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Uttam, S.

Publications and source records attributed to Uttam, S..

12 recordsLinked to original sources

Overcoming segmentation bottlenecks in brain tissue for spatial proteomic inference at population scale

In spatial proteomics across large cohorts, downstream estimates from tens of thousands of images depend on accurate cell segmentation. Yet pretrained segmentation models struggle with morphologically complex cell bodies in human brain tissue, and how domain adaptation affects downstream discovery remains unclear. Here, we introduce SPInfer, a workflow for spatial proteomic inference developed using 5,832 manually annotated cell bodies from 120 immunofluorescence images of the human prefrontal cortex. After benchmarking eight segmentation methods spanning classical, convolutional, and foundation models, we adapted Cellpose-SAM, raising cell segmentation F1 from 0.37 to 0.84 and recovering cell compositions concordant with matched single-nucleus RNA-seq and spatial transcriptomics. Across 14,765 images from 69 postmortem donors, identical Alzheimer's disease pathology models found no significant associations after false discovery rate correction using zero-shot masks, versus four using fine-tuned masks; three linked higher OLIG2-positive fractions to greater neurofibrillary tangle and plaque burden. Using the fine-tuned masks, a graph attention network over nuclear neighborhoods classified four cell types without marker information, and differential expression analysis linked cell morphology to gene expression. This provides a pipeline for fine-tuning foundation models to segment complex tissues, enabling biological discovery in spatial proteomics at the population scale.

bioinformatics↗

SpaReg: sparsity-based 3D reconstruction of tissue microenvironments at native resolution across morphological and spatial molecular modalities

Tissue microenvironments comprise cellular and acellular components whose three-dimensional (3D) architecture guides disease fate. Direct imaging of intact specimens by light-sheet and multiphoton microscopy, and computational reconstruction from serial sections, have established that 3D spatial context reveals cell and tissue organization inaccessible at single planes. Computational reconstruction in particular can leverage archived human tissue, benefiting from the cost-effectiveness, robustness, scalable storage, workflow compatibility, and century-long pathobiology knowledge of histology, and can integrate multiple spatial modalities. However, sectioning can introduce tears and folds, and computational alignment can further distort tissue integrity. Here we introduce SpaReg, a sparsity-based 3D reconstruction method spanning histology, spatial proteomics and spatial transcriptomics. Across multiple organs, SpaReg robustly reconstructs large tissue volumes with preserved subcellular morphology despite sectioning artifacts. On a standardized histology benchmark, SpaReg achieves the best balance between 3D reconstruction accuracy and tissue integrity, and on spatial transcriptomics benchmarks it ranks among the leading methods while scaling to hundreds of sections and millions of cells in a dataset that several existing methods fail to process. Preservation of subcellular morphology by SpaReg also enables training of a Hematoxylin and Eosin (H&E)-based epithelial, T and B cell classifier, generating single-cell-resolved 3D maps directly from H&E. Applied to pancreatic tissue containing pancreatic ductal adenocarcinoma arising from an intraductal papillary mucinous neoplasm, these maps reveal that 2D sections overestimate immune exclusion, and resolve lymphoid aggregates in 3D. SpaReg, therefore, provides a scalable foundation for morphologically faithful, multimodal 3D atlases and spatially informed disease modeling

systems biology↗

Microplastics inhibit macrophage bioenergetics impairing homeostatic function and immune responsiveness

Since the 1950s, micro- and nanoplastics (MNPs) have become omnipresent, representing a novel environmental hazard which continually deposits in our airways. Pulmonary macrophages (pMacs) orchestrate the balance between inflammation and tolerance required for homeostasis of the lung and are among the first immune cells to encounter inhaled MNPs. Yet, how pMacs react to plastic deposition in the lung and implications for disease remain unknown. Here, we exposed mice in vivo, human precision-cut lung slices (hPCLS) ex vivo, and monocyte-derived macrophages and cell lines to polystyrene MNPs in vitro. MNP deposition in the lung and extrapulmonary tissues was determined over a 1-week period and pMacs from MNP-laden lungs isolated for RNA-sequencing. We compared the effects of MNPs or diesel exhaust particulate exposures on hPCLS viability and metabolism, monocyte-derived macrophage transcription, and macrophage mitochondrial function, inflammation, and antigen presentation. MNPs readily translocated the lung and were observed in all organs examined within 1-day. pMacs from MNP-exposed mice expressed transcriptional pathways associated with endocrine system disorders, tissue remodeling, and malignant disease. Macrophage phagocytosis was impaired through decreased mitochondrial function which could be rescued pharmacologically. MNPs inhibited the ability of macrophages to effectively present OVA-antigen preventing TCR-specific activation, an effect that could be restored by blocking PD-1/PD-L1. These findings indicate that MNPs impair macrophages via unique mechanisms linking phagocytic and bioenergetic dysfunction. Loss of antigen-presenting capabilities in MNP-laden macrophages may compromise immunosurveillance. As such, MNPs have the potential to increase susceptibility to lung disease independent of the conventional mechanisms of inflammation and oxidative stress. Clinical relevanceO_LIBioaccumulation of micro- and nanoplastics in macrophages impairs their ability to function as antigen-presenting cells increasing susceptibility to pathogenic and malignant disease. C_LIO_LIPulmonary macrophages residing in micro- and nanoplastic laden lungs possess transcriptional profiles associated with endocrine system disorders, gastrointestinal disease, and cancers. C_LI

immunology↗

MitoChontrol: Adaptive mitochondrial filtering for robust single-cell RNA sequencing quality control

SummaryMitochondrial transcript abundance is a standard quality control metric in single-cell RNA sequencing, but fixed percentage thresholds fail to account for the substantial variation in mitochondrial content across cell types and tissues, risking both retention of compromised cells and exclusion of transcriptionally active viable cell populations. We present MitoChontrol, a cell-type-aware probabilistic framework for mitochondrial quality control that models the mitochondrial transcript fraction within transcriptionally coherent clusters as a Gaussian mixture distribution. Compromised-cell components are identified from the upper tail of each cluster-specific distribution, and filtering thresholds are defined as the point at which the posterior probability of cellular compromise exceeds a user-definded confidence value. Applied to controlled perturbation experiments and a pancreatic ductal adenocarcinoma single-cell dataset, MitoChontrol selectively removes transcriptionally compromised cells while preserving biologically elevated but viable populations, outperforming fixed-threshold and outlier-based approaches. Availability and ImplementationMitoChontrol is implemented in Python and integrates directly with AnnData-based workflows. It is freely available under the GNU General Public License v3 (GPL-3.0) at: https://github.com/uttamLab/MitoChontrol (DOI: https://doi.org/10.5281/zenodo.19423054)

bioinformatics↗

Novel Predictive Spatial Biomarker in Non-Small Cell Lung Carcinoma: The Diversity of Niches Unlocking Treatment Sensitivity (DONUTS)

Probabilistic spatial modelling techniques developed on large-scale tumor-immune Atlases ([~]35M individually mapped cells; 50,000 high power fields) were used to characterize predictive features of treatment-responsive lung cancer. We identified CD8+FoxP3+ cell density as a robust pre-treatment biomarker for outcomes across disease stages and therapy types. In parallel, single-cell RNAseq studies of CD8+FoxP3+ T-cells revealed an activated, early effector phenotype, substantiating an anti-tumor role, and contrasting with CD4+FoxP3+ T-regulatory cells. A spatial biomarker was developed using an empirical probabilistic model to define the immediate cell neighbors or niche surrounding CD8+FoxP3+ cells and proximity to the tumor-stromal boundary. The resultant Diversity of Niches Unlocking Treatment Sensitivity (DONUTS) are more prevalent than the CD8+FoxP3+ cells themselves, mitigating sampling error in small biopsies. Further, the DONUTS only require four markers, are additive to PD-L1, and associate with tertiary lymphoid structure counts. Taken together, the DONUTS represent a next-generation predictive biomarker poised for clinical implementation. HIGHLIGHTSO_LILarge-scale tumor-immune Atlases drive robust computational biomarker development C_LIO_LICD8+FoxP3+ cells are anti-tumor T-cells and predict response to therapy C_LIO_LIThe niches or spatial donuts around CD8+FoxP3+ cells boost biomarker performance C_LIO_LICD8+FoxP3+ donuts are hallmarks of a larger immune organization that includes TLS C_LI

pathology↗

The PTPN1 and PTPN2 phosphatases are Cooperative Regulators of Cancer Cell Immune Evasion

Immune evasion by cancer cells remains a major barrier to the success of immune checkpoint blockade (ICB). Here, we identify the phosphatases PTPN1 and PTPN2 as cooperative regulators of tumor immune resistance. Dual genetic ablation of PTPN1/2 in cancer cells enhances Type I and II interferon signaling, MHC-I and CXCL9 expression, and sensitizes tumor cells to cytotoxic T lymphocyte-mediated killing. The small-molecule inhibitor KQ791 phenocopies these effects and synergizes with anti-PD1 therapy to suppress tumor growth in murine models, including immunotherapy-refractory cancers. Mechanistically, PTPN1/2 loss augments STAT1/3/5 signaling and primes cancer cells for immunogenic cell death via IFN{gamma}/TNF-induced pathways. Moreover, PTPN1/2 inhibition enhances antigen release and cross-presentation, promoting robust antigen-specific CD8 T cell responses. These findings highlight PTPN1&2 as essential mediators of cancer immune evasion and support their inhibition as a strategy to broaden the effectiveness of immune checkpoint blockade in solid tumors.

cancer biology↗

Local Mean Suppression Filter for Effective Background Identification in Fluorescence Images

We present an easy-to-use, nonlinear filter for effective background identification in fluorescence microscopy images with dense and low-contrast foreground. The pixel-wise filtering is based on comparison of the pixel intensity with the mean intensity of pixels in its local neighborhood. The pixel is given a background or foreground label depending on whether its intensity is less than or greater than the mean respectively. Multiple labels are generated for the same pixel by computing mean expression values by varying neighborhood size. These labels are accumulated to decide the final pixel label. We demonstrate that the performance of our filter favorably compares with state-of-the-art image processing, machine learning, and deep learning methods. We present three use cases that demonstrate its effectiveness, and also show how it can be used in multiplexed fluorescence imaging contexts and as a denoising step in image segmentation. A fast implementation of the filter is available in Python 3 on GitHub.

bioinformatics↗

Translational control in the spinal cord regulates gene expression and pain hypersensitivity in the chronic phase of neuropathic pain

Sensitization of spinal nociceptive circuits plays a crucial role in neuropathic pain. This sensitization depends on new gene expression that is primarily regulated via transcriptional and translational control mechanisms. The relative roles of these mechanisms in regulating gene expression in the clinically relevant chronic phase of neuropathic pain are not well understood. Here, we show that changes in gene expression in the spinal cord during the chronic phase of neuropathic pain are substantially regulated at the translational level. Downregulating spinal translation at the chronic phase alleviated pain hypersensitivity. Cell-type-specific profiling revealed that spinal inhibitory and excitatory neurons exhibited substantial changes in translation after peripheral nerve injury. Notably, increasing translation selectively in all inhibitory neurons or parvalbumin-positive (PV+) interneurons, but not excitatory neurons, promoted mechanical pain hypersensitivity. Furthermore, increasing translation in PV+ neurons decreased their intrinsic excitability and spiking activity. Conversely, reducing translation in spinal PV neurons prevented the nerve injury-induced decrease in excitability but did not alleviate mechanical hypersensitivity. Together, these findings advance our understanding of translational control mechanisms in the spinal cord during neuropathic pain and highlight their cell-type- and phase-specific contributions to gene expression and pain hypersensitivity.

neuroscience↗

UNSEG: unsupervised segmentation of cells and their nuclei in complex tissue samples

Multiplexed imaging technologies have made it possible to interrogate complex tumor microenvironments at sub-cellular resolution within their native spatial context. However, proper quantification of this complexity requires the ability to easily and accurately segment cells into their sub-cellular compartments. Within the supervised learning paradigm, deep learning based segmentation methods demonstrating human level performance have emerged. However, limited work has been done in developing such generalist methods within the label-free unsupervised context. Here we present an unsupervised segmentation (UNSEG) method that achieves deep learning level performance without requiring any training data. UNSEG leverages a Bayesian-like framework and the specificity of nucleus and cell membrane markers to construct an a posteriori probability estimate of each pixel belonging to the nucleus, cell membrane, or background. It uses this estimate to segment each cell into its nuclear and cell-membrane compartments. We show that UNSEG is more internally consistent and better at generalizing to the complexity of tissue morphology than current deep learning methods. This allows UNSEG to unambiguously identify the cytoplasmic compartment of a cell, which we employ to demonstrate its use in an exemplar biological scenario. Within the UNSEG framework, we also introduce a new perturbed watershed algorithm capable of stably and automatically segmenting a cluster of cell nuclei into individual cell nuclei that increases the accuracy of classical watershed. Perturbed watershed can also be used as a standalone algorithm that researchers can incorporate within their supervised or unsupervised learning approaches to extend classical watershed, particularly in the multiplexed imaging context. Finally, as part of developing UNSEG, we have generated a high-quality annotated gastrointestinal tissue (GIT) dataset, which we anticipate will be useful for the broader research community. We demonstrate the efficacy of UNSEG on the GIT dataset, publicly available datasets, and on a range of practical scenarios. In these contexts, we also discuss the possibility of bias inherent in quantification of segmentation accuracy based on F1 score. Segmentation, despite its long antecedents, remains a challenging problem, particularly in the context of tissue samples. UNSEG, an easy-to-use algorithm, provides an unsupervised approach to overcome this bottleneck, and as we discuss, can help improve deep learning based segmentation methods by providing a bridge between unsupervised and supervised learning paradigms.

bioinformatics↗

Single-cell RNA sequencing reveals time- and sex-specific responses of spinal cord microglia to peripheral nerve injury and links ApoE to neuropathic pain

Activation of microglia in the spinal cord following peripheral nerve injury is critical for the development of long-lasting pain hypersensitivity. However, it remains unknown whether distinct microglia subpopulations or states contribute to different stages of pain development and maintenance. We show, using single-cell RNA-sequencing, that nerve injury induces the generation of a male-specific inflammatory microglia subtype, and demonstrate increased proliferation of microglia in males as compared to females. We also show time- and sex-specific transcriptional changes in different microglial subpopulations following injury. Apolipoprotein E (Apoe) is the top upregulated gene in microglia at chronic time points after nerve injury in mice and polymorphisms in the APOE gene in humans are associated with chronic pain. Single-cell analysis of human spinal cord microglia reveals a subpopulation with a disease-related transcriptional signature. Our data provide a detailed analysis of transcriptional states of mouse and human spinal cord microglia, and identify a previously unrecognized role for ApoE in neuropathic pain.

neuroscience↗

Unsupervised cellular phenotypic hierarchy enables spatial intratumor heterogeneity characterization, recurrence-associated microdomains discovery, and harnesses network biology from hyperplexed in-situ fluorescence images of colorectal carcinoma

LEAPH is an unsupervised machine learning algorithm for characterizing in situ phenotypic heterogeneity in tissue samples. LEAPH builds a phenotypic hierarchy of cell types, cell states and their spatial configurations. The recursive modeling steps involve determining cell types with low-ranked mixtures of factor analyzers and optimizing cell states with spatial regularization. We applied LEAPH to hyperplexed (51 biomarkers) immunofluorescence images of colorectal carcinoma primary tumors (N=213). LEAPH, combined with pointwise mutual information (PMI), enables the discovery of phenotypically distinct microdomains, composed of spatially configured computational phenotypes. LEAPH identified a subset of microdomains visualized as the spatial configuration of recurrence-specific signaling networks whose intracellular and intercellular interactions support cancer stem cell maintenance and immunosuppression in the evolving tumor microenvironment. The LEAPH framework, when combined with microdomain discovery and microdomain-specific network biology, has the potential to provide insights into pathophysiological mechanisms, identify novel drug targets and inform therapeutic strategies for individual patients.

cancer biology↗

A spatial analytics computational and systems biology platform predicts risk of colorectal cancer recurrence and identifies emergent spatial domain networks associated with recurrence

An unmet clinical need in solid tumor cancers is the ability to harness the intrinsic spatial information in primary tumors that can be exploited to optimize prognostics, diagnostics and therapeutic strategies for precision medicine. We have developed a transformational spatial analytics (SpAn) computational and systems biology platform that predicts clinical outcomes and captures emergent spatial biology that can potentially inform therapeutic strategies. Here we apply SpAn to primary tumor tissue samples from a cohort of 432 chemo-naive colorectal cancer (CRC) patients iteratively labeled with a highly multiplexed (hyperplexed) panel of fifty-five fluorescently tagged antibodies. SpAn predicted the 5-year risk of CRC recurrence with a mean area under the ROC curve of 88.5% (SE of 0.1%), significantly better than current state-of-the-art methods. SpAn also inferred the emergent network biology of the tumor spatial domains revealing a synergistic role of known features from CRC consensus molecular subtypes that will enhance precision medicine.

cancer biology↗