Formyl peptide receptor-2 (FPR2) belongs to the G protein-coupled receptor (GPCR) family and plays a critical role in the development of various tumors. However, the roles and mechanisms of FPR2 in glioblastoma (GBM) remain poorly understood. In this study, we observed significant upregulation of FPR2 in glioma cell lines and tissues, and elevated FPR2 expression levels are correlated with poor patient survival. Furthermore, we found that FPR2 suppresses the autophagy mediated by BECN1 and ATG5 in GBM cells. Using Western blot analysis, we revealed that FPR2 regulates GBM cell invasion via the PI3K/AKT signaling pathway. Additionally, we demonstrated that knocking down FPR2 expression in GBM cells reduced tumor cell migration and invasion in vitro and tumor growth in vivo. The inhibition of FPR2 led to cell cycle arrest at the G2/M phase and increased apoptosis. Finally, our findings indicate that FPR2 may prevent autophagy-induced epithelial‒mesenchymal transition (EMT)-like changes by preventing autophagy-induced degradation of Snail. Our findings suggest that FPR2 promotes GBM cell migration and invasion through the inhibition of autophagy and the activation of the PI3K/AKT signaling pathway, highlighting the potential of inducing autophagy as a therapeutic approach to inhibit invasion in GBM with high FPR2 expression.

Respiratory diseases pose a significant global public health challenge. Extensive research indicates that respiratory conditions are influenced by lung microbiota; however, the relationships between alterations in pulmonary microbiota and various respiratory diseases remain unclear. This study explores the characteristics and distinctions of lung microbial communities in patients with lung cancer (LC), chronic obstructive pulmonary disease (COPD), and community-acquired pneumonia (CAP). The research involved 114 patients and employed culturomics and 16S rRNA gene sequencing to analyze bronchoalveolar lavage fluid samples. Through culturomics, 168 bacterial species were identified, with variations in bacterial profiles observed across the different diseases. Sequencing results indicated that the dominant phyla among the three groups were Bacillota, Bacteroidota, Pseudomonadota, Actinomycetota, and Fusobacteriota, consistent with the culturomics findings. Notably, the CAP group exhibited higher species richness compared to the LC and COPD groups, with significant differences in beta-diversity among the three groups. Specific bacterial genera, such as Alloprevotella, Abiotrophia, and Mycoplasma, were distinguished as indicative taxa for the LC, COPD, and CAP groups, respectively. Utilizing random forest modeling and receiver operating characteristic curve analysis, several key bacterial genera were identified as capable of differentiating between these diseases. The study highlights distinct differences in lung microbiota among patients with LC, COPD, and CAP, potentially serving as a reference for diagnosis, suggesting that disease-specific microenvironments may influence local microbial communities, thus providing evidence for associations between lung microbiota and various respiratory diseases that warrant further investigation.IMPORTANCEThe human lung microbial community plays a crucial role in various respiratory diseases by regulating the lung's immune system and maintaining lung homeostasis. However, there is a paucity of comparative studies examining the characteristics of the pulmonary microbiome in common respiratory diseases, such as lung cancer (LC), chronic obstructive pulmonary disease (COPD), and community-acquired pneumonia (CAP). This study aims to explore the differences in lung microbiomes among these conditions. By employing culturomics and 16S rRNA sequencing technology, we identified significant variations in their lung microbiota. Notably, Alloprevotella, Abiotrophia, and Mycoplasma were identified as indicative taxa for the LC, COPD, and CAP groups, respectively. This research is essential for enriching the database of cultivable lung bacteria and investigating the interactions between specific strains and diseases at the species level, and identifying potential biomarkers and therapeutic targets.

MicroRNA-503 (miR-503) is encoded within the X-linked MIR503HG locus and the miR-424/503 cluster, where its output is shaped by guide-strand identity, target availability, competing endogenous RNA (ceRNA) dosage, and tumor-lineage context. This review focuses on solid tumors and synthesizes evidence on miR-503 biogenesis, strand usage, upstream regulation, target selection, tumor-microenvironmental constraints, and translational relevance. In many epithelial cancers, microRNA-503-5p (miR-503-5p) is reduced and is associated with repression of cell-cycle, angiogenic, and survival pathways. Malignant mesothelioma provides the strongest reported oncogenic context, whereas the evidence in selected glioblastoma settings remains limited. We propose a provisional, evidence-informed target-context framework in which net polarity reflects the interaction of strand availability, lineage-restricted target repertoires, ceRNA dosage, epigenetic state, and tumor-microenvironmental composition. The framework is hypothesis-generating rather than a validated unified mechanism. We further assess miR-503 as a candidate biomarker and therapeutic target while distinguishing biological associations from clinically actionable evidence and separating miR-503-specific data from general miRNA delivery-platform studies.

Background:There is growing evidence that long non-coding RNAs (lncRNAs) play crucial roles in cancer progression and therapy. Our previous study showed that the lncRNA plasmacytoma variant translocation 1 (PVT1) regulates tumor growth and metastasis in breast cancer (BC). As a conventional chemotherapeutic drug, doxorubicin (DOX) resistance continues to be a major challenge in BC treatment. This study aimed to explore the role and underlying mechanism of PVT1 in doxorubicin-resistant BC. Methods:Quantitative reverse transcription polymerase chain reaction (qRT-PCR) and Western blotting (WB) were carried out to detect gene and protein expression levels. The extent of ferroptosis was measured based on the cellular glutathione (GSH) levels and total or lipid reactive oxygen species (ROS) levels. An in-situ tumor implantation model in nude mice was employed to validate the mechanism in vivo. Transcriptome analysis was conducted to identify downstream target genes. Results:This study found that PVT1 was highly expressed in the plasma of drug-resistant patients and drug-resistant cell lines. Silencing PVT1 reduced cellular glutathione level, increased reactive oxygen species (ROS) and lipid peroxidation (LPO), while ferroptosis inhibition in rescue experiments partially reversed the oxidative stress. In-vivo study confirmed that silencing PVT1 increased the sensitivity of BC cells to doxorubicin treatment. Transcriptomic sequencing revealed that solute carrier family 3 member 2 (SLC3A2) was the most potential target gene of PVT1, which was confirmed in PVT1-silenced cell models. Conclusion:Mechanistically, PVT1 increased SLC3A2 expression, thus inhibiting ferroptosis and promoting doxorubicin resistance in BC, indicating that PVT1 could be a promising therapeutic target for doxorubicin-resistant BC patients.

Initially characterized as a component of the extracellular matrix (ECM) in cartilage, cartilage intermediate layer protein 2 (CILP2) is now recognized as a pleiotropic secretory protein with far-reaching roles in physiology and disease. This review synthesizes evidence establishing CILP2 as a key modulator at the nexus of metabolic dysfunction, cancer, and other pathologies. Genomic studies have firmly established the NCAN-CILP2 locus as a hotspot for genetic variants influencing dyslipidemia and cardiovascular risk. Functionally, CILP2 is upregulated by metabolic stress, including high glucose and oxidatively modified LDL (oxLDL), and actively contributes to pathologies such as dyslipidemia, diabetes, and sarcopenia by impairing glucose metabolism and mitochondrial function. Its role extends to fibrosis and neurodevelopment, promoting hypertrophic scar formation and neurogenesis through interactions with ATP citrate lyase (ACLY) and Wnt3a, respectively. More recently, CILP2 has emerged as an oncoprotein, overexpressed in multiple cancers, including pancreatic ductal adenocarcinoma and colorectal cancer. It drives tumor proliferation and metastasis and correlates with tumor microenvironment remodeling through mechanisms involving Akt/EMT signaling and immune infiltration. The dysregulation of CILP2 in patient serum and its correlation with disease severity and poor prognosis highlight it as a promising biomarker and a compelling therapeutic target across a spectrum of human diseases.

Immune checkpoint inhibitors (ICIs) have changed the treatment of non-small cell lung cancer (NSCLC), but response, acquired resistance and immune-related adverse events (irAEs) remain variable. Gut microbiome features and microbial metabolites may contribute to this variation through systemic immunity, gut-lung communication and the tumor immune microenvironment. This structured narrative review synthesizes direct and near-direct NSCLC or lung-cancer immunotherapy evidence, including cohorts ranging from 37 to 556 patients, a phase III chemoimmunotherapy ancillary cohort with 270 baseline fecal samples and recent TOPOSCORE-based community-ecology studies. Clinical evidence reports recurrent but inconsistent associations among microbial diversity, Akkermansia-related states, community topology, functional microbial features, survival, treatment-duration questions and toxicity, with substantial variation by region, treatment setting and endpoint. Mechanistic studies support plausible pathways involving short-chain fatty acids (SCFAs), bile acids, tryptophan-related metabolites, inosine and exploratory bacterial extracellular vesicle-associated signals. Few studies, however, connect microbiome, metabolite, immune and clinical outcome data within the same patients. We use an evidence-boundary framework to state what each evidence layer can support. In the current evidence base, microbiome signals are better suited to prospective validation, trial design and communication of uncertainty than to routine microbiome testing or intervention outside regulated studies.

Background Breast cancer is the leading cause of cancer-related mortality among women. Laminin subunit alpha 3 (LAMA3), a constituent of the extracellular matrix, is associated with tumor progression. However, its clinical relevance and function remain inadequately understood. Methods We conducted a systematic evaluation of LAMA3 expression in breast cancer by assessing plasma, cell lines, and tissues using mass spectrometry, qRT-PCR, Western blotting, and immunohistochemistry (IHC). The colocalization of LAMA3 with tumor and stromal markers was detected by immunofluorescence. Tumor and stromal regions were digitally segmented using QuPath software to compute compartment-specific histochemical scores. The correlation of LAMA3 with clinical characteristics was evaluated using Chi-square and nonparametric statistical tests. The impact of LAMA3 expression on survival was analyzed using Kaplan-Meier survival curves and Cox proportional hazards regression models. Bioinformatics analyses were performed to investigate potential underlying mechanisms. Results Plasma LAMA3 protein levels were elevated in patients, but its mRNA and protein levels were reduced in breast cancer cell lines and tissues. Analysis on TIMER 2.0 database showed LAMA3 was positively related to cancer-associated fibroblasts and epithelial cells infiltration in breast cancer tissues. Multiplex immunofluorescence revealed LAMA3 colocalized with cancer-associated fibroblasts and tumor epithelial cells. Although LAMA3 protein levels were reduced in breast cancer tissues, high stromal—but not tumor—LAMA3 expression was significantly associated with advanced histological grade, TNM stage, molecular subtype, recurrence, and poorer survival outcomes. Multivariate analysis indicated stromal LAMA3 as an independent prognostic factor for survival in breast cancer, with enhanced predictive power when combined with lymph node metastasis. Bioinformatic analyses suggested that LAMA3 protein was correlated with epithelial-mesenchymal transition and extracellular matrix-receptor interaction pathways in breast cancer. Conclusions Stromal LAMA3, expressed in the tumor microenvironment, is a new potential prognostic biomarker for breast cancer, emphasizing the significance of spatial context in biomarker discovery and suggesting its use in risk stratification.

BackgroundMacrococcus caseolyticus is a Gram-positive bacterium mainly isolated from dairy products and animal skin and is usually associated with animal infections. M. caseolyticus comprises two subspecies, M. caseolyticus subsp. caseolyticus and M. caseolyticus subsp. hominis. Here, we report a fatal bloodstream infection caused by M. caseolyticus subsp. caseolyticus in China and characterize the clinical isolate by genomic and phenotypic analyses.MethodsStrain WH712 was isolated from the blood culture of a 91-year-old male patient and identified by matrix-assisted laser desorption ionization/time-of-flight mass spectrometry. Whole-genome sequencing was performed using the Illumina HiSeq platform. Antimicrobial susceptibility testing was conducted using the AutoMic-i600 system, and biofilm-forming capacity was evaluated using a 96-well microtiter plate assay.ResultsWH712 was initially identified as M. caseolyticus by MALDI-TOF MS and confirmed as M. caseolyticus subsp. caseolyticus by whole-genome analysis. Homology-based genomic analysis identified putative homologs of bopD, ami, srtE, and pfbA, which have been associated in other bacteria with biofilm-related regulation, adhesion, and cell-surface functions. These findings suggest that WH712 may harbor genomic features relevant to host colonization and persistence. The isolate was phenotypically susceptible to most tested antibiotics but showed intermediate resistance to clindamycin, possibly associated with a vgaB homolog and efflux-related homologs, including macB and sdrM. Phenotypic testing demonstrated that WH712 had strong biofilm-forming capacity, comparable to that of Staphylococcus aureus ATCC 29213, which may have contributed to bacterial persistence and the poor clinical outcome.ConclusionsThis study reports a fatal human bloodstream infection associated with M. caseolyticus subsp. caseolyticus in China. Whole-genome analysis and phenotypic testing showed that this clinical isolate had a strong biofilm-forming phenotype, which may have contributed to bacterial persistence. However, the poor clinical outcome should be interpreted primarily in the context of the patient’s advanced age, severe comorbidities, and impaired host defenses.

Pseudomonas fulva (P. fulva) is a rare human pathogen, with few reported cases of infection caused by this bacterium. We report a case of an elderly patient with P. fulva infection who developed peritoneal dialysis-related peritonitis after peritoneal dialysis. A bacterial strain was isolated from peritoneal dialysis fluid and identified as P. fulva by matrix-assisted laser desorption ionization-time of flight mass spectrometry (MALDI-TOF MS) and 16S rRNA sequencing. The patient recovered after treatment with cefotaxime. A comprehensive review of P. fulva infections in pathogenic diagnosis, clinical treatment, and prognosis were presented in this paper.

A novel Erwinia strain BC051422T was isolated from the blood of a patient at the Central Hospital of Wuhan, Wuhan, PR China in 2022. The strain was found to be Gram stain negative, facultatively anaerobic, motile, and rod-shaped. A preliminary analysis based on the 16S rRNA gene sequence and multi-locus sequence analysis of the atpD, infB, rpoB, and gyrB gene revealed that this strain is closely related to members of the genus Erwinia. The strain was subjected to whole genome sequencing and both average nucleotide identity (ANI) and in silico DNA–DNA hybridization (isDDH) values between strain BC051422T and type strains of all known species in Erwiniaceae were 68.8 to 83.4% and 19.2 to 35.5%, respectively, which are lower than the 95% (ANI) and 70% (isDDH) cut-off for delineation of bacterial species. The major cellular fatty acids of strain BC051422T is C16:0, C16:1 ω7c/C16:1 ω6c, and C17: 0 cyclo, which are similar to other Erwinia species. The genomic DNA G + C content of strain was 55.95 mol%. Strain BC051422T can be differentiated from other Erwinia species by its ability to ferment sucrose, but is negative for mannose, rhamnose, melibiose, and sorbitol. Genotypic and phenotypic characteristics indicate that strain BC051422T represent a novel species of the genus Erwinia, for which the names Erwinia wuhanensis sp. nov. is proposed. The type strain of Erwinia wuhanensis sp. nov. is BC051422T (= GDMCC 1.4074T = JCM 36319T).

Mycoplasma pneumoniae (MP) is a leading cause of community-acquired pneumonia (CAP), accounting for 10-40% of cases in children. In China, the high prevalence of macrolide-resistant MP (MRMP) and recurrent MP epidemics place a significant burden on the healthcare system. Leveraging data from over 1.6 million cases, this study provides a comprehensive analysis of the epidemiological characteristics of MP across China. Seasonal patterns analysis revealed three distinct transmission zones in China. Transmission Zone 1 exhibited two annual epidemic peaks, while Zones 2 and 3 showed a single annual peak of distinct timings. Notably, winter travel to popular tourist destinations appears to influence MP infection patterns in China. Age- and sex- specific analysis indicated male newborns aged [0-1) years face a 1.67 times higher risk of MP infection compared to females. Conversely, females aged [23-38) years have a higher infection risk, likely due to their caregiving roles. The proportion of MRMP surged from 80.00% to 93.02% between July 2023 and May 2024, with a median growth rate of 10.21%. This rapid increase contrasts sharply with the modest 5.3% rise observed from 2011 to 2019, and we attribute this escalation in part to the growing prevalence of the T1-3R clade strain in China. These findings have important implications for the identification of high-risk population, place, and time for more targeted efforts of prevention and treatment. Furthermore, the rapidly increased proportion of MRMP in the 2023-2024 season raises a concerning signal regarding antibiotic use.

Objectives:Urinary tract infection is one of the most prevalent forms of bacterial infection, and prompt and efficient identification of pathogenic bacteria plays a pivotal role in the management of urinary tract infections. In this study, we propose a novel approach utilizing aptamer-functionalized graphene quantum dots integrated with an artificial intelligence detection system (AG-AI detection system) for rapid and highly sensitive detection of Escherichia coli (E. coli). Methods:Firstly, graphene quantum dots were modified with the aptamer that can specifically recognize and bind to E. coli. Therefore, the fluorescence intensity of graphene quantum dots was positively correlated with the concentration of E. coli. Finally, the fluorescence images were processed by artificial intelligence system to obtain the result of bacterial concentration. Results:The AG-AI detection system, with wide linearity (103-109 CFU/mL) and a low detection limit (3.38×102 CFU/mL), can effectively differentiate between E. coli and other urinary tract infection bacteria. And the result of detection system is in good agreement with MALDI-TOF MS. Conclusions:The detection system is an accurate and effective way to detect bacteria in urinary tract infections.

Lung nodules are critical indicators for early lung cancer detection, yet accurately distinguishing between benign and malignant lesions remains a clinical challenge. This review summarizes advances in predictive models for lung nodule risk assessment, spanning classical clinical-imaging models, biomarker-based approaches, and artificial intelligence (AI)-driven tools. While classical models provide a foundational framework, their performance often varies across populations. Biomarkers and AI models significantly enhance diagnostic precision by capturing molecular and imaging features imperceptible to the human eye. However, issues such as generalizability, standardization, and data security persist. The most promising direction lies in multimodal integration, combining clinical, imaging, biomarker, and AI data to achieve superior accuracy with an area under the curve (AUC) >0.90. Future efforts should focus on multi-center validation, standardized biomarker assays, and data secure, scalable AI systems to translate these innovations into routine clinical practice, enabling personalized and early lung cancer diagnosis.

Micrococcus antarcticus (M. antarcticus) is an aerobic Gram-positive spherical actinobacterium that was initially isolated from Chinese Great-Wall station in Antarctica in 2000. M. antarcticus was considered to be of low pathogenicity, no previous cases of human infection by this organism have been reported. Here we describe the first report with community-acquired pneumonia (CAP) caused by M. antarcticus. An 87-year-old female was presented to the Central Hospital of Wuhan in November 2023 with a chief complaint of cough, sputum production, and chest tightness for 2 weeks. Microbial culture of the patient’s bronchoalveolar lavage fluid (BALF) and identification of the isolates using Matrix-assisted laser desorption ionization/time of flight mass spectrometry (MALDI-TOF MS) and 16S rRNA gene sequencing revealed M. antarcticus infection. Combined with clinical symptoms, laboratory and imaging examination, the patient was diagnosed with CAP. Then cefoperazone/sulbactam and levofloxacin was administrated, the patient’s condition was improved and she was discharged after a week after admission, no abnormalities were detected during a 5-month follow-up. This case highlights that M. antarcticus, first identified from a patient with CAP, is an extremely rare pathogenic microorganism. Clinicians should be aware of its potential as a pathogen in the diagnosis and treatment of CAP.

IntroductionNon-coding RNAs (ncRNAs), which are incapable of encoding proteins, are involved in the progression of numerous tumors by altering transcriptional and post-transcriptional processing. Recent studies have revealed prominent features of ncRNAs in pyroptosis, a type of non-apoptotic programmed cellular destruction linked to an inflammatory reaction. Drug resistance has arisen gradually as a result of anti-apoptotic proteins, therefore strategies based on pyroptotic cell death have attracted increasing attention. We have observed that ncRNAs may exert significant influence on cancer therapy, chemotherapy, radio- therapy, targeted therapy and immunotherapy, by regulating pyroptosis.Areas coveredLiteratures were searched (December 2023) for studies on cancer therapy for ncRNAs-mediated pyroptotic cell death.Expert opinionThe most universal mechanical strategy for ncRNAs to regulate target genes is competitive endogenous RNAs (ceRNA). Besides, certain ncRNAs could directly interact with proteins and modulate downstream genes to induce pyroptosis, resulting in tumor growth or inhibition. In this review, we aim to display that ncRNAs, predominantly long non-coding RNAs (lncRNAs), microRNAs (miRNAs) and circular RNAs (circRNAs), could function as potential biomarkers for diagnosis and prognosis and produce new insights into anti-cancer strategies modulated by pyroptosis for clinical applications.

Stutzerimonas nitrititolerans (S. nitrititolerans) is a rare human pathogenic bacterium and has been inadequately explored at the genomic level. Here, we report the first case of carbapenem-resistant S. nitrititolerans isolated from the peritoneal dialysis fluid of a patient with chronic renal failure. This study analyzed the genomic features, antimicrobial resistance, and virulence factors of the isolated strain through whole genome sequencing (WGS). The bacterial isolate from the peritoneal dialysis fluid was named PDI170223, and preliminary identification was conducted through Matrix-assisted laser desorption ionization/time of flight mass spectrometry (MALDI-TOF MS). WGS of the strain PDI170223 was performed using the Illumina platform, and a phylogenetic tree was constructed based on the 16S rRNA gene sequences. Antimicrobial susceptibility test (AST) was conducted using the TDR-200B2 automatic bacteria identification/drug sensitivity tester. S. nitrititolerans may emerge as a human pathogen due to its numerous virulence genes, including those encoding toxins, and those involved in flagellum and biofilm formation. The AST results revealed that the strain is multidrug- and carbapenem-resistant. The antimicrobial resistance genes of S. nitrititolerans are complex and diverse, including efflux pump genes and β⁃lactam resistance genes. The analysis of virulence factors and antimicrobial resistance of S. nitrititolerans provides clinical insight into the pathogenicity and potential risks of this bacterium. It is crucial to explore the mechanisms through which S. nitrititolerans causes diseases and maintains its antimicrobial resistance, thereby contributing to development of effective treatment and prevention strategies.

Accumulating studies suggest that Huaier exerts anti-tumor effects through intricate mechanisms. Despite extensive research on its efficacy in lung cancer, further investigation is required to elucidate the molecular mechanism of Huaier. The involvement of long noncoding RNAs (lncRNAs) in the anti-lung cancer effects of Huaier remains unknown. In this study, we found Huaier suppressed cell viability, migration and invasion in non-small cell lung cancer (NSCLC) cells. LncRNA sequencing analysis revealed Deleted in lymphocytic leukemia 2 (DLEU2) to be significantly downregulated in Huaier-treated NSCLC cells. Furthermore, DLEU2 silencing was observed to suppress NSCLC progression, while DLEU2 overexpression attenuated the anti-tumor effects of Huaier in NSCLC, thereby promoting cell viability, migration and invasion of NSCLC. The ceRNA role of DLEU2 had been demonstrated in NSCLC, which directly interacted with miR-212-5p to rescue the repression of E74 Like ETS Transcription Factor 3 (ELF3) by this microRNA. Additionally, Huaier was found to regulate the expression of miR-212-5p and ELF3. Functionally, miR-212-5p inhibitor or ELF3 overexpression reversed the effects of DLEU2 silencing or Huaier treatment, resulting in increased colony formation, migration and invasion in NSCLC. Taken together, these results illuminate the mechanism underlying Huaier's anti-tumor effects via the DLEU2/miR-212-5p/ELF3 signaling pathway, which offers novel insights into the anti-tumor effects of Huaier and constitutes a promising therapeutic target for the treatment in NSCLC.

BackgroundAdults with community-acquired pneumonia (CAP) in China suffer high morbidity. CAP is caused by a multitude of pathogens; however, pathogen-directed clinical symptoms are often lacking. Therefore, patients lacking an accurate microbiological diagnosis are administered with empirical antimicrobials.MethodsWe collected bronchoalveolar lavage fluid, as well as clinical and laboratory data from 650 adult patients with CAP admitted to three hospitals in Hubei, Sichuan, and Zhejiang provinces in China. Specimens were cultured and tested using real-time reverse transcription qPCR (RT-qPCR) assays for the presence of 42 respiratory bacteria and viruses. CAP was investigated with respect to regions, genders, and age and patterns of infections or co-infections. Employing clinical guidelines adapted for diagnosis, we assessed retrospectively the appropriate pathogen-directed therapy and compared it with the initial empirical therapies.ResultsOur study identified that 21.38% (139/650) of the patients were classified as having Severe CAP (S-CAP), with a higher prevalence among males, older adults, and during the warm season. Bacterial pathogens were detected in 35.53% (231/650) of cases. K. pneumoniae, H. influenzae, and S. aureus were the most prevalent bacteria across different demographics and regions. Viral pathogens were found in 48.76% (317/650) of patients Epstein-Barr, Human rhinovirus, and Cytomegalovirus were the most common viruses. Co-infections were present in 24.31% (158/650) of cases, with viral-bacterial co-infections being the most frequent. The RT-qPCR demonstrated significantly higher detection rates for key pathogens compared to standard culture methods. It showed potential in optimizing antimicrobial prescriptions by allowing for de-escalation in 18.30% (95/518) of patients, among which reducing the number of excessive antibiotics mainly comprised decreasing the use of 2nd or 3rd generation cephalosporins (5.79%, 30/518) and β-lactamase inhibitor combinations.ConclusionThe study highlights the significant burden of S-CAP, particularly among specific demographics and seasons. The prevalence of bacterial and viral pathogens, along with the high rate of co-infections, emphasizes the need for comprehensive diagnostic approaches. The RT-qPCR assays emerge as a superior diagnostic tool, offering enhanced pathogen detection capabilities and facilitating more precise antimicrobial therapy. This could lead to improved patient outcomes and contribute to the rational use of antimicrobials, addressing the growing concern of antibiotic resistance.

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