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Salehi, A.

Publications and source records attributed to Salehi, A..

10 recordsLinked to original sources

Pathogen-specific antimicrobial activity prediction with biological large language model-based methods

Driven by the rise of antimicrobial resistance, antimicrobial peptides (AMPs) have emerged as promising therapeutics capable of targeting multidrug-resistant pathogens. Because identifying AMPs and their specific targets requires costly and labor-intensive wet-lab experiments, in silico methods to prioritize candidates are highly valuable. However, current computational methods often lack pathogen specificity or fail to incorporate crucial targeted proteomic and genomic contexts. To bridge this gap, we developed triAMPh, a robust, zero-shot framework for pathogen-specific peptide bioactivity prediction. triAMPh integrates a heterogeneous graph attention network-based link predictor (HLP), Extreme Gradient Boosting, and a multilayer perceptron trained on features from biological large language models (bLLMs). Our novel HLP constructs a knowledge graph that maps peptides and pathogens as distinct nodes, connected by similarity and bioactivity edges. The model extracts information through semantic traversals, prioritizing neighboring nodes and their biological contexts. Benchmarking shows that triAMPh provides unbiased, peptide- and pathogen-centered zero-shot predictions, matching or outperforming state-of-the-art methods across all metrics except precision. Ultimately, triAMPh offers a powerful computational tool to accelerate wet-lab AMP discovery while demonstrating the capability of bLLMs to capture complex, pathogen-specific bioactivity patterns.

bioinformatics↗

Selective Immune Silencing by Targeted TGF-β Agonists

Depletion of pathogenic T and B cells is a pillar of therapies for autoimmune, inflammatory, and transplantation-related immunological diseases. However, adverse events, safety concerns in immunocompromised patients, and disease relapse limit clinical utility. Here, we exploit the immunosuppressive properties of a transforming growth factor beta (TGF-{beta}) mimic repurposed from helminths for cell type-specific therapeutic silencing, as a new approach to complement existing therapies. Mouse CD4 and CD8 T cell-targeted TGF-{beta} agonists selectively and potently silence antigen-specific T cell responses in OVA-immunized mice by suppressing pro-inflammatory effector, cytotoxic, and T follicular helper programs, while skewing cells toward a quiescent state biased toward regulatory and type 17 T cell phenotypes. Similarly, human CD4 and CD8 T cell-targeted TGF-{beta} agonists precisely and effectively suppress live-attenuated influenza vaccine (LAIV)-induced T cell activation and expansion in human spleen organoids. Correspondingly, CD4 T cell-targeted TGF-{beta} agonist effectively ameliorated disease activity and promoted disease remission in CD4 T cell-driven models of autoimmune neuroinflammation and allergic airway inflammation, demonstrating efficacy in both prophylactic and established inflammatory settings. Moreover, both CD4 and CD8 T cell-targeted TGF-{beta} agonists ameliorated disease activity in graft-versus-host disease. Additionally, a human CD19 B cell-targeted TGF-{beta} agonist robustly inhibits germinal center B cell-to-plasmablast maturation and antibody responses in LAIV-stimulated human spleen organoids. These early-stage results suggest that cell-selective TGF-{beta} agonism merits further investigation as a versatile therapeutic approach for the precise silencing of pathogenic adaptive immune responses.

immunology↗

Cytokine Regulation of Human Antibody Responses to Influenza Vaccines

Studies show that human vaccine responses widely vary. Here, we analyzed data measuring 66 cytokines from 4 different inactivated influenza vaccine (IIV) cohorts over 5 seasons (N=581) and identified a significant correlation between baseline/day 0 serum IL-18 and IFN-{beta} concentrations and the vaccine-specific antibody response on day 28, suggesting these factors may have an adjuvant-like effect. To investigate this further, we tested the impact of 19 cytokines on the development of anti-influenza antibody response when administered together with the IIV vaccine in human tonsil and spleen organoids. We found that Type I IFNs (IFN-{beta} and others), IL-21, IL-12, IL-10, but not IL-18 or IFN-{gamma}, enhanced the antibody response. The live attenuated influenza vaccine (LAIV) induced a stronger antibody response than the inactivated one in organoids. Adding a single cytokine, IFN-{beta}, to IIV stimulation recapitulated most of the live vaccine-specific cytokine activation program. It increased the antibody response of the inactivated vaccine to that of the LAIV. Two other antibody-boosting cytokines, IL-12 and IL-21, were induced by LAIV but not by Type I IFNs, indicating different cytokines can affect different pathways leading to a robust antibody response. We then generated cytokine mRNA lipid nanoparticles (LNPs) to test the effect of cytokines on IIV response in a mouse model of immunization. We found that IL-21-LNPs augmented the quantity and breadth of the antibody responses, while IFN-{beta} LNPs enhanced durability. These findings identified parallel cytokine pathways regulating human vaccine responses and provide a rationale for using cytokines as adjuvants to mimic the effectiveness of live-attenuated vaccines without the risk of viral replication.

immunology↗

Shedding of mitochondrial Voltage-Dependent Anion Channel-1 (VDAC1) Reflects COVID-19 Severity and Reveals Macrophage Dysfunction

COVID-19 severity correlates with lymphopenia and increased pro-inflammatory cytokines. However, the dysfunction of tissue macrophages in COVID-19 patients during the inflammatory cytokine storm has not been fully elucidated. Hospitalized COVID-19 patients were divided into three groups based on their symptomatic severity: exhibiting mild, moderate, or severe symptoms. Patients exhibited successively increased serum levels of mitochondrial voltage-dependent anion channel 1 (VDAC1) at days 0, 3, 7, 10, and 14, returning to those of non-infected subjects at day 28. Serum level of VDAC1 was positively correlated with COVID-19 severity and with increased white blood cell (WBC), neutrophil, lymphocyte, procalcitonin (PCT), and gamma-glutamyltransferase (GT) levels. Peripheral blood mononuclear cells (PBMCs) from hospitalized COVID-19 patients showed increased VDAC1 content concomitant with a reduced ATP content. Culture of monocytes, isolated from healthy individuals, and differentiated into polarized M1 macrophages, together with a cytokine mixture (IL-1{beta}, IFN-{gamma}, and TNF-), to mimic the inflammatory cytokine storm, for 24 h markedly increased VDAC1 and Monocyte chemoattractant protein-1 (MCP-1) release in culture medium. The presence of the cytokine mixture reduced the ATP content, cell viability, and the phagocytic capability of macrophages. Co-staining of VDAC1 and the plasma membrane marker Na+/K+-ATPase showed that cytokine-treatment mistargeted VDAC1 to the cell surface of macrophages. All these effects were prevented by VDAC1 inhibition using VBIT-4, VDAC1-specific antibody (VDAC1-ab), or metformin. Our findings indicate that increased VDAC1 expression and cell surface mistargeting in immune cells might be associated with cell dysfunction, potentially contributing to the severity of COVID-19 infection. The data also indicate serum VDAC1 as a biomarker of COVID-19 severity and the use of VDAC1 inhibitors as potential drug candidates restoring macrophages and PBMCs function in individuals severely affected by COVID-19.

pathology↗

Mining the UniProtKB/Swiss-Prot database forantimicrobial peptides

The ever-growing global health threat of antibiotic resistance is compelling researchers to explore alternatives to conventional antibiotics. Antimicrobial peptides (AMPs) are emerging as a promising solution to fill this need. Naturally occurring AMPs are produced by all forms of life as part of the innate immune system. High-throughput bioinformatics tools have enabled fast and large-scale discovery of AMPs from genomic, transcriptomic, and proteomic resources of selected organisms. Public protein sequence databases, comprising over 200 million records and growing, serve as comprehensive compendia of sequences from a broad range of source organisms. Yet, large-scale in silico probing of those databases for novel AMPs has never been reported. In the present study, we propose an AMP mining workflow to predict novel AMPs from the UniProtKB/Swiss-Prot database using the AMP prediction tool, AMPlify, as its discovery engine. Using this workflow, we identified 8,008 novel putative AMPs from all eukaryotic sequences in the database. Focusing on the practical use of AMPs as suitable antimicrobial agents with applications in the poultry industry, we prioritized 40 of those AMPs based on their similarities to known chicken AMPs in predicted structures. In our tests, 13 out of the 38 successfully synthesized peptides showed antimicrobial activity against Escherichia coli and/or Staphylococcus aureus.

bioinformatics↗

Maternal n-3 enriched diet reprograms neurovascular transcriptome and blunts inflammation in neonate

Infection during perinatal period can adversely affect brain development, predispose infants to ischemic stroke and have lifelong consequences. We previously demonstrated that diet enriched in n-3 polyunsaturated fatty acids (PUFA) transforms brain lipid composition and protects from neonatal stroke. Vasculature is a critical interface between blood and brain providing a barrier to systemic infection. Here we examined whether maternal PUFA-enriched diets exert reprograming of endothelial cell signalling in 9-day old mice after endotoxin (LPS)-induced infection. Transcriptome analysis was performed on brain microvessels from pups born to dams maintained on 3 diets: standard, n-3 or n-6 enriched. N-3 diet enabled higher immune reactivity in brain vasculature, while preventing imbalance of cell cycle regulation and extracellular matrix cascades that accompanied inflammatory response in standard diet. LPS response in blood and brain was blunted in n-3 offspring. Cerebral angioarchitecture analysis revealed modified vessel complexity after LPS. Thus, n-3-enriched maternal diet partially prevents imbalance in homeostatic processes and alters inflammation rather than affects brain vascularization during early life. Importantly, maternal diet may presage offspring neurovascular outcomes later in life.

neuroscience↗

Longitudinal dynamics of microvascular recovery after acquired cortical injury

Acquired brain injuries due to trauma damage cortical vasculature, which in turn impairs blood flow to injured tissues. There are reports of vascular morphological recovery following traumatic brain injury (TBI), but the remodeling process has not been examined longitudinally in detail after injury in vivo. Understanding the dynamic processes that influence recovery is thus critically important. We evaluated the longitudinal and dynamic microvascular recovery and remodeling up to 2 months post injury using live brain miniscope and 2-photon microscopic imaging. The new imaging approaches captured dynamic morphological and functional recovery processes at high spatial and temporal resolution in vivo. Vessel painting documented the initial loss and subsequent temporal morphological vascular recovery at the injury site. Miniscopes were used to longitudinally image the temporal dynamics of vascular repair in vivo after brain injury in individual mice across each cohort. We observe near-immediate nascent growth of new vessels in and adjacent to the injury site that peaks between 14-21 days post injury. 2-photon microscopy confirms new vascular growth and further demonstrates differences between cortical layers after cortical injury: large vessels persist in deeper cortical layers (>200 m), while superficial layers exhibit a dense plexus of fine (and often non-perfused) vessels displaying regrowth. Functionally, blood flow increases mirror increasing vascular density. Filopodia development and endothelial sprouting is measurable within 3 days post injury that rapidly transforms regions devoid of vessels to dense vascular plexus in which new vessels become increasingly perfused. Within 7 days post injury, blood flow is observed in these nascent vessels. Behavioral analysis reveals improved vascular modulation after 9 days post injury, consistent with vascular regrowth. We conclude that morphological recovery events are closely linked to functional recovery of blood flow to the compromised tissues, which subsequently leads to improved behavioral outcomes.

neuroscience↗

Vascular topology is acutely impacted by experimental febrile status epilepticus

Febrile status epilepticus (FSE) is an important risk factor for temporal lobe epilepsy and early identification is vital. In a rat model of FSE, we identified an acute novel MRI signal in the basolateral amygdala (BLA) at 2 hours post FSE that predicted epilepsy in adulthood. This signal remains incompletely understood and hypothesized that it might derive from changes to vascular topology. Experimental FSE was induced in rat pups and compared to normothermic littermate controls. We examined cerebral vascular topology at 2 hours, using a novel vessel painting and analysis protocol. Blood vessel density of the cortical vasculature was significantly reduced in FSE rats, and this effect was lateralized, as reported for the MRI signal. The middle cerebral artery (MCA) exhibited abnormal topology in FSE pups but not in controls. In the BLA, significant vessel junction reductions and decreased vessel diameter were observed, together with a strong trend for reduced vessel length. In summary, FSE results in acute vascular topological changes in the cortex and BLA that may underlie the acute MRI signal that predicts progression to future epilepsy. The altered vasculature may be amenable to intervention treatments to potentially reduce the probability of progression to epilepsy following FSE.

neuroscience↗

A novel technology for objective, accurate and non-invasive early diagnosis and monitoring of Alzheimer’s disease in clinics and clinical trials

We have developed a novel medical image processing technology for objective, accurate, and non-invasive diagnosis, prognosis, and monitoring of Alzheimers disease using standard clinical brain MRI (magnetic resonance imaging) and basic clinical cognitive assessment. The technology is a robust, highly accurate, fully automated, high-throughput, cloud-based platform, which operates in a fully integrated and controlled environment. In diagnosis mode, our technology performs with 91% balanced accuracy on blind testing to diagnose the current neurocognitive status, and in prognosis mode or early detection at mild cognitive impairment (MCI) stage with 88% balanced accuracy on blind testing to predict progression from MCI to Alzheimers dementia (AD) within 5 years. Such prognostic capability is currently non-existent, even in specialty clinics and hospitals, a major factor in Alzheimers clinical trial failures. The algorithms diagnostic certainty precisely mirrors the diagnostic confidence of an expert cognitive neurologist for both MCI (Spearmans Rho = 1) and AD (Rho = 1). In addition to widespread clinical applications, this novel technology can enable correct patient selection and therapeutic effect monitoring in clinical trials of Alzheimers disease, the crucial elements to finding a cure.

neuroscience↗

Large-scale RNA editing profiling in different adult chicken tissues

RNA editing is a post-transcription maturation process that diversifies genomically encoded information and can lead to diversity and complexity of transcriptome, especially in the brain. Thanks to next-generation sequencing technologies, a large number of editing sites have been identified in different species, especially in human, mouse and rat. While this mechanism is well described in mammals, only a few studies have been performed in the chicken. Here, we developed a rigorous computational strategy to identify RNA editing sites in eight different tissues of the chicken (brain, spleen, colon, lung, kidney, heart, testes and liver), based on RNA sequencing data alone. We identified 68 A-to-G editing sites in 46 genes. Only two of these were previously reported in chicken. We found no C-to-U sites, attesting the lack of this type of editing mechanism in the chicken. Similar to mammals, the editing sites were enriched in non-coding regions, rarely resulted in change of amino acids, showed a critical role in nervous system and had a low guanosine level upstream of the editing site and some enrichment downstream from the site. Moreover, in contrast to mammals, editing sites were weakly enriched in interspersed repeats and the frequency and editing ratio of non-synonymous sites were higher than those of synonymous sites.\n\nInterestingly, we found several tissue-specific edited genes including GABRA3, SORL1 and HTR1D in brain and RYR2 and FHOD3 in heart that were associated with functional processes relevant to the corresponding tissue. This finding highlighted the importance of the RNA editing in several chicken tissues, especially the brain. This study extends our understanding of RNA editing in chicken tissues and establish a foundation for further exploration of this process.

genetics↗