Search Results (872)

Parathyroid allotransplantation is a promising treatment for hypoparathyroidism, yet immune rejection and fibrosis remain significant barriers. This study evaluates a novel immunoprotective culture system utilizing a moderate-intensity static magnetic field (SMF) to modulate lymphocyte migration without compromising graft functionality. Human parathyroid cells were encapsulated and divided into 10 experimental groups, co-cultured with Jurkat T-lymphocytes, and either exposed to SMF or maintained as controls. Over 72 h, we analyzed parathormone (PTH) secretion, cell viability (via proliferation assays), and molecular expression patterns of key markers (VitDR, PTH, GCM2, and CaSR). Lymphocyte dynamics were monitored through comparative imaging and cytokine profiling (IL-1α, IL-1β, and IL-2). SMF exposure significantly altered Jurkat cell behavior; while lymphocytes in unexposed groups aggregated around microcapsules, they were effectively repelled and migrated away from the graft interface under SMF exposure. Crucially, this biophysical manipulation was safe: no significant differences in PTH secretion or viability were observed across groups. All groups maintained essential genetic markers. Our findings demonstrate that SMF exposure induces lymphocyte migration away from the capsule without compromising parathyroid cell characteristics or functionality. Integrating encapsulation with SMF represents a novel, non-pharmacological, non-invasive immunoprotective strategy for parathyroid allotransplantation, offering a technological alternative to systemic immunosuppression. Full article

Cross-kingdom pathogenesis—human and animal pathogens colonizing and persisting in plants—is transforming our understanding of microbial ecology, food safety, and public health. This review translates incoming research that demonstrates plants as more than mute carriers to dynamic ecological interfaces where human and zoonotic pathogens, such as Salmonella enterica, Escherichia coli O157:H7, and Listeria monocytogenes, will adhere, internalize, and, in some cases, potentially evade host defenses. Such pathogens exploit evolutionarily conserved molecular processes like Type III secretion system 1 (TTSS), biofilm formation, quorum sensing, and small RNA-mediated immune sabotage that have allowed them to cross biological kingdom boundaries. To provide an entry point for pathogens, environmental conditions (e.g., contaminated irrigation water, manure application, wildlife access, and mechanical wounding) promote pathogen transfer to and penetration into plant tissues through stomata hydathodes above ground or roots below ground. Once inside, pathogens confront a range of plant immune responses, indigenous microbiota, and abiotic stresses such as UV radiation exposure, nutrient starvation, and osmotic fluctuations. Nonetheless, biofilm production, metabolic versatility, and virulence gene expression contribute to their persistence. Interactions with plant pathogens and microbiomes additionally shape colonization dynamics, for example, through co-survival and niche manipulation. With the acceleration of these processes due to climate change, urbanization, and intensified agriculture, cross-kingdom pathogenesis becomes a rising concern for One Health. Critical knowledge gaps, including seedborne transmission, microbiome engineering, and predictive modeling, are pointed out in the review along with emerging mitigation strategies, including point-of-care diagnostics and microbial biocontrol. In conclusion, this review advocates for interdisciplinary collaboration from microbiology, plant science, and One Health perspectives to predict and mitigate cross-kingdom threats to global food production. Full article

The mitogen-activated protein kinase (MAPK) pathways, ERK, JNK, and p38, are key regulators of immune responses during viral infections. These signaling cascades control cytokine production, T cell activity, and antigen presentation. However, many viruses can hijack MAPK pathways to avoid immune detection, promote their replication, and establish chronic infection. In this review, we discuss how different viruses, including HSV-1, HBV, HCMV, and SARS-CoV-2, manipulate MAPK signaling to alter host cell functions. A particular focus is given to the CD1d–iNKT cell axis, which plays a critical role in early antiviral responses but is often disrupted through MAPK-dependent mechanisms. We explore how changes in MAPK signaling affect antigen-presenting cells, drive T cell exhaustion, and reprogram immune cell metabolism, factors that contribute to viral immune evasion. The review also examines therapeutic strategies aimed at targeting MAPKs to improve antiviral immunity. These include small-molecule inhibitors and immune modulators that may enhance antiviral responses while limiting side effects. We emphasize the importance of context, as MAPK-targeted therapies must be carefully timed and tailored to avoid suppressing protective immunity or triggering unwanted inflammation. Overall, this review highlights the therapeutic potential and challenges of targeting MAPK pathways in viral infections and encourages further research into selective, host-directed antiviral strategies. Full article

Gut dysbiosis, defined as a disruption in the structure or function of the intestinal microbiota, is increasingly recognized as a key contributor to inflammatory, metabolic, and neuropsychiatric diseases. Conventional interventions such as broad-spectrum antibiotics, generic probiotics, and fecal microbiota transplantation (FMT) often show limited and inconsistent efficacy because they lack specificity, durability, and robust safety controls. In contrast, recent advances in DNA-based technologies are reshaping the therapeutic landscape by enabling targeted, programmable, and mechanistically informed modulation of the gut ecosystem. This review presents an integrated overview of three major domains driving this shift: CRISPR-based systems that selectively delete, silence, or reprogram microbial genes; synthetic biology-driven live therapeutics engineered to sense disease-associated cues and execute controlled responses; and metagenomics-informed strategies that tailor interventions to patient-specific microbial gene profiles and functional deficits. Additionally, we examine the continued evolution of FMT toward DNA-optimized workflows and defined microbial consortia that offer safer, more standardized alternatives to crude donor material. Across these domains, we discuss delivery platforms (including bacteriophages, conjugative plasmids, extracellular vesicles, and synthetic nanoparticles), and compare their efficiency, specificity, and scalability. We further highlight how DNA-guided interventions interface with host immunity—shaping Treg/Th17 balance, mucosal barrier function, and inflammatory signaling—while also analyzing ecological and evolutionary risks, biocontainment strategies, and regulatory classification gaps that will govern clinical translation. Together, these developments signal a transition from empirical microbiome manipulation to rational ecosystem engineering. DNA-guided therapies hold strong promise for precise and personalized management of gut-related diseases, but their success will depend on rigorous ecological risk assessment, long-term monitoring, and adaptive regulatory frameworks alongside continued technological innovation. Full article

Some parasitic infections promote or inhibit vascular growth in their hosts to increase parasite survival through immune evasion and tissue dissemination. This review focuses on how the most prevalent protozoan and helminth parasites in humans, such as Plasmodium, Toxoplasma, Leishmania, Trypanosoma, Entamoeba, Schistosoma, and Taenia, manipulate angiogenic pathways for their own benefit. This knowledge reveals that angiogenesis is central to the pathophysiology and therapeutic targeting of parasitic diseases. Importantly, parasites and/or their excretory/secretory factors, which modulate vascular responses, are potential treatments for chronic degenerative diseases in which angiogenesis is crucial to disease progression, such as cancer. Full article

Cell-based immuno-biosensors are novel platforms for studying immune responses of biological cells, with real-time insights more similar to physiological and pathological conditions. These systems utilize living immune cells as their main components, enabling them to detect disease-related biomarkers and cellular traits in a way that is often highly sensitive and label-free. Integration with microfluidics and organ-on-chip technologies has facilitated precise manipulational control over the cellular microenvironment. Not only has this resulted in high-throughput screening, but it also enabled smaller, more portable systems which can be used at the point of care. In this work, we review the recent advance in microfluidic cell-based immuno-biosensing associated with immune cells such as neutrophils, macrophages, T cell and dendrite cells. Some of the exciting developments include fusion with methods such as advanced imaging, electrical impedance sensing and application of machine learning to phenotyping. We will also elaborate on the issues related to the standardization of these systems, cell heterogeneity, and the challenges for translating these technologies for clinical application. Taken together, such integrated platforms have potential to fill the gap left in-between cellular immunology with biosensor engineering. Full article

Lysin motif (LysM) domain-containing proteins are widespread in prokaryotes and eukaryotes, and play crucial roles in microbe-host interactions. In recent decades, a large number of LysM domain-containing proteins have been identified and confirmed to participate in various biological processes, including microbial growth, fungal pathogenesis, and recognition of pathogens by plant immune receptors. Emerging evidence has shown that some LysM domain-containing proteins in plant pathogenic fungi have evolved as key virulence factors. They manipulate host immune responses mainly by interfering with the plant’s perception of chitin, a core pathogen-associated molecular pattern (PAMP) of fungal cell walls. However, the functions of LysM domain-containing proteins in plant pathogenic fungi have not been systematically summarized. In this review, we discuss the latest advances in the structural characteristics, classification, and functional mechanisms of these proteins, as well as their applications in plant disease control. We also propose the current challenges and future research directions in this field. This review aims to deepen the understanding of the molecular mechanisms underlying plant-fungal interactions mediated by LysM domain-containing proteins and provide theoretical references for developing novel and environmentally friendly strategies for fungal disease management in agriculture. Full article

As populations around the world continue to age, promoting healthy ageing has become a key public health priority. Nutrition plays a vital role in maintaining physical and cognitive function later in life, and omega-3 polyunsaturated fatty acids (PUFA) are essential components of cell membranes and are known for their anti-inflammatory and cardio-protective effects. Chronic inflammation and oxidative stress are major contributors to age-related decline, and omega-3s help mitigate these processes by modulating immune responses and improving endothelial function. This systematic review aims to examine the potential of omega-3 fatty acids to reduce inflammatory markers and improve overall health. Moreover, it aims to present the most effective dietary interventions in dairy cows that increase PUFA content in milk. PubMed, Web of Science, Scopus, and the Cochrane Library databases were searched for relevant articles published up to November 2025. Evidence suggests that older adults who consume higher levels of PUFA tend to have better cardiovascular health, preserved cognitive function, and a lower risk of age-related diseases such as Alzheimer’s and arthritis, and reduce the risk of frailty and disability in later years. Dietary manipulation to enhance PUFA in bovine milk represents a promising strategy for improving human nutrition while potentially benefiting cow health. Full article

Porphyromonas gingivalis is described as a keystone pathogen associated with periodontal disease (PD), which exhibits enhanced representation upon microbial dysbiosis in such a chronic inflammatory disease. This oral pathogen drives and contributes to a dysregulated immune response, resulting in stages of aggressive destructive immune activation and inflammation punctuated by immune suppression, which underlies the relapsing–remitting nature of this disease. The understanding of key mechanisms and balance between protective innate, adaptive immune responses and dysregulated responses, linked to changes in the oral mucosal microbial environment, will afford researchers the potential to manipulate oral mucosal environments for clinical benefit. This review focuses on the dynamic interactions between the oral pathogen P. gingivalis and the immune system with an emphasis on immune evasion and how the potential correction of these mechanisms may benefit future therapeutic interventions, leading to the successful treatment of PD. Full article

Classical swine fever virus (CSFV) remains a significant threat to the global swine industry, causing a highly contagious and often fatal disease in pigs. This review comprehensively examines the molecular biology of CSFV and the intricate mechanisms it employs to establish infection. We detail the structure and functions of viral proteins, highlighting their roles in virus entry, replication, and immune evasion. A major focus is placed on the virus–host interaction, specifically how CSFV subverts host innate immune responses and hijacks critical cellular processes, including metabolism and cell death pathways. The virus strategically manipulates host cell death programs (apoptosis, mitophagy, necroptosis) and exploits intracellular transport systems to promote its propagation. Furthermore, we summarize recent advances in understanding the cellular receptors involved in CSFV entry and the role of exosomes in viral spread. This synthesis of current knowledge aims to provide a deeper insight into the pathogenesis of CSFV and identify potential vulnerabilities that could be targeted for the development of novel antiviral strategies. Full article

Glioblastoma multiforme (GBM) is the most lethal primary brain tumor in adults. Emerging evidence endorses that gut dysbiosis contributes to GBM progression through the gut–brain axis (GBA), promoting inflammation and therapeutic resistance via abnormal short-chain fatty acid production and cytokine dysregulation. Exosomes, naturally occurring nanovesicles (30–150 nm), offer promising therapeutic potential due to their blood–brain barrier permeability, biocompatibility, and versatile cargo capacity. This review examines exosome engineering strategies for dual targeting: inhibiting alterations in gut microbiome and inducing regulated cell death mechanisms such as apoptosis and ferroptosis in GBM. We describe exosome engineering with detailed focus on cargo loading approaches (e.g., genetic modification, electroporation, and sonication), exosome surface functionalization with specific ligands (e.g., antibodies), and exosome biogenesis pathway manipulation. Engineered exosomes can deliver anti-inflammatory agents and gut microbiome modulators to restore GBA homeostasis while simultaneously transporting tumor-suppressive non-coding RNAs (e.g., miRNAs, siRNAs) and therapeutic agents to induce apoptosis by overcoming temozolomide resistance, and trigger ferroptosis-inducing components in GBM stem cells. Preclinical studies make obvious that this dual-targeting approach ought to enhance therapeutic efficacy by creating systemic immunity and eliminating tumor cells. However, clinical translation brings forth challenges, such as manufacturing, targeting specificity, and standardized quality control, and warrants further study. Full article

Tumor Mutational Burden (TMB) is a critical biomarker used to determine patient eligibility for immunotherapy with immune checkpoint inhibitors. However, its gold-standard assessment via whole exome sequencing is limited by high costs, technical complexity, and lengthy processing times. To address these challenges, we investigated whether Ultra-High-Frequency (UHF) electromagnetic wave sensing could serve as an alternative method for evaluating TMB. We analyzed the dielectrophoresis crossover frequency spectrum and corresponding electromagnetic signature (EMS) of cancer cells using a lab-on-a-chip biosensor that integrates microfluidics with dielectrophoresis-based electro-manipulation. Across seven solid tumor cell lines exhibiting diverse TMB levels, EMS exhibited an upward shift correlated with higher TMB, suggesting a relationship between mutational load and electromagnetic behavior. To further explore this connection, we artificially increased the somatic variant burden by exposing cells to the mutagen N-ethyl-N-nitrosourea (ENU). EMS measurements reliably detected the induced increase in variant load in ENU-treated cells. Overall, these findings demonstrate that EMS can detect both intrinsic TMB differences and experimentally induced increases in mutational burden, enabling refined categorization of cancer cells. Although further validation is required, this work lays the foundation for developing complementary, rapid, and accessible tools to support cancer cell stratification and guide immunotherapy decision-making. Full article

Chromatin dynamics are usually modulated by histone epigenetic post-translational modifications, which rapidly and reversibly govern accessibility and transcriptional responsiveness. During microbial infection, this regulatory layer becomes a highly contested interface where host defense mechanisms and pathogen-driven subversion strategies converge and compete. Many infectious agents exploit chromatin to reprogram gene expression, creating cellular environments that are conducive to infection, proliferation, and persistence. Diverse strategies have been described for viruses, bacteria, fungi, protozoa and nematodes, including the direct secretion of acetyltransferases and methyltransferases, interference with host chromatin-binding proteins, subcellular localization of transcriptional factors or epigenetic regulators, and metabolic availability manipulation. Concurrently, host cells activate immune and stress-response genes to mount rapid, adaptable antimicrobial responses. Recent advances in genome-wide, single-cell, and spatial omics profiling have begun to reveal the temporal and cell-type-specific dynamics of the host genome at the core of infection. This review synthesizes current insights into how chromatin is rewired by the major categories of pathogens during infection, highlighting representative case studies across infective agents and the functional consequences for immunity and cell fate. In addition, we discuss emerging techniques for epigenomic and transcriptomic data collection, and the potential of targeted host-directed therapeutic strategies. Chromatin regulation is thus a promising field of study and a possible target for next-generation interventions. Full article

Head and neck squamous cell carcinoma (HNSCC) remains a major global health challenge due to its aggressive behavior, late-stage diagnosis, and high incidence of therapy resistance. At the cellular level, these clinical limitations are driven by profound alterations in oncogenic signaling, stress adaptation, DNA damage response pathways, and immune regulation within the tumor microenvironment. Advances in nanotechnology offer powerful opportunities to address these challenges by enabling targeted interference with cellular processes that govern tumor growth, survival, and therapy resistance. “Ancient” (i.e., established, long-studied) nanostructures, including mineral-based nanoparticles, natural biopolymers, and plant-derived nanovesicles, provide inherently biocompatible and bioactive platforms capable of modulating cellular signaling, redox balance, and immune responses. In parallel, emerging nanosystems—such as nanobodies, engineered exosomes, DNA origami, and stimuli-responsive smart nanoparticles—allow precise molecular targeting, controlled cargo release, and direct manipulation of intracellular pathways and intercellular communication. This manuscript synthesizes historical and contemporary developments in nanostructure design, highlighting how the integration of ancient materials with advanced nanotechnology can reshape therapeutic strategies for HNSCC. By targeting key cellular and microenvironmental processes, including DNA damage response signaling, redox homeostasis, immune regulation and stress-adaptive survival mechanisms, rather than drug delivery alone, these integrated nano-platforms offer promising avenues to overcome resistance mechanisms, reprogram the tumor microenvironment, and improve therapeutic precision and patient outcomes. Full article

Emerging evidence suggests that certain cestodes, including Taenia solium, may actively modulate the host’s hormonal and immune environment to facilitate their survival. This study aimed to determine whether patients diagnosed with neurocysticercosis (NCC) exhibit immunoendocrine alterations associated with infection. A clinical study was conducted in Honduras, enrolling 11 adult NCC patients (9 female, 2 male) and 11 age- and sex-matched healthy controls. Serum concentrations of seven hormones and two cytokines were evaluated. Compared to controls, NCC patients showed significantly elevated levels of 17β-Estradiol (E2), Progesterone (P4), Androstenedione (A4), Luteinizing Hormone (LH), Follicle-Stimulating Hormone (FSH), Interleukin-6 (IL-6), and Interleukin-10 (IL-10). Conversely, Free testosterone (FT) and Dihydrotestosterone (DHT) levels were significantly reduced. These findings support the hypothesis that T. solium may manipulate host immunoendocrine pathways to promote its establishment and persistence within the central nervous system. Full article