The phenomenon of bacterial resistance has emerged as a significant challenge to global public health. Due to the increasing prevalence of antibiotic resistance, there has been interest in developing antimicrobial peptides (AMPs) as alternative antimicrobial therapies. However, AMPs resistance is not uncommon; it is simply subject to complex ecological and physiological limitations. While AMPs demonstrate potent antimicrobial activity in experimental and preclinical studies, their clinical efficacy remains limited. This review mainly summarizes the two methods of peptide hybridization and conjugation to combat drug-resistant bacteria. Hybridization has given AMPs new vitality, which overall enhance their antimicrobial spectrum, reduce toxicity, and enhance the bactericidal effect on drug-resistant strains. We also reviewed the conjugation of AMPs with various active molecules, such as antibiotics, antibodies, fatty acids, photosensitizers, phosphodiester oligomers, and nanoparticles. This review provides ideas for the design of hybrid peptides and coupled peptides in the future, and these AMPs have been shown to have an effect on drug-resistant strains after hybridization or coupling, thereby making the originally ineffective AMPs regain sensitivity. The transformation of natural AMPs has been effective in the laboratory to some extent, and give it clinical exploration value. Their clinical performance still falls short of that of conventional antibiotics due to challenges related to pharmacokinetics, safety, and reduced activity under clinically relevant conditions. To break through the bottleneck of clinical transformation of AMPs, it is necessary to continue to deepen multi-dimensional research on their physicochemical properties and make good use of artificial intelligence technology for intelligent design and high-throughput verification of hybrid peptides or conjugated peptides.

Fungal infections represent a significant and growing threat to public health, exacerbated by an expanding population of immunocompromised individuals and the increasing prevalence of resistance to conventional antifungal agents. Drug repurposing offers a strategic and efficient pathway for antifungal discovery, leveraging existing pharmacotherapies to reduce development costs and mitigate safety risks. This study evaluated the antifungal potential of pinaverium bromide, an FDA-approved antispasmodic drug for functional gastrointestinal disorders, against the prevalent pathogen Candida albicans. Our in vitro analyses revealed that pinaverium bromide demonstrated standalone antifungal activity and acted synergistically with amphotericin B or azole drugs. Moreover, it effectively attenuated key virulence factors of C. albicans, including hyphal formation and biofilm development. The therapeutic efficacy of both monotherapy and combination therapy with amphotericin B or voriconazole was validated in two murine models of systemic candidiasis. Mechanistically, pinaverium bromide disrupted mitochondrial function, induced apoptotic cell death, and impaired iron homeostasis in C. albicans. When combined with amphotericin B, it potentiated the drug’s effect by amplifying reactive oxygen species accumulation and enhancing membrane permeabilization. These findings support the potential of pinaverium bromide as a novel antifungal agent, either when used alone or in combination with established antifungal therapies.

Journal Article Accepted manuscript Human umbilical cord mesenchymal stem cells treated anti-MDA5 antibody-positive dermatomyositis with interstitial lung disease: a case report Get access Runlu Zhou, Runlu Zhou The Second Clinical Medical School of Nanjing Medical University, Nanjing, Jiangsu, ChinaDepartment of Respiratory and Critical Care Medicine, The Second Affiliated Hospital of Nanjing Medical University, Nanjing, Jiangsu, China Search for other works by this author on: Oxford Academic PubMed Google Scholar Xiao Jin, Xiao Jin The Second Clinical Medical School of Nanjing Medical University, Nanjing, Jiangsu, ChinaDepartment of Respiratory and Critical Care Medicine, The Second Affiliated Hospital of Nanjing Medical University, Nanjing, Jiangsu, China Search for other works by this author on: Oxford Academic PubMed Google Scholar Juan Li, Juan Li Department of Respiratory and Critical Care Medicine, The Second Affiliated Hospital of Nanjing Medical University, Nanjing, Jiangsu, China Search for other works by this author on: Oxford Academic PubMed Google Scholar Yucong He, Yucong He The Second Clinical Medical School of Nanjing Medical University, Nanjing, Jiangsu, ChinaDepartment of Respiratory and Critical Care Medicine, The Second Affiliated Hospital of Nanjing Medical University, Nanjing, Jiangsu, China Search for other works by this author on: Oxford Academic PubMed Google Scholar Tianming Gao, Tianming Gao Department of Respiratory and Critical Care Medicine, The Second Affiliated Hospital of Nanjing Medical University, Nanjing, Jiangsu, China Search for other works by this author on: Oxford Academic PubMed Google Scholar Chenghua Zhu, Chenghua Zhu Department of Respiratory and Critical Care Medicine, The Second Affiliated Hospital of Nanjing Medical University, Nanjing, Jiangsu, China Search for other works by this author on: Oxford Academic PubMed Google Scholar Yan Wang, Yan Wang Jiangsu Cell Tech Medical Research Institute, Nanjing, Jiangsu, 211166, China Search for other works by this author on: Oxford Academic PubMed Google Scholar Ganzhu Feng Ganzhu Feng Department of Respiratory and Critical Care Medicine, The Second Affiliated Hospital of Nanjing Medical University, Nanjing, Jiangsu, China Correspondence to Ganzhu Feng, Address: No. 121 Jiangjiayuan Rd, Gulou District, Nanjing 210011, Jiangsu, China, Email: fgz62691@163.com Search for other works by this author on: Oxford Academic PubMed Google Scholar Rheumatology, keae285, https://doi.org/10.1093/rheumatology/keae285 Published: 22 May 2024 Article history Received: 09 October 2023 Revision received: 27 March 2024 Accepted: 25 April 2024 Published: 22 May 2024

The development of vaccines represents a promising and safe strategy to combat multidrug-resistant (MDR) Acinetobacter baumannii (A. baumannii) infections. In this study, we designed and evaluated a dendritic cell (DC)-targeting multiepitope peptide-based biomimetic nanovaccine for its immunogenicity and protective efficacy in a murine model. Bioinformatics tools were employed to predict and screen B- and T-cell epitopes derived from the OmpW protein of A. baumannii, followed by immunological validation. The dominant epitopes were sequentially linked using 6-aminocaproic acid to synthesize a multiepitope peptide, rOmpW. Subsequently, rOmpW was encapsulated within polylactic-co-glycolic acid (PLGA) nanoparticles coated with neutrophil membranes (NM), and the surface was functionalized with a DC-targeting peptide (DCpep) to construct the biomimetic nanovaccine, DCpep-NM-PLGA-rOmpW. This biomimetic nanovaccine elicited robust Th1 and Th17 cellular immune responses, as well as humoral immunity, and demonstrated significant protective efficacy in a murine model of acute lethal pneumonia caused by A. baumannii. These findings underscore the translational potential of this biomimetic nanovaccine as a prophylactic strategy against A. baumannii infections.

Acinetobacter baumannii has become a challenge to treat clinically because of the increased number of extensively drug-resistant strains. Vaccination is an effective way to prevent and control A. baumannii infection. In this study, we constructed an A. baumannii nanovaccine Chitosan-PLGA-rOmp22 (CS-PLGA-rOmp22), and evaluated its immunogenicity and protective effects after intranasal immunization. BALB/c mice that received intranasal immunization with the CS-PLGA-rOmp22 nanovaccine displayed long-lasting local mucosal and systemic immunity, and could resist A. baumannii challenge. The CS-PLGA-rOmp22 penetrated the nasal mucosa and promoted the maturation and activation of dendritic cells (DCs) in vitro. Moreover, the immunoprotective effect of intranasal vaccination was comparable to that of subcutaneous immunization. Our findings suggest that this nanovaccine is a potential candidate for preventing A. baumannii infection after mucosal administration.

Inflammasome-mediated pyroptosis and cytokine release are crucial host defenses against intracellular pathogens. Mycobacterium tuberculosis (M. tb) is a successful intracellular pathogen, and it is largely unclear how it evades immune clearance and persists in macrophages. This study investigated whether the Rv2647 protein acts as a key virulence factor of M. tb and explored the potential mechanism of inhibiting macrophage pyroptosis and promoting M. tb survival. The results showed Rv2647 promoted NLRP3 degradation via enhancing its ubiquitination, which led to the inactivation of NLRP3/caspase-1/GSDMD and reduction of IL-1β secretion, thereby inhibiting macrophage pyroptosis and facilitating M. tb survival. Furthermore, Rv2647-mediated enhancement of NLRP3 ubiquitination and degradation depended on its binding to ISG15, competitively inhibiting ISGylation of NLRP3. The study identified Rv2647 as the key virulence factor that promoted M. tb survival by inhibiting macrophage pyroptosis, whose mechanism was to competitively inhibit the ISGylation of NLRP3 and enhance its ubiquitination, thus suppressing NLRP3/caspase-1/GSDMD-mediated pyroptosis. This finding highlighted Rv2647 as a promising drug target or vaccine antigen for tuberculosis prevention and control.

Tuberculosis is a widely spread disease caused by Mycobacterium tuberculosis (Mtb). The pathogenicity of the pathogen is closely associated with the immune defense mechanisms of the host cells. As key cellular degradation and metabolic centers, lysosomes critically regulate tuberculosis infection. When Mtb invades the host, it is taken up by macrophages and enters phagosomes. Subsequently, the phagosomes fuse with lysosomes and form phagolysosomes, which eliminate the pathogenic bacteria through the acidic environment and hydrolytic enzymes within lysosomes. However, Mtb can interfere with the normal functions of lysosomes through various strategies. It can secrete specific factors (such as ESAT-6, ppk-1, and AcpM) to inhibit the acidification of lysosomes, enzyme activity, and the fusion of phagosomes and lysosomes, thereby enabling Mtb proliferation within host cells. An in-depth exploration of the mechanism of the interaction between Mtb and lysosomes will both uncover bacterial immune evasion strategies and identify novel anti-tuberculosis therapeutic targets.

Biofilm-associated refractory pneumonia represents a growing clinical challenge, where the protective extracellular matrix not only confers drug resistance but also promotes persistent infections. While topologically structured physical bactericidal systems show potential for biofilm disruption, their reliance on passive diffusion limits penetration efficiency, and biofilm regeneration following treatment remains problematic. Inspired by phage invasion mechanisms, a biohybrid nanomotor integrating sono-sensitive antibiotics is developed for combating multidrug-resistant Klebsiella pneumonia (MDR-KPN)-induced lung infections. The asymmetric heterostructured nanomotor consists of hollow mesoporous Prussian blue-lomefloxacin/mesoporous CuxO (CuO/Cu2O composite) Janus nanoparticle (HP-L/MCu JNPs), which can actively target and dismantle biofilms through integrated mechanical and chemical action. The innovative design of nanomotor leverages two complementary functionalities: CuxO nanospheres provide autonomous propulsion for mechanical biofilm penetration, and the Prussian blue subunit enables ultrasound-triggered antibiotic release; meanwhile, ultrasound-activated antibiotics generate cytotoxic singlet oxygen (1O2) that induces irreparable DNA damage in surviving bacteria. Transcriptomic analysis confirms this combined mechanical-chemical action effectively disperses biofilms while preventing bacterial recovery. In vivo validation demonstrates the therapeutic potential of this biomimetic strategy, which merges physical destruction with catalytic chemistry to overcome biofilm-associated treatment resistance. This approach establishes a new paradigm for addressing persistent bacterial infections through integrated nanoarchitectonics.

Background Bronchiectasis (BE) is a chronic respiratory disease. Acute BE exacerbation caused by recurrent infections can lead to hemoptysis and even asphyxia, with high mortality and long hospitalization. This study aimed to identify novel diagnostic metabolic biomarkers for predicting acute exacerbation and severity of BE. Methods A liquid chromatography–mass spectrometry (LC–MS)-based untargeted metabolomic analysis was performed for serum samples from 45 patients with acute BE exacerbation and 15 healthy controls. The diagnostic value of the candidate metabolites was evaluated using receiver operating characteristic (ROC) curves. Results Based on bronchiectasis severity index (BSI) scores, patients with acute BE exacerbation were classified into mild, moderate, and severe BE groups. Compared to healthy controls, the abundance of 4-acetamidobutyric acid was elevated in the mild, moderate, and severe groups (p < 0.05), with no significant difference among the three groups. In the severe BE group, the abundances of taurochenodecoxycholic acid, oleamide, hexadecanamide, and glycodeoxycholic acid were significantly elevated from those in mild and moderate BE groups (p < 0.05), with Youden index (YI) ≥ 0.8 for all metabolites; the combination of these 4 metabolites had an area under the ROC curve (AUROC) of 0.99, a sensitivity of 100 % and a specificity of 93.3 % for identifying severe BE. Pathway analysis reveals that abnormally enriched metabolites in BE patients are associated with PI3K-Akt signaling pathway, mTOR signaling pathway, FoxO signaling pathway, renin-angiotensin system signaling pathway, asthma signaling pathway, and FcεRI signaling pathway, where prostaglandin D2 exerts direct or indirect impacts on these pathways. Conclusion 4-Acetamidobutyric acid can serve as a biomarker for predicting acute BE exacerbation, while taurochenodecoxycholic acid, oleamide, hexadecanamide, and glycodeoxycholic acid are robust biomarkers for predicting severe BE. Prostaglandin D2 plays a crucial role in promoting the pathogenesis of pulmonary inflammatory cell recruitment, cell autophagy, and pulmonary fibrosis during acute BE exacerbation. Overall, this study identifies biomarkers for predicting acute BE exacerbation and provides new targets for drug development.

Suraxavir marboxil (GP681) is an antiviral drug inhibiting the polymerase acidic protein (PA) of RNA polymerase, of influenza. It has shown therapeutic activity against influenza A and B virus infections in preclinical studies. In this multicenter randomized, double-blind, placebo-controlled, phase 3 trial, we aimed to investigate the efficacy and safety of single-dose suraxavir marboxil (40-mg oral dose) in otherwise healthy outpatients aged 5–65 years with uncomplicated influenza unaccompanied by severe issues. From 28 July 2022 to 31 October 2023, 591 outpatients aged 5–65 years with uncomplicated influenza underwent randomization in 46 research centers in China and were randomly assigned in a 2:1 ratio to receive suraxavir marboxil (40 mg) or placebo within 2 days of symptom onset. The primary outcome was time to alleviation of influenza symptoms (TTAS) (from the start of treatment until body temperature returned to 37.2 °C or less and all seven influenza symptoms (cough, sore throat, headache, nasal congestion, feverishness or chills, muscle or joint pain, and fatigue) resolved for at least 21.5 h) within 15 days by treatment. The secondary endpoints included virological indicators, system and respiratory symptoms, PA variant mutation and adverse events. The median TTAS was significantly shorter in the group that received suraxavir marboxil compared to the placebo group (42.0 h versus 63.0 h, P = 0.002). Suraxavir marboxil was associated with more rapid decrease in viral load from baseline than placebo by 1 day after administration, with a mean change of −2.2 ± 1.3 compared to −1.3 ± 1.7 log10 copies per ml (P < 0.001) in the placebo group. Adverse events were reported in 28.4 NCT05474755 . Suraxavir marboxil, an antiviral drug designed to inhibit the polymerase acidic protein of influenza, alleviates symptoms in individuals with influenza faster than placebo in a phase 3 trial conducted in China.

The increasing prevalence of carbapenem-resistant and extensively drug-resistant Acinetobacter baumannii (XDR-Ab) poses a critical challenge in treating hospital-acquired pulmonary infections. In this study, we developed a biomimetic neutrophil membrane-coated nanoparticle system, NM@PCN-TIG, for the targeted delivery of tigecycline (TIG). The system utilizes the porphyrin-based metal-organic framework (MOF) PCN-224 as the core of the nanoparticle, encapsulating TIG and coated with a neutrophil membrane (NM) to enhance immune evasion and targeting of infection sites. Its loading efficiency, controlled release properties, cytotoxicity, and bactericidal activity under ultrasound mediation were systematically evaluated in vitro and in vivo. Our results demonstrated that NM@PCN-TIG significantly enhanced the bactericidal efficacy of TIG, increased reactive oxygen species (ROS) production, and promoted macrophage polarization toward an anti-inflammatory phenotype. This innovative biomimetic TIG nanosystem shows great potential as a platform for addressing XDR-Ab-induced pneumonia.

ABSTRACT Opportunistic fungal infections, particularly caused by Candida albicans , remain a common cause of high morbidity and mortality in immunocompromised patients. The escalating prevalence of antifungal drug resistance necessitates the immediate exploration of alternative treatment strategies to combat these life-threatening fungal diseases. In this study, we investigated the antifungal efficacy of firsocostat, a human acetyl-CoA carboxylase (ACC) inhibitor, against C. albicans . Firsocostat alone displayed moderate antifungal activity, while combining it with voriconazole, itraconazole, or amphotericin B exhibited synergistic effects across almost all drug-sensitive and drug-resistant C. albicans strains tested. These observed synergies were further validated in two mouse models of oropharyngeal and systemic candidiasis, where the combination therapies demonstrated superior fungicidal effects compared to monotherapy. Moreover, firsocostat was shown to directly bind to C. albicans ACC and inhibit its enzymatic activity. Sequencing spontaneous firsocostat-resistant mutants revealed mutations mapping to C. albicans ACC, confirming that firsocostat has retained its target in C. albicans . Overall, our findings suggest that repurposing firsocostat, either alone or in combination with other antifungal agents, holds promising potential in the development of antifungal drugs and the treatment of candidiasis.

Pseudomonas aeruginosa (P. aeruginosa), a common opportunistic pathogen, is highly prone to chronic infection and is almost impossible to eradicate, especially attributed to virulence factors and adaptive mutations. In the present study, pseudomonas effector candidate 1 (Pec 1), a novel virulence factor of P. aeruginosa, was investigated, which inhibited bacterial clearance by the host and aggravated lung injury. Further, it demonstrated that Pec 1 inhibited miR-155 via suppressing integrin β3 expression, thereby activating PI3K-AKT-mTOR and inhibiting autophagy in macrophages. Additionally, the identification of Pec 1 in sputum was related to the bacterial load and assisted in rapid diagnosis of P. aeruginosa infection. This finding underlined the importance of Pec 1 in the pathogenesis of P. aeruginosa infection and indicated that Pec 1 could be a vital independent virulence factor during chronic infection with P. aeruginosa, providing new insights in rapid diagnosis, therapeutic targets, and vaccine antigens of P. aeruginosa infection.

Lung cancer is one of the most malignant tumors with fastest morbidity and mortality. Small cell lung cancer (SCLC) is the most malignant pathological type of lung cancer with early metastasis and poor prognosis. At present, there is a lack of effective indicators to predict prognosis of SCLC patients. Delta-like 3 protein (DLL3) is selectively expressed on the surface of SCLC and is involved in proliferation and invasion. Neuron-specific enolase (NSE) is an enolase isoenzyme that is generally regarded as a biomarker for SCLC and may correlate with stage of SCLC, prognosis and chemotherapy response. NSE can be influenced by different types of factors. To explore the associations between expression levels of DLL3 in tumor tissues with platinum/etoposide chemotherapy response, and assess the prognostic values of DLL3, NSE and other potential prognostic factors in advanced SCLC patients were herein studied. Ninety-seven patients diagnosed with SCLC in Zhongda Hospital from 2014 to 2020 were enrolled in the study. Serum NSE levels were tested using ELISA methods before any treatment. The expression of DLL3 in tumor tissue was detected by Immunohistochemistry (IHC). We investigated the relationship of DLL3 expression with chemotherapy and survival. Progression free survival (PFS) and overall survival (OS) were estimated by the Kaplan–Meier method. Multivariate Cox-proportional hazard regression was used to identify predictors of PFS and OS. DLL3 was detected in 84.5% (82/97) of all patients’ tumor samples by IHC, mainly located on the surface of SCLC cells. Lower DLL3 expression was associated with longer PFS and better chemotherapy response. OS had no significant differences. Multivariate analysis by Cox Hazard model showed that, high DLL3 expression and maximum tumor size >5 cm were independent risk factors for PFS, where NSE < 35 ng/mL and age < 70 were independent prognostic factors for OS. Early stage was independent prognostic factors for PFS and OS (P < .05 log-rank). DLL3 was expressed in the most of SCLCs. DLL3 expression level in the tumor and NSE level in the serum may be useful biomarkers to predict the prognosis of SCLC. DLL3 may be a potential therapeutic target for SCLC in the future.

Novel antimicrobial strategies are urgently needed to treat extensively drug-resistant (XDR) bacterial infections due to the high mortality rate and lack of effective therapeutic agents. Herein, nanoengineered human umbilical cord mesenchymal stem cells (hUC-MSCs), named PMZMU, are designed as a sonosensitizer for synergistic sonodynamic-nano-antimicrobial therapy against gram-negative XDR bacteria. PMZMU is composed of a bacterial targeting peptide (UBI29-41) modified hUC-MSCs membrane (MSCm), a sonosensitizer meso-tetra(4-car-boxyphenyl) porphine doped mesoporous organo-silica nanoparticle and an acidity-responsive metal-organic framework ZIF-8. This innovative formulation enables efficient loading of polymyxin B, reduces off-target drug release, increases circulation and targeting efficacy, and generates reactive oxygen species upon ultrasound irradiation. PMZMU exhibits remarkable in vitro inhibitory activity against four XDR bacteria: Klebsiella pneumoniae, Acinetobacter baumannii, Pseudomonas aeruginosa (PA), and Escherichia coli. Taking advantage of the bacterial targeting ability of UBI29-41 and the inflammatory chemotaxis of hUC-MSC, PMZMU can be precisely delivered to lung infection sites thereby augmenting polymyxin B concentration. PMZMU-mediated sonodynamic therapy significantly reduces bacterial burden, relieves inflammatory damage by promoting the polarization of macrophages toward M2 phenotype, and improves survival rates without introducing adverse events. Overall, this study offers promising strategies for treating deep-tissue XDR bacterial infections, and guides the design and optimization of biomimetic nanomedicine.

Background: Non-small cell lung cancer (NSCLC) is a malignant form of lung cancer, and its prognosis could be improved by identifying key therapeutic targets. Thus, this study investigates the potential role of F-box Only Protein 33 (FBXO33) in NSCLC. Methods: The expression levels of FBXO33 in NSCLC were determined using University of Alabama at Birmingham Cancer Data Analysis Portal (UALCAN) prediction, and its correlation with overall survival (OS) was analyzed via Kaplan-Meier survival analysis. These results were validated through quantitative polymerase chain reaction (qPCR), western blot (WB), and immunofluorescence (IF). We modulated FBXO33 expression by overexpression or knockdown and analyzed its effects on cell growth, proliferation, migration, invasion, and stemness characteristics in NSCLC cell lines. Additionally, the interaction between FBXO33 and Myelocytomatosis (Myc) and its impact on Myc ubiquitination were examined. An in vivo NSCLC xenograft model was used to corroborate the in vivo experimental results. Results: The study found an inverse correlation between FBXO33 expression in NSCLC and OS. Lower FBXO33 expression enhanced the growth, proliferation, migration, invasion, and stemness characteristics of NSCLC cell lines. FBXO33 interacted with Myc to promote its ubiquitination and subsequent degradation, which suppressed NSCLC development. Conclusion: FBXO33 is expressed at low levels in NSCLC and correlates with lower OS. Overexpression of FBXO33 promotes Myc ubiquitination and degradation and inhibits tumor cell proliferation, migration and stemness characteristics, thereby impeding NSCLC progression.

The evidence from clinical studies suggests that lung carcinoma (LC) patients exhibit dysregulation in lipid metabolism. However, the causal relationship between plasma lipidome and LC, and whether inflammatory proteins mediate, remains to be determined. Genetic data for 179 plasma lipids and 91 inflammatory proteins were obtained from the latest published genome-wide association studies. Genetic data on LC and subtypes were from the largest available meta-analysis. The causal relationship between plasma lipidome and LC was determined by the two-sample Mendelian randomization (MR) method. Mediation MR analysis was employed to ascertain whether inflammatory proteins mediate the impact of plasma lipidome on LC. We identified 39 causal relationships between genetically predicted plasma lipidome and LC and subtypes. These relationships involve the influence of phosphatidylcholines, phosphatidylethanolamines, diacylglycerols, triacylglycerols, sphingomyelins, and Sterol esters. Additionally, the mediating role of 5 inflammatory proteins in the causal relationship between plasma lipidome and LC and subtypes was determined. Our results highlight the complex network of plasma lipidome and inflammatory proteins regulating LC. Integrating plasma lipidome and inflammatory proteins into clinical practice may open new avenues for the prevention and treatment of LC.

Background The development of vaccines is an effective and safe strategy to combat multidrug-resistant (MDR) Acinetobacter baumannii (A. baumannii) infections. This study aimed to prepare a DC-targeting multiepitope peptide biomimetic nanovaccine and evaluate its immune response and protective effect in mice. Results The B-cell and T-cell epitopes of the OmpW protein from A. baumannii were predicted and screened using bioinformatics methods and identified by immunological means. The selected dominant epitopes were conjugated in series with 6-aminocaproic acid, and a multiepitope peptide, rOmpW, was chemically synthesized. Then, rOmpW was encapsulated with polylactic-co-glycolic acid (PLGA) and a neutrophil membrane (NM), and the surface was modified with DC-targeting peptide (DCpep) to construct the biomimetic nanovaccine DCpep-NM-PLGA-rOmpW. This biomimetic nanovaccinecan induce strong Th1 and Th17 cellular immune responses and humoral immunity. The biomimetic nanovaccine produced efficient immunological protection in an acute lethal pneumonia model of A. baumannii. Conclusions Our results indicate the potential translational value of this biomimetic nanovaccinefor preventing A.baumannii infection.