Abstract: Feline calicivirus, herpesvirus, and panleukopenia virus are major infectious viruses to cause serious diseases in cats, yet their current trivalent vaccines have limitations in immune efficacy and duration of protection. This study assessed the immune-enhancing effects of novel adjuvants (feline IL-15, IL-23, and metabolic modulators) on vaccine responses. Forty mice were randomly assigned to four groups: Group A (composite adjuvants), Group B (metabolic regulatory molecules and Mn adjuvant), Group C1 (Mn adjuvant), and Group C2 (blank commercial vaccine). Results showed that Group A had significantly higher neutralizing antibody titers against calicivirus post-booster immunization, while both Group A and B exhibited enhanced antibody responses against herpesvirus and parvovirus. Notably, Group A displayed increased proportions of memory T cells, follicular B cells, and activated B cells. These findings suggest that the combination of feline IL-15, IL-23, and metabolic modulators are safe and effective immunoadjuvants for the trivalent feline vaccines to promote immune cell differentiation and antibody production, thus representing a promising strategy to optimize vaccine efficacy.

Abstract: Biofilm formation is important for microbial survival, adaptation, and persistence within mutualistic and pathogenic systems in the Vibironaceae. Biofilms offer protection against environmental stressors, immune responses, and antimicrobial treatments by increasing host colonization and resilience. This review examines the mechanisms of biofilm formation in Vibrio species focusing on quorum sensing, cyclic-di-GMP signaling and host specific adaptations that influence biofilm structure and function. We discuss how biofilms differ between mutualistic and pathogenic species based on environmental and host signals. Recent advances in omics technologies such as transcriptomics and metabolomics have enhanced research in biofilm regulation under different conditions. Horizontal gene transfer and phase variation promotes greater fitness of bacterial biofilms due to the diversity of environmental isolates that utilize biofilms to colonize host species. Despite progress, questions remain regarding the long-term effects of biofilm formation and persistence on host physiology and biofilm community dynamics. Research integrating multidisciplinary approaches will help advance our understanding of biofilms and their implications for influencing microbial adaptation, symbiosis, and disease. These findings have applications in biotechnology and medicine, where genetic manipulation of biofilm regulation can enhance or disrupt microbiome stability and pathogen resistance, eventually leading to targeted therapeutic strategies.

Abstract: Absidia represents the most species-rich genus within the family Cunninghamellaceae, with its members commonly isolated from diverse substrates, particularly rhizosphere soil. In this study, four novel Absidia species (A. irregularis sp. nov., A. multiformis sp. nov., A. ovoidospora sp. nov., and A. verticilliformis sp. nov.) were discovered from south and southwestern Chinese soil samples through integrated morphological and molecular phylogenetic analyses. Phylogenetic analyses based on concatenated ITS, SSU, LSU, Act, and TEF1α sequence data reconstructed trees that strongly supported the monophyly of these four new taxa each. Key diagnostic features include A. irregularis (closely related to A. oblongispora) exhibiting irregular colony morphology, A. multiformis (sister to A. heterospora) demonstrating polymorphic sporangiospores, A. ovoidospora (forming a clade with A. panacisoli and A. abundans) producing distinctive ovoid sporangiospores, and A. verticilliformis (next to A. edaphica) displaying verticillately branched sporangiophores. Each novel species is formally described with comprehensive documentation, including morphological descriptions, illustrations, Fungal Names registration identifiers, designated type specimens, etymological explanations, maximum growth temperatures, and taxonomic comparisons. This work constitutes the sixth installment in a series investigating early-diverging fungal diversity in China, expanding the recognized Absidia species to 71. The findings enhance our understanding of mucoralean biodiversity in Asian tropical and subtropical ecosystems.

Abstract: Ecological sustainable development is of great importance in the present age. The traditional free-range feeding mode of Tibetan aromatic pigs in Tibet is gradually being replaced by a semi-housed feeding mode due to the development of modern economic industry. In this study, we analysed the physicochemical properties and microbial composition of the soil under the original ecological environment and semi-housed feeding mode. The study revealed that the activities of Tibetan balsam pigs resulted in the disruption of the original shallow ecological structure of the soil, while the presence of faeces led to an increase in bacterial flora and the spoilage of fodder. Furthermore, the soil under the semi-housed mode exhibited an accumulation of nitrogen, potassium and organic carbon in the shallow layer. The abundance of species was found to be significantly lower than that observed in the original soil environment. At the soil's gate level, the abundances of Proteobacteria ( 31.05% and 32.33%), Bacteroidota (10.48% and 24.90%), and Firmicutes (38.32% and 4.31%) were higher. In contrast, the abundances of Chloroflexi (0.63% and 1.78%), Verrucomicrobiota (0.64% and 1.9 2%), and Planctomycetota (0.82% and 2.67%) were lower. At the level one Metabolism pathway, the Metabolism of terpenoids and polyketides, Lipid metabolism and Xenobiotics biodegradation and metabolism were significantly different (P< 0.05). Glycan biosynthesis and metabolism and Biosynthesis of other secondary metabolites were highly significantly different (P< 0.01). In conclusion, the results of this experiment have demonstrated the significant impact of the semi-enclosed mode on the shallow soil layer. In order to facilitate targeted adjustments for later soil ecological restoration or sustainable use, it is crucial to consider the soil's physicochemical properties and microbial structure.

Abstract: Early biomarkers are needed to predict the long-term persistence of rheumatic symptoms in patients infected with chikungunya virus (CHIKV). This nested case-control study aimed to assess immunological factors during the early phases of CHIKV infection to pre-dict the risk of post-CHIK chronic rheumatism (pCHIK-CR) in adult patients of two pro-spective cohorts. We evaluated 46 febrile patients (median age: 33.5 years, IQR:19 years; women: 50.0%) with CHIKV infection confirmed during the 2014-2015 outbreak in San-tander, Colombia. Participants were classified by a rheumatologist as either cases (pCHIK-CR) or controls (WoRM, without rheumatic manifestations). We quantified serum levels of IL-4, IL-6, IL-8/CXCL-8, IL-27, CCL-2, CXCL-9, CXCL-10 and IgG using Luminex and ELISA assays during the acute and subacute phases of infection. Then, we evaluated the association of these immune factors with the case-control status using piecewise lo-gistic regression adjusted for age and sex. There were non-linear associations between IL-8/CXCL-8, CXCL-9 and CXCL-10 with pCHIK-CR. Elevated levels of IL-8/CXCL-8 (< 35.7 pg/mL), CXCL-9 (≥2,000 pg/mL), CXCL-10 (≥36,800 pg/mL), significantly reduced the risk of pCHIK-CR (adjusted ORs: 0.85, 0.96 and 0.94, respectively). These results suggest that higher levels of IL-8/CXCL-8, CXCL-9 and CXCL-10, measured in the early stages of CHIKV infection, may predict chronic disease risk. This suggests that an early and strong immune response may enhance CHIKV control and reduce the risk of persistent joint symptoms. Given their expression patterns and timing, these three immune factors may be considered promising biomarker candidates for assessing the risk of chronic rheuma-tism. These findings should be validated in additional cohort studies.

Abstract: Understanding the long-term dynamics of SARS-CoV-2 neutralizing antibodies is critical for evaluating vaccine-induced protection and informing booster strategies. In this longitudinal study, we analyzed 114 serum samples from 19 individuals across six time points over a three-year period following mRNA vaccination (Comirnaty) and natural SARS-CoV-2 infection. Using pseudotype-based neutralization assays against nine SARS-CoV-2 variants, including major Omicron subvariants (BA.1–BA.5, BQ.1.1, XBB), and anti-S1 IgG ELISA, we observed that antibody levels peaked after the third vaccine dose (mean ELISA ratio ± SD: 8.89 ± 1.65 S/C) and remained relatively stable two years later (mean: 7.53± 1.17 S/C). Neutralization titers rose markedly after the second and third doses, with the highest neutralization observed at two years post-booster. Strong correlations were found between anti-S1 IgG levels and mean neutralization titers for pre-Omicron variants (r = 0.79–0.93; p&lt;0.05), but only moderate for Omicron subvariants (r ≈ 0.50–0.64). Notably, hybrid immunity (vaccination plus infection) resulted in higher neutralization titers at the final time point compared to vaccine-only participants. The lowest neutralization was observed against XBB, underscoring the immune evasiveness of emerging variants. These findings support the importance of booster vaccination and highlight the added durability of hybrid immunity in long-term protection.

Abstract: Objective: We aimed to investigate the association between pyroptosis and the outer membrane virulence factor of H. pylori in patients with gastritis and ulcers. Methods: DNA, RNA, and protein were extracted from a single tissue sample taken from the antrum region of the stomach of volunteer patients. The expression of bacterial outer membrane virulence genes in these tissues was analyzed at the gene level, and the expression levels of major pyroptosis markers were compared between H. pylori-infected and uninfected ulcer and gastritis patient groups. Results: Results showed that infection by H. pylori induced alterations in the expression levels of ASC, NLRP3, caspase-1, GSDMD, IL-18, and IL-1β, suggesting an association between pyroptosis markers and gastritis or ulcers related to H. pylori. Statistically significant variations in the correlations between increased levels of target markers and active caspase-1 across different patient cohorts demonstrated the effective detection of pyroptosis. Both pro and active forms of caspase-1, GSDMD, IL-18, and IL-1β were evaluated within the sample, leading to the identification of patients displaying indications of pyroptosis. The vacA m2 allele, which elicits a significant and contrasting ASC response in individuals with gastritis and ulcer, along with its increased prevalence and GSDMD upregulation in ulcerative conditions, in conjunction with the babB gene, are crucial for comprehending the interplay between the virulence determinants of H. pylori and pyroptosis in bacteria-associated pathologies. These findings underscore a deficiency in the current body of literature. Conclusion: This study holds considerable importance as it represents the first examination of the interrelation between pathogen virulence factors and pyroptosis in diseases associated with H. pylori. Grasping this interrelationship is vital for elucidating the intracellular alterations induced by H. pylori, and its pathogenicity, and for the development of novel targeted therapeutic interventions.

Abstract: Colistin resistance, driven by chromosomal mutations and the spread of plasmid-mediated MCR genes, has emerged as a critical challenge in combating multidrug-resistant gram-negative bacteria. This resistance compromises the efficacy of colistin, leading to higher treatment failure rates, prolonged hospitalizations, and increased mortality. Recent studies highlight key mechanisms, including lipid A modifications, that enable bacteria to evade colistin’s effects. The global spread of MCR genes exacerbates the issue, underlining the need for improved diagnostics and rapid detection of resistant strains to prevent adverse patient outcomes. To combat this growing threat, a multifaceted approach is essential, involving enhanced antimicrobial stewardship, stricter infection control measures, and continued research into alternative therapies and diagnostic methods. Collaborative efforts from researchers, healthcare providers, policymakers, and the pharmaceutical industry are crucial to preserving colistin’s effectiveness and mitigating the broader impact on public health.

Abstract: Triple-negative breast cancer (TNBC) is an aggressive breast cancer subtype with limited treatment options. While immune checkpoint inhibitors (ICIs) targeting PD-1/PD-L1 have shown clinical benefit, response rates remain variable, and mechanisms of resistance are not fully understood. Emerging evidence suggests that the tumor microbiome can influence immune responses and therapy outcomes. This study investigates the role of Staphylococcus aureus in modulating PD-L1 expression and immune evasion in TNBC. We examined the internalization, persistence, and functional impact of S. aureus in three TNBC cell lines (MDA-MB-468, MDA-MB-231, MDA-MB-453) and the non-tumorigenic MCF-12A breast epithelial cell line. Bacterial uptake and intracellular survival were assessed using an optimized gentamicin protection assay, colony-forming unit quantification, and transmission electron microscopy for up to seven days. Flow cytometry was used to analyze PD-L1 and TLR2 surface expression, while western blot assessed STAT1 activation. Cells were infected with viable S. aureus or treated with the TLR2 agonists S. aureus lipoteichoic acid and Pam3CSK4, a synthetic triacylated lipopeptide that specifically activates TLR2, alone or in combination with IFN-γ. Our findings demonstrate that S. aureus invades and persists within breast cells in a subtype-dependent manner. Notably, intracellular S. aureus, in the presence of IFN-γ, induces PD-L1 expression, contributing to immune checkpoint regulation. The degree of PD-L1 upregulation varied across TNBC subtypes, with MDA-MB-468 (basal-like) and MDA-MB-231 (mesenchymal stem-like) cells exhibiting the highest response. In MDA-MB-231 cells, which express high levels of TLR2, TLR2 agonists enhanced PD-L1 expression independently of IFN-γ. Across all cell lines, TLR2 agonists in combination with IFN-γ further increased PD-L1 expression, suggesting a synergistic effect between bacterial signaling and inflammatory pathways. These findings provide evidence that S. aureus modulates immune checkpoint pathways in TNBC, potentially contributing to immune evasion and ICI resistance. This highlights the need for further investigation into microbial influences on tumor progression and suggest that targeting bacterial interactions may enhance immunotherapy efficacy in TNBC.

Abstract: Fungal infections caused by Candida spp. cause potentially fatal infections with high morbidity and mortality rates, particularly in immunocompromised individuals. Their resistance to conventional antifungal drugs is closely associated with biofilm formation, which increasingly limits available therapeutic options, making medical practice a major challenge worldwide. In this context, plant derived compounds are an excellent alternative to be investigated. The objective of this study was to evaluate the antifungal potential of the flavonoid diosmin (DIO) and its synergistic capacity with commercial antifungals against clinical isolates of Candida spp. Susceptibility testing by broth microdilution method showed antifungal activity of DIO against all isolates tested, with minimum inhibitory concentration (MIC90) values ​​ranging from 1150 to 2251 µg/mL. Furthermore, we report the ability of DIO to inhibit biofilm and mature biofilm formation, with a greater inhibitory effect on fungal biofilm formation; this effect with DIO was significantly greater in most cases than that shown by amphotericin B (AFB). Intracellular leakage experiments (260/280 nm) showed damage to the cell membrane. This indicates that the antifungal action of DIO could be associated with damage to the cell membrane integrity and consequent death of these pathogens. Synergism experiments with DIO and fluconazole (FLZ) and DIO and AFB revealed a significant synergistic effect against Candida spp. These results highlight the antifungal and synergistic potential of the flavonoid DIO against antifungal resistant Candida spp. Furthermore, these findings serve as a basis for future studies aimed at elucidating DIO's antimicrobial mechanisms of action and contribute to the search for novel compounds from natural sources with antimicrobial potential.

Abstract: Background: Currently, there are two major theories for the pathogenesis of sepsis: hyperimmune and hypoimmune. Hyperimmune theory suggests that cytokine storm causes the symptoms of sepsis. On the contrary, hypoimmune theory suggests that immunosuppression causes the manifestations of sepsis. Methods: By using microarray study on peripheral leukocytes from septic patients, this study implies that hyperactivity of TH17 immunity are noted in sepsis patients. Results: I find out that innate immunity related genes are significantly up-regulated including CD14, TLR1,2,4,5,8, HSP70, CEBP proteins, AP1(JUNB, FOSL2), TGF-β, IL-6, TGF-α, CSF2 receptor, TNFRSF1A, S100A binding proteins, CCR2, formyl peptide receptor2, amyloid proteins, pentraxin, defensins, CLEC5A, whole complement machinery, CPD, NCF, MMP, neutrophil elastase, caspases, IgG and IgA Fc receptors(CD64, CD32), ALOX5, PTGS, LTB4R, LTA4H, and ICAM1. Majority of adaptive immunity genes are down-regulated including MHC related genes, TCR genes, granzymes/perforin, CD40, CD8, CD3, TCR signaling, BCR signaling, T & B cell specific transcription factors, NK killer receptors, and TH17 helper specific transcription factors(STAT3, RORA, REL). In addition, Treg related genes are up-regulated including TGFβ, IL-15, STAT5B, SMAD2/4, CD36, and thrombospondin. Conclusions: Thus, Th17 with Treg over-presentation plays important roles in the pathophysiology of sepsis.

Abstract: With the increasing detection of artemisinin resistance to front-line antimalarials in Africa and notwithstanding the planned roll-out of RTS’S and R21 in Africa, the search for new vaccines with high efficacy remains an imperative. Towards this endeavor, we performed in silico screening to identify Plasmodium falciparum gametocyte stage genes that could be targets of protection or diagnosis. Through the analysis, we identified a gene, Pf3D7_1105800, coding for a Plasmodium falciparum subtilisin-like do-main-containing protein (PfSDP). Genetic diversity assessment revealed the Pfsdp gene to be relatively conserved across continents with signs of directional selection. Using RT qPCR and western blots, we observed that Pfsdp is expressed in all parasite developmental stages at the transcript and protein levels. Immunofluorescence assays found PfSDP protein colocalizing with PfMSP-1 and partially with Pfs48/45 at the asexual and sexual stages, respectively. Further, we demonstrated that anti-PfSDP peptide-specific antibodies inhibited erythrocyte invasion by 20-60% in a dose-dependent manner, suggesting that PfSDP protein might play a role in merozoites invasion. We also discovered that PfSDP protein is immunogenic in children from different endemic areas with antibody level increasing from acute infection to day 7 post-treatment, followed by a gradual decay. The limited effect of antibodies on erythrocyte invasion could imply that it might be more involved in other processes in the development of the parasite.

Abstract: Endocytosis is a specialized transport mechanism in which the cell membrane folds inward to enclose large molecules, fluids, or particles, forming vesicles that are transported within the cell. It plays a crucial role in nutrient uptake, immune responses, and cellular communication. However, many pathogens exploit the endocytic pathway to invade and survive within host cells, allowing them to evade the immune system and establish infection. Endocytosis can be classified as clathrin-dependent (CDE) or clathrin-independent (CIE), based on the mechanism of vesicle formation. Unlike CDE, which involves the formation of clathrin-coated vesicles that bud from the plasma membrane, CIE does not rely on clathrin-coated vesicles. Instead, other mechanisms facilitate membrane invagination and vesicle formation. CIE encompasses a variety of pathways, including caveolin-mediated, Arf6-dependent, and flotillin-dependent pathways. In this review, we discuss key features of CIE pathways, including cargo selection, vesicle formation, routes taken by internalized cargo, and the regulatory mechanisms governing CIE. Many viruses and bacteria hijack host cell CIE mechanisms to facilitate intracellular trafficking and persistence. We also revisit the exploitation of CIE by bacterial and viral pathogens, highlighting recent discoveries in entry mechanisms, intracellular fate, and host-pathogen interactions. Understanding how pathogens manipulate CIE in host cells can inform the development of novel antimicrobial and immunomodulatory interventions, offering new avenues for disease prevention and treatment.

Abstract: Helicobacter pylori is a motile bacterial pathogen that causes severe gastric diseases globally. H. pylori motility and chemotaxis are key colonization factors. Motility and chemotaxis are studied in many microbes, including H. pylori, using soft agar assays. In these assays, bacteria are inoculated into low-percentage agar and expand in a motility and chemotaxis-dependent manner. H. pylori similarly expand in soft agar but if a plate is inoculated at multiple points, the expanded H. pylori colonies do not merge and leave gaps. The basis of these gaps was unknown. We report here that gap formation was not affected by media components such as nutrient and agar concentrations, nor did it require chemotaxis but did rely on quorum sensing. To broaden our understanding of this H. pylori property, an H. pylori Tn7 transposon library was screened for mutants that lost gap formation. Fourteen mutants were obtained, and the transposon sites mapped to genes encoding outer membrane proteins, cysteine rich proteins, phosphatidyl glycerophosphate synthase, an endorestriction nuclease and several hypothetical proteins. Our results suggest that H. pylori may use specific proteins to avoid contact with other H. pylori, a behavior that may relate to previous observations that different H. pylori strains do not mix populations in stomach glands.

Abstract: Multiple immune cells and stromal components comprise the tumor microenvironment (TME). In this complex TME, tumor-associated macrophages (TAMs) are spatially heterogeneous. Tumor heterogeneity affects tissue remodeling, immune response, angiogenesis, and metastatic potential. This review highlights the roles of macrophages in TME, immunoregulation, and immunotherapy. Also, intricate relationships between TAMs and various immune cells in the TME and immune evasion have been explored comprehensively. TAM heterogeneity and complex interactions with immune cell types may lead to potential therapeutic approaches. Similarly, classic immune checkpoint inhibitors like anti-PD-L-1 and anti-PD-1 offer promising tumor therapies. TAMs regulate PD-1/PD-L1 immunosuppression by suppressing T cell recruitment and function using cytokines, superficial immune checkpoint ligands, and exosomes. TAM’s functions and mechanisms in PD-1/PD-L1 blocker resistance are described in detail. The insights into intricate relationships of TAMs with the immune cells within TME and the role of immune checkpoint inhibitors will further help explore potential future therapeutic advances.

Abstract: Background: Salmonella infections in poultry pose significant public health and economic challenges due to contamination of meat and eggs and the rise of antimicrobial resistance. Innovative control strategies are needed to reduce Salmonella in poultry flocks. Methods: We explored a novel approach integrating a live attenuated Salmonella vaccine and IgY antibody therapy. Several indigenous plant extracts were screened as natural attenuating agents for Salmonella. The most effective (garlic and onion extracts) were used to attenuate a cocktail of five wild-type Salmonella serovars (S. Montevideo, S. Yeerongpilly, S. Augustenborg, S. Kentucky, and S. Typhimurium). Chickens were immunized with the plant-attenuated Salmonella vaccine, and the resulting egg yolk IgY antibodies were harvested. We assessed in vitro bacterial growth inhibition, vaccine safety and immunogenicity (via ELISA for anti-Salmonella IgY), and performed statistical analyses to evaluate significance. Results: Garlic and onion extracts markedly inhibited Salmonella growth in vitro, yielding significantly smaller colonies (1.0–1.5 mm) compared to untreated controls (4.1 mm, p < 0.05). Combining garlic and onion achieved complete inhibition (no visible colonies), indicating a potent attenuation effect. Plant-extract attenuation did not compromise immunogenicity: chickens vaccinated with the attenuated strains developed high titers of anti-Salmonella IgY, with ELISA optical density values (~1.2 at 1:500 dilution) far above the negative cut-off (0.35). The IgY antibodies showed strong agglutination of Salmonella and are expected to confer passive protection. Recent studies corroborate that orally administered anti-Salmonella IgY can reduce intestinal colonization and shedding in chickens. Conclusion: This study demonstrates a feasible, cost-effective strategy for Salmonella control in poultry by using indigenous plant extracts to create a live attenuated vaccine and harnessing resultant IgY antibodies for therapy.

Abstract: Background: Metabolic dysfunction-associated steatotic liver disease (MASLD) is a common cause of chronic liver disease and is closely associated with metabolic ab-normalities and cardiovascular risks. Butyrate, a short-chain fatty acid produced by gut microbiota, has the potential to enhance liver health by modulating inflammation and supporting gut barrier integrity. This study aimed to investigate and compare the effects of sodium butyrate and calcium butyrate in patients with MASLD. Methods: In this single-center, randomized clinical trial, 181 patients with MASLD were enrolled and assigned to receive either sodium butyrate (n=121) or calcium butyrate (n=60) supplementation at a daily dose of 1000 mg. The primary endpoint was the change in liver steatosis, measured using the Controlled Attenuation Parameter (CAP) via Fi-broScan®. Secondary endpoints included liver stiffness, biochemical parameters, se-rum and fecal calprotectin levels, stool short-chain fatty acid levels, and microbiome composition. A subgroup analysis compared responders (a ≥5% reduction in CAP) to non-responders. Results: There were no significant changes in CAP values for either group (ΔCAP: sodium butyrate, 0.84; calcium butyrate, –0.23; p=0.70). Sodium butyrate significantly reduced serum trimethylamine N-oxide, while calcium butyrate led to a decrease in fecal calprotectin levels. Responders demonstrated a lower body mass in-dex, higher levels of high-sensitivity C-reactive protein and HbA1c, and distinct mi-crobiome profiles, characterized by lower abundance of Subdoligranulum and higher abundance of Catenibacterium. Conclusions: Although butyrate supplementation did not significantly improve liver steatosis as measured by CAP, the differing effects on metabolic and inflammatory markers suggest that there may be potential benefits for specific subgroups of patients with MASLD.

Abstract: Notch-mediated signaling pathways represent a system that is conserved from an evolutionary point of view, demonstrating a key role in determining cell fate in development; in fact, Notch operates at multiple levels during tissue and organ organization, intervening in the key processes of organogenesis. As a consequence of this, a dysregulation of the Notch-mediated pathways leads to the onset of various pathological conditions such as autoimmune diseases or tumors. The activation of Notch-mediated molecular pathways has also been demonstrated in the development of salivary glands (SGs) and in associated pathologies. Although the numerous advances made in recent years have clarified various aspects of the activation of transductional cascades involving Notch in SGs development and diseases, there are still many aspects that require experimental investigation. In this review, we report, for therapeutic purposes, what is present in the literature relating to the mechanisms regulating the development of Notch-mediated SGs and the most recent discoveries relating to SGs pathologies that derive from alterations of the Notch-mediated pathways.

Abstract: Sporothrix schenckii is a pathogenic fungus of worldwide distribution and one of the etiological agents of sporotrichosis. The cell wall is the first point of contact with host cells; therefore, its composition has been widely studied. It has a cell wall composed of chitin, β-glucans, and glycoproteins modified with N-linked and O-linked glycans. Protein O-linked glycosylation is mediated by two gene families of genes, PMT and MNT. Therefore, we evaluated the relevance of protein O-linked glycosylation during the interaction of S. schenckii with the host. Independent silencing of the MNT1 and PMT2 was accomplished by interference RNA. Morphological analyses revealed defects in cell morphology in both yeast and mycelial cells; however, these defects differed between MNT1 and PMT2 silencing. Subsequently, the cell wall was characterized, and silencing of these genes markedly changed cell wall organization. When the silenced strains interacted with human peripheral blood mononuclear cells, a reduced ability to stimulate the proinflammatory cytokines IL-6 and TNFα was found. However, the PMT2-silenced mutants also stimulated higher levels of IL-10 and IL-1β. Interaction with macrophages and neutrophils was also altered, with increased phagocytosis and decreased extracellular trap formation in both sets of silenced strains. Survival assays in Galleria mellonella larvae showed that silencing of any of these genes reduced the ability of S. schenckii to kill the host. In addition, the mutant strains showed defects in the adhesion to extracellular matrix proteins. These data indicate that MNT1 and PMT2 are relevant for cell wall synthesis and interaction with the host.

Abstract: Plastic pollution, particularly in the form of nanoplastics, has emerged as a significant global environmental concern, affecting ecosystems and human health. This review examines the complex interactions between fungi and nanoplastics, emphasizing the dual role of fungi in plastic degradation and potential pathogenicity. Fungi possess unique enzymatic machinery that allows them to degrade various plastic materials, offering promising bioremediation strategies. However, the presence of nanoplastics can impact fungal physiology, potentially altering metabolic pathways, enhancing virulence, and contributing to antifungal resistance. The interactions between nanoplastics and fungi raise critical questions about their ecological roles and implications for human health. This review underscores the need for further research into the mechanisms of nanoplastic-fungi interactions, the effects on fungal communities, and the potential for increased resistance to antifungal agents. Understanding these dynamics is essential for developing effective strategies to address the challenges posed by plastic pollution and fungal infections. The findings highlight the importance of interdisciplinary approaches in addressing the intertwined issues of environmental sustainability and public health.