGCNA), ten NnWOX genes and their co-expressed genes were assigned to the modules that were significantly related to the cotyledon and seed coat. We further performed RT-qPCR experiments, validating the expression levels of ten NnWOX genes in the co-expression networks. Our study reveals comprehensive genomic features of NnWOX genes in lotus, providing a solid basis for further function studies.

Role of Type VI secretion system in pathogenic remodeling of host gut microbiota during Aeromonas veronii infection.

Intestinal microbial disturbance is a direct cause of host disease. The bacterial Type VI secretion system (T6SS) often plays a crucial role in the fitness of pathogenic bacteria by delivering toxic effectors into target cells. However, its impact on the gut microbiota and host pathogenesis is poorly understood. To address this question, we characterized a new T6SS in the pathogenic Aeromonas veronii C4. First, we validated the secretion function of the core machinery of A. veronii C4 T6SS. Second, we found that the pathogenesis and colonization of A. veronii C4 is largely dependent on its T6SS. The effector secretion activity of A. veronii C4 T6SS not only provides an advantage in competition among bacteria in vitro, but also contributes to occupation of an ecological niche in the nutritionally deficient and anaerobic environment of the host intestine. Metagenomic analysis showed that the T6SS directly inhibits or eliminates symbiotic strains from the intestine, resulting in dysregulated gut microbiome homeostasis. In addition, we identified three unknown effectors, Tse1, Tse2, and Tse3, in the T6SS, which contribute to T6SS-mediated bacterial competition and pathogenesis by impairing targeted cell integrity. Our findings highlight that T6SS can remodel the host gut microbiota by intricate interplay between T6SS-mediated bacterial competition and altered host immune responses, which synergistically promote pathogenesis of A. veronii C4. Therefore, this newly characterized T6SS could represent a general interaction mechanism between the host and pathogen, and may offer a potential therapeutic target for controlling bacterial pathogens.

Active targeting tumor therapy using host-guest drug delivery system based on biotin functionalized azocalix[4]arene.

Host-guest drug delivery systems (HGDDSs) provided a facile method for incorporating biomedical functions, including efficient drug-loading, passive targeting, and controlled drug release. However, developing HGDDSs with active targeting is hindered by the difficult functionalization of popular macrocycles. Herein, we report an active targeting HGDDS based on biotin-modified sulfonated azocalix[4]arene (Biotin-SAC4A) to efficiently deliver drug into cancer cells for improving anti-tumor effect. Biotin-SAC4A was synthesized by amide condensation and azo coupling. Biotin-SAC4A demonstrated hypoxia responsive targeting and active targeting through azo and biotin groups, respectively. DOX@Biotin-SAC4A, which was prepared by loading doxorubicin (DOX) in Biotin-SAC4A, was evaluated for tumor targeting and therapy in vitro and in vivo. DOX@Biotin-SAC4A formulation effectively killed cancer cells in vitro and more efficiently delivered DOX to the lesion than the similar formulation without active targeting. Therefore, DOX@Biotin-SAC4A significantly improved the in vivo anti-tumor effect of free DOX. The facilely prepared Biotin-SAC4A offers strong DOX complexation, active targeting, and hypoxia-triggered release, providing a favorable host for effective breast cancer chemotherapy in HGDDSs. Moreover, Biotin-SAC4A also has potential to deliver agents for other therapeutic modalities and diseases.

Data mining and safety analysis of traditional immunosuppressive drugs: a pharmacovigilance investigation based on the FAERS database.

OBJECTIVE: The purpose of this study aimed to explore the new and serious adverse events(AEs) of Tacrolimus(FK506), cyclosporine(CsA), azathioprine(AZA), mycophenolate mofetil(MMF), cyclophosphamide(CTX) and methotrexate(MTX), which have not been concerned. METHODS: The FAERS data from January 2016 and December 2022 were selected for disproportionality analysis to discover the potential risks of traditional immunosuppressive drugs. RESULTS: Compared with CsA, FK506 has more frequent transplant rejection, and is more related to renal impairment, COVID-19, cytomegalovirus infection and aspergillus infection. However, CsA has a high infection-related fatality rate. In addition, we also found some serious and rare AE in other drugs which were rarely reported in previous studies. For example, AZA is closely related to hepatosplenic T-cell lymphoma with high fatality rate and MTX is strongly related to hypofibrinogenemia. CONCLUSION: The AEs report on this study confirmed that the results were basically consistent with the previous studies, but there were also some important safety signals that were inconsistent with or not mentioned in previous published studies. EXPERT OPINION: The opinion section discusses some of the limitations and shortcomings, proposing the areas where more effort should be invested in order to improve the safety of immunosuppressive drugs.

A centrosome-related gene signature for predicting the overall survival of uveal melanoma.

Background: Centrosome aberration (CA) plays a vital role in tumorigenesis and metastasis under pathophysiological conditions. The existence of CA was first reported in uveal melanoma (UVM) recently. Our study aimed to investigate the association of centrosome-related genes with UVM prognosis. Methods: The Cancer Genome Atlas (TCGA)-UVM and Gene Expression Omnibus series (GSE) 22138 were included in the study. Least absolute shrinkage and selection operator (LASSO) and Cox regression were combined to screen out key genes and construct a centrosome-related gene signature. Kaplan-Meier (KM) survival curves were used to evaluate the survival differences between the 2 groups. Gene enrichment, immune infiltration, and mutation profile were used to explore the underlying mechanism. Results: A centrosome-related gene signature was constructed: Risk score =-3.27071 × MAP6 - 5.03735 × CCDC40 - 2.68459 × PRKCD + 1.826349 × IGFBP4 + 11.66582 × RAB6C - 4.86899 × CCND3. The survival possibilities of the two groups were significantly different. The high-risk group showed cancer progression, inflammation, and immune restriction characteristics when compared with the low-risk group. BAP1 mutation was associated with high risk and SF3B1 mutation was associated with low risk according to the signature. Conclusions: Our study first investigated the role of centrosome-related genes in UVM overall survival (OS). We then constructed a centrosome-related gene signature for UVM, which provides new insights into the role of CA in UVM and identifies novel centrosome-related biomarkers.

Palmitoylation alters LDHA activity and pancreatic cancer response to chemotherapy.

Lactate dehydrogenase A (LDHA) serves as a key regulator of the Warburg Effect by catalyzing the conversion of pyruvate to lactate in the final step of glycolysis. Both the expression level and enzyme activity of LDHA are upregulated in cancers, however, the underlying mechanism remains incompletely understood. Here, we show that LDHA is post-translationally palmitoylated by ZDHHC9 at cysteine 163, which promotes its enzyme activity, lactate production, and reduces reactive oxygen species (ROS) generation. Replacement of endogenous LDHA with a palmitoylation-deficient mutant leads to reduced pancreatic cancer cell proliferation, increased T-cell infiltration, and limited tumor growth; it also affects pancreatic cancer cell response to chemotherapy. Moreover, LDHA palmitoylation is upregulated in gemcitabine resistant pancreatic cancer cells. Clinically, ZDHHC9 is upregulated in pancreatic cancer and correlated with poor prognoses for patients. Overall, our findings identify ZDHHC9-mediated palmitoylation as a positive regulator of LDHA, with potentially significant implications for cancer etiology and targeted therapy for pancreatic cancer.

Genome-wide DNA N6-methyladenosine in Aeromonas veronii and Helicobacter pylori.

BACKGROUND: DNA N6-methyladenosine (6mA), as an important epigenetic modification, widely exists in bacterial genomes and participates in the regulation of toxicity, antibiotic resistance, and antioxidant. With the continuous development of sequencing technology, more 6mA sites have been identified in bacterial genomes, but few studies have focused on the distribution characteristics of 6mA at the whole-genome level and its association with gene expression and function. RESULTS: This study conducted an in-depth analysis of the 6mA in the genomes of two pathogenic bacteria, Aeromonas veronii and Helicobacter pylori. The results showed that the 6mA was widely distributed in both strains. In A. veronii, 6mA sites were enriched at 3' end of protein-coding genes, exhibiting a certain inhibitory effect on gene expression. Genes with low 6mA density were associated with cell motility. While in H. pylori, 6mA sites were enriched at 5' end of protein-coding genes, potentially enhancing gene expression. Genes with low 6mA density were closely related to defense mechanism. CONCLUSIONS: This study elucidated the distribution characteristics of 6mA in A. veronii and H. pylori, highlighting the effects of 6mA on gene expression and function. These findings provide valuable insights into the epigenetic regulation and functional characteristics of A. veronii and H. pylori.

TNFSF15 inhibits progression of diabetic retinopathy by blocking pyroptosis via interacting with GSDME.

Diabetic retinopathy is a common microvascular complication of diabetes and a leading cause of blindness. Pyroptosis has emerged as a mechanism of cell death involved in diabetic retinopathy pathology. This study explored the role of GSDME-mediated pyroptosis and its regulation by TNFSF15 in diabetic retinopathy. We found GSDME was upregulated in the progression of diabetic retinopathy. High glucose promoted GSDME-induced pyroptosis in retinal endothelial cells and retinal pigment epithelial cells, attributed to the activation of caspase-3 which cleaves GSDME to generate the pyroptosis-executing N-terminal fragment. TNFSF15 was identified as a binding partner and inhibitor of GSDME-mediated pyroptosis. TNFSF15 expression was increased by high glucose but suppressed by the caspase-3 activator Raptinal. Moreover, TNFSF15 protein inhibited high glucose- and Raptinal-induced pyroptosis by interacting with GSDME in retinal cells. Collectively, our results demonstrate TNFSF15 inhibits diabetic retinopathy progression by blocking GSDME-dependent pyroptosis of retinal cells, suggesting the TNFSF15-GSDME interaction as a promising therapeutic target for diabetic retinopathy.

Analysis of instability of starch-based Pickering emulsion under acidic condition of pH < 4 and improvement of emulsion stability.

Starch-based Pickering emulsions exhibit high interfacial stability in a certain range of mild pH environments. On the contrary, many studies have reported that when the pH value is <4, it often leads to different degrees of emulsion instability. In this paper, the microscopic state of starch granules in the emulsion and its effect on the stability of the emulsion were observed and analyzed by atomic force microscope (AFM) in tapping mode. At the same time, Pickering emulsions in acidic environment were prepared by using the gel properties of methyl cellulose (MC) in synergy with esterified high amylose maize starch (M-HAMS) granules. The results show that in the emulsion with pH 3, the excessive H + ion inhibits the swelling of M-HAMS granules and prevents it from forming a stable gel structure, which is the main cause of emulsion instability. The polarity of MC with water contact angle (WCA) of 81.8° is similar to that of M-HAMS granules with WCA of 80.1°, and a uniform and ordered micro-nanostructure is formed in the aqueous phase. The prepared acidic (pH 3-4) emulsion has good stability during the observation period of 30 days.

Clinical significance of platelet mononuclear cell aggregates in patients with sepsis and acute respiratory distress syndrome.

BACKGROUND: The diagnosis of sepsis combined with acute respiratory distress syndrome (ARDS) has increased owing to the enhanced awareness among medical professionals and the continuous development of modern medical technologies, while early diagnosis of ARDS still lacks specific biomarkers. One of the main pathogenic mechanisms of sepsis-associated ARDS involves the actions of various pathological injuries and inflammatory factors, such as platelet and white blood cells activation, leading to an increase of surface adhesion molecules. These adhesion molecules further form platelet-white blood cell aggregates, including platelet-mononuclear cell aggregates (PMAs). PMAs has been identified as one of the markers of platelet activation, here we hypothesize that PMAs might play a potential biomarker for the early diagnosis of this complication. AIM: To investigate the expression of PMAs in the serum of patients with sepsis complicated by ARDS and its clinical significance. METHODS: We selected 72 hospitalized patients diagnosed with sepsis as the study population between March 2019 and March 2022. Among them, 30 patients with sepsis and ARDS formed the study group, while 42 sepsis patients without ARDS comprised the control group. After diagnosis, venous blood samples were immediately collected from all patients. Flow cytometry was employed to analyze the expression of PMAs, platelet neutrophil aggregates (PNAs), and platelet aggregates (PLyAs) in the serum. Additionally, the Acute Physiology and Chronic Health Evaluation (APACHE) II score was calculated for each patient, and receiver operating characteristic curves were generated to assess diagnostic value. RESULTS: The study found that the levels of PNAs and PLyAs in the serum of the study group were higher than those in the control group, but the difference was not statistically significant (P > 0.05). However, the expression of PMAs in the serum of the study group was significantly upregulated (P < 0.05) and positively correlated with the APACHE II score (r = 0.671, P < 0.05). When using PMAs as a diagnostic indicator, the area under the curve value was 0.957, indicating a high diagnostic value (P < 0.05). Furthermore, the optimal cutoff value was 8.418%, with a diagnostic sensitivity of 0.819 and specificity of 0.947. CONCLUSION: In summary, the serum levels of PMAs significantly increase in patients with sepsis and ARDS. Therefore, serum PMAs have the potential to become a new biomarker for clinically diagnosing sepsis complicated by ARDS.