Staphylococcus aureus is a major opportunistic pathogen that causes a wide spectrum of human and animal diseases. Capsule is one of the key virulence factors of S. aureus. Approximately 90% of S. aureus isolates produce capsular polysaccharides (CPs) that envelop the entire bacterial cells. CPs can suppress the phagocytosis of S. aureus by innate immune cells, promote intracellular survival, and reduce the killing efficacy of antimicrobial agents. As a result, CPs are versatile candidates for vaccine development. The synthesis of S. aureus CPs is controlled by the cap operon, which contains 16 genes encoding functional enzymes involved in the biosynthesis and transport of CPs. During S. aureus growth, cap operon expression is strictly regulated. The control region of the cap operon is characterized by two promoters: a housekeeping sigma factor A (SigA)-dependent promoter and a stress-responsive sigma factor B-dependent promoter. Many transcription factors, including both positive and negative regulatory molecules, are timely involved in the regulatory network of S. aureus capsule synthesis. Moreover, environmental conditions such as medium composition and carbon dioxide levels further modulate CP production. In this review, the structure and function of S. aureus CPs are introduced, and the biosynthesis of S. aureus CPs is discussed. Moreover, the regulation of S. aureus CP production is summarized, the factors affecting CP production are outlined, and the preparation of S. aureus CPs is reviewed. The advanced information presented here may provide useful references for further research on the production and function of S. aureus CPs.

The correlation between microbes and autoimmunity is well established, but many underlying mechanisms remain obscure. Thus, this paper attempts to elucidate the role of infectious agents (bacteria, viruses, etc.) in autoimmune diseases. To offer a concise framework for many relevant research findings, the following general conceptual model is proposed and discussed: autoimmune diseases arise from alterations in cells, tissues, or organs, caused by infectious agents. These alterations evolve with time, beginning as subtle, often undetectable changes. As the alterations become more severe, they can be identified by the immune system, which may subsequently attack the infected cells. This process allows for new explanations of relationships between triggers of autoimmunity and infectious agents, the time lag between infection and autoimmune response, the progressive nature of autoimmune diseases, and the role of virus persistence. It can also offer a new point of view on molecular mimicry and epitope spreading. The roles of genetic predisposition, sex, stress, dietary habits, the “hygiene hypothesis,” and the healing effects of β-interferon also fit into this framework. In addition, the side effects of malignancy treatments using immune checkpoint inhibitors can also be explained. Adhering to the framework, it is concluded that treatments should aim to eliminate the cause of these evolving alterations, namely, the infectious agents. Presumably, they could be based on antibiotics and antiviral drugs. Future research directions are suggested for evaluating the proposed conceptual model.

The pulmonary immune system serves as a critical frontline in the host’s defense against invading pathogens. Understanding the dynamic interplay between invading pathogens and the host’s immune defenses is essential for the development of innovative therapeutic strategies. This review explores the complex mechanisms underlying pulmonary immune responses, with a focus on the balance between pathogen virulence and host immunity. Relevant publications - including peer-reviewed articles, clinical studies, and technological advancements published between 2020 and 2025 - were identified through searches of electronic databases such as Google Scholar, PubMed, Scopus, and Web of Science. The findings reveal that pathogens employ sophisticated strategies to evade immune detection, such as modulation of host cell signaling pathways and the secretion of virulence factors. Conversely, the host mounts protective immune responses characterized by rapid activation of innate immunity, cytokine-mediated signaling, and the development of adaptive immune memory. Notably, recent studies have reported several novel biomarkers associated with enhanced pathogen clearance and tissue repair, highlighting their potential as therapeutic targets. This review provides new insights into pulmonary immune responses, highlighting the delicate balance between pathogen evasion and host defense mechanisms. By identifying key immune regulators and pathogen-specific vulnerabilities, it highlights potential targets for innovative treatments to enhance pulmonary immunity. These findings underscore the importance of interdisciplinary approaches in advancing knowledge of respiratory infections and immune defense.

Obesity is a multifactorial disease that results in the excessive accumulation of adipose tissue in humans. It poses a major global public health crisis, as it increases the risk of several pathologies. The gut microbiome is considered a potential modulator in the development of obesity, alongside environmental factors, lifestyle, and genetic makeup. The qualitative and quantitative composition of the gut microbiome is greatly influenced by the type, quality, and quantity of diet. We have found that a vegetarian diet facilitates the growth and development of beneficial bacteria in the gut. This review discusses the relationship between the human gut microbiome, energy balance, and various obesity-related diseases. The metabolic products of the gut microbiome (such as short-chain fatty acids and secondary bile acids) and their effects on the gut microbiome, intestinal barrier function, and immune homeostasis are explored in the context of obesity. However, the specific roles of individual gut microbiota species and their interactions with the gut environment, host genetics, and medications (including antibiotics) require further investigation. We also discuss the potential of the gut microbiome in managing obesity-related diseases through dietary modifications, with reference to dietary fiber, resistant starch, gluten, high-fat diets, and proteins and carbohydrates from both vegetarian and animal sources.

With the development of next-generation sequencing and other technologies, there has been an exponential increase in DNA, RNA, and protein sequences and protein structures in the last two decades, paralleled with the advancement of user-friendly bioinformatics tools. Furthermore, the enormous improvement in computational power and accumulation of massive amounts of data has given rise to the development of big data analysis, which can unveil novel patterns, associations, and trends. In view of the unprecedented biological data explosion, we have recently developed a platform known as Mx. BIOME, which provides a collection of some of the most popular and cutting-edge tools in the fields of bioinformatics and big data analysis. Such a collection would facilitate end-users to identify suitable tools for analyzing their specific datasets. Further studies and reviews on various in silico tools are necessary to compare the advantages and limitations.

Adherent-invasive Escherichia coli (AIEC) has been implicated in Crohn’s disease (CD) pathogenesis. We aimed to evaluate the impact of dietary factors on the presence of AIEC in patients with CD and to identify AIEC-associated mucosa microbial signatures in regions with different urbanization levels. A total of 112 CD patients and healthy controls were recruited from a rural area in China (Yunnan). Clinical demographics, food additive questionnaires, and ileal biopsies were collected from subjects in rural China. AIEC was isolated from biopsy samples by an antibiotic protection assay. Correlation between AIEC presence and food additives was evaluated using multivariate logistic regression. In addition, a secondary dataset of an urban CD cohort (Hong Kong) was included for microbiome analysis. AIEC was detected in the ileal mucosa in 20.83% of patients with CD in rural China. Multivariate analysis showed that living in an urban area was associated with the presence of AIEC in CD patients. Carrageenan consumption was positively correlated with AIEC presence in CD. AIEC-positive CD patients with primary education consumed more carrageenan than AIEC-negative CD patients (p=0.008). AIEC presence in CD patients was associated with 23 microbial genera in both urban and rural areas. AIEC-positive CD patients showed a decrease in anti-inflammatory pathways. AIEC colonizes the gut mucosa of CD patients in a rural area of China, with its presence significantly associated with higher carrageenan consumption. These findings suggest a potential link between dietary emulsifiers, microbial dysbiosis, and AIEC-related CD pathogenesis.

Brachyspira pilosicoli is a globally prevalent, anaerobic, Gram-negative spirochete that causes intestinal spirochetosis in birds, pigs, and humans. It colonizes the large intestine, causing colitis, diarrhea, and impaired growth. Despite its pathogenic relevance, the outer membrane proteins of B. pilosicoli remain largely uncharacterized. In this study, we computationally identified a total of 42 outer membrane β-barrel (OMBB) proteins within the B. pilosicoli proteome using a consensus-based computational framework. Structural models generated using AlphaFold 3 confirmed the β-barrel architectures of the predicted proteins. Structure- and sequence-based functional annotations revealed homologs of b-barrel assembly machinery BamA protein, lipopolysaccharide-assembly protein LPS-assembly protein D, TolC, transporter proteins, enzymes, diffusion channels, and porins. Notably, seven of the predicted OMBB proteins were previously unannotated in UniProt and the National Center for Biotechnology Information; we report their putative functions here for the 1st time. Sequence variation analysis among the homologs of OMBB proteins across nine B. pilosicoli strains revealed that many of the variations were present within surface-exposed loop regions, suggesting roles in host interaction and immune modulation. Our in silico study expands the functional repertoire of B. pilosicoli outer membrane proteins, highlighting potential targets for diagnostics, vaccine development, and therapeutic interventions.

Porcine epidemic diarrhea virus (PEDV) causes acute watery diarrhea and high mortality in neonatal piglets, resulting in substantial economic losses to the global swine industry. Here, we successfully isolated a PEDV strain, designated CHN-CQ-2021, from PEDV-positive diarrheic samples collected from a pig farm in Chongqing, China. Electron microscopy observation revealed that the CHN-CQ-2021 strain exhibited typical coronavirus morphology and could be recognized by PEDV-specific antibodies. Phylogenetic analysis of its full-length genome and S gene further classified this isolate as a G2b variant strain. Importantly, 1-day-old newborn piglets were orally challenged with CHN-CQ-2021 at 2 × 10⁶ 50% tissue culture infectious dose/mL. Compared with the control group, the infected piglets developed severe diarrhea with 100% mortality. In addition, viral RNA was detected in rectal swabs and multiple tissues, including the intestinal tract and brain, with macroscopic/microscopic intestinal lesions and viral antigen distribution confirmed using histopathology and immunohistochemistry. These findings demonstrate the presence of a pathogenic PEDV strain in Chongqing, China, capable of causing severe neonatal piglets’ enteric disease.

Dolutegravir (DTG), a key component of antiretroviral therapy (ART), has demonstrated potent virologic suppression and superior efficacy compared to standard regimens in HIV management. However, concerns about its long-term safety persist, with emerging evidence suggesting potential adverse effects. Notably, studies have reported an increased risk of neural tube defects in infants born to women exposed to DTG during pregnancy, as well as associations with neuropsychiatric effects and sideroblastic anemia. This cross-sectional study investigated plasma folate and malondialdehyde (MDA) levels—markers of antioxidant status and oxidative stress, respectively—in HIV-positive patients receiving DTG-based ART at the University of Nigeria Teaching Hospital, Enugu. A total of 120 participants were recruited, comprising 40 treatment-naïve patients initiating DTG-based ART, 40 patients on DTG-based ART for 6 months, and 40 HIV-negative controls. Plasma folate was measured using chemiluminescence immunoassay, while MDA levels were determined spectrophotometrically. Results showed significantly elevated MDA levels in both treatment-naïve (5.72 ± 3.61 μmol/L) and 6-month DTG-treated patients (8.94 ± 5.03 μmol/L) compared to controls (1.19 ± 0.18 μmol/L). Conversely, folate concentrations were markedly lower in the DTG groups (2.23 ± 1.52 and 1.89 ± 0.54 ng/mL, respectively) than in controls (11.11 ± 1.31 ng/mL). These findings suggest that DTG-based ART may elevate oxidative stress while reducing antioxidant levels, underscoring the need for careful monitoring of its biochemical effects in HIV-positive individuals.

Glioblastoma multiforme (GBM) is the most common malignant primary tumor of the central nervous system (CNS), accounting for the majority of brain tissue tumors and CNS neoplasms. GBM has an incidence rate of 3.2/100,000 people in the United States, with an abysmal survival rate of 15 months with treatment and under 3 months for untreated patients. GBM remains incurable, with no disease-modifying treatment available. As a grade IV astrocytoma, GBM is highly aggressive, characterized by rapid proliferation, high metabolic demands, substantial angiogenesis, and diffuse infiltration of healthy parenchyma. The GBM genome is highly heterogeneous, with unpredictable amplification patterns, dysregulation, and mutational activation of receptor tyrosine kinase genes, tumor suppressor genes, and growth factor signaling. GBM’s indistinct tumor margins, its highly adaptive interaction with the brain microenvironment, and the existence of the blood-brain barrier and the blood-brain tumor barrier further limit effective anti-GBM therapeutic strategies. Hence, anti-GBM drug discoveries and molecular techniques that aim for patient-specific treatment stratification are of profound clinical and therapeutic significance. The current paper aims to outline the fundamental pathophysiology, tumorigenicity, and immunosuppressive mechanism of GBMs, review current treatment options for GBMs, and examine the contemporary challenges and advances in anti-GBM drug discovery and delivery. Finally, the paper aims to shed light on the emergence of small-molecule inhibitors, immune checkpoint inhibitors, and vaccination therapy as potentially efficacious therapeutic strategies for treating GBM.

Nocardia is an opportunistic pathogen that can present as pulmonary, central nervous system, or disseminated infection in immunocompromised host. However, primary cutaneous Nocardia infections have distinctive presentations in immunocompetent hosts. When infecting a host with an intact immune system, the infection tends to be more insidious, delaying accurate diagnosis and leading to inadequate treatment and persistent infection. Herein, we present a rare case of post-operative cutaneous nocardiosis in a 57-year-old immunocompetent patient with a delay in therapy resulting in a prolonged non-healing wound. Nineteen case reports were reviewed to identify trends in immune status, exposure, treatment regimens, and responses to therapy in both immunocompromised and immunocompetent patients with Nocardia farcinica cutaneous infection. This case report summarizes characteristics of patient populations where N. farcinica might be suspected and emphasizes the importance of a thorough environmental and occupational history in the case of immunocompetent patients. It also addresses challenges in the treatment of cutaneous N. farcinica as related to empiric therapy, antibiotic resistance, and duration of treatment, ultimately providing an algorithm to approach the management of primary cutaneous nocardiosis.

Erythropoietin-producing hepatocellular receptor A8 (EphA8) is a type I transmembrane protein that belongs to the largest erythropoietin-producing hepatocellular (Eph) family among receptor tyrosine kinases. By binding to its membrane-bound ephrin-A or ephrin-B ligands on adjacent cells, Eph receptors form complexes and mediate bidirectional signaling activities, triggering cell-cell adhesion and repulsion. Increased expression of EphA8 correlates with poor prognosis in some types of cancer. Therefore, developing sensitive monoclonal antibodies (mAbs) for EphA8 has been desired for treatment, diagnosis, and further basic research. In particular, there are no anti-EphA8 mAbs that can be used for flow cytometry. A novel, specific, and sensitive anti-human EphA8 mAb, which applies to flow cytometry, clone Ea₈Mab-9 (mouse immunoglobulin G1, kappa), was established using the Cell-Based Immunization and Screening method. Ea₈Mab-9 reacted with EphA8-overexpressed Chinese hamster ovary-K1 cells (CHO/EphA8) and EphA8-overexpressed LN229 glioblastoma cells (LN229/EphA8) in flow cytometry. Notably, Ea₈Mab-9 did not recognize other members of the Eph receptor family. Furthermore, Ea₈Mab-9 demonstrated a high binding affinity for CHO/EphA8 and LN229/EphA8, with dissociation constants of 1.3 × 10-9 M and 1.6 × 10-9 M, respectively. The reaction of Ea₈Mab-9 with CHO/EphA8 was completely blocked by a recombinant EphA8 protein. Ea₈Mab-9 could be useful for analyzing the EphA8-related biological responses using flow cytometry, owing to its high affinity and specificity.