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Beebe, D. J.

Publications and source records attributed to Beebe, D. J..

18 recordsLinked to original sources

Droplet-array culture enables single-cell isolation of bacteria directly from blood

Bacteremia and sepsis require rapid diagnosis and treatment, but these are often hampered by slow or inconclusive blood culture results. Here we describe an alternative to traditional blood culture, leveraging common laboratory equipment and a droplet array to isolate and expand bacteria in a single step. The method neutralizes inhibitory whole-blood components through lysis, concentrates sample bacteria, and uses a droplet array to enable single-bacteria isolation and subsequent in-droplet expansion. Seven species of bacteria (four gram negative, three gram positive) were spiked into 1 mL of whole blood at a concentration of approximately 100 colony-forming units (CFU) and subsequently processed. The mean time to colorimetric detection via WST-8 dye was 11.5 h (range 9-13 h), compared with [≥] 28 h typically required for conventional blood culture and subculture. Colony counts per droplet followed a Poisson distribution for both gram-negative ({lambda} = 0.288) and gram-positive ({lambda} = 0.320) organisms, and means of 86.2% and 88.4% of occupied droplets, respectively, contained a single CFU. This method eliminates the need for additional subculture after positive blood culture. By partitioning the sample, the workflow limits competitive exclusion and preserves the composition of polymicrobial samples, while yielding viable colonies substantially faster than conventional methods. Blood processing at low CFU counts (3-5 CFU/mL) with both S. aureus and E. coli consistently recovered viable bacteria (1-3 CFU/mL).

microbiology↗

Exclusive liquid repellency isolation (ELRi) microliter scale isolation technique unmasks T-cell migration defects to CCL21 in pediatric asthma

Exclusive Liquid Repellency Isolation (ELRi) is a novel, chip-free platform designed for efficient microscale immune cell isolation. Leveraging the inherent exclusive liquid repellency (ELR) properties of polypropylene tubes with an oil overlay, ELRi ensures that small sample volumes, as low as 8 L, have no contact with container walls, preventing cell loss. Here we describe ELRi and demonstrate magnetic bead-based isolation of diverse immune cells, including T cells, and monocytes, from whole blood. The platforms utility is highlighted in its application to pediatric asthma research, where sample volume is highly restricted. It has been reported that the T cell homing receptor CCR7 is downregulated in cells from asthmatic patients, but a direct functional link to impaired cell migration remains unconfirmed (1, 2). Using ELRi-isolated cells, we provide the first functional evidence that T cells from asthmatic children exhibit significantly impaired chemotaxis toward the CCR7 ligand, CCL21. By simplifying RBC depletion and enabling such functional assays alongside RNA sequencing from the same tiny sample, ELRi overcomes the limitations of large-volume flow cytometry or cell-specific sorting methods. Easily integrated into lab workflows and scalable for various needs, ELRi facilitates more frequent, minimally invasive, and functionally informative immune profiling of restricted volume samples.

immunology↗

CXCL13-CXCR5 Signaling in CD8⁺ T Cell Recruitment and Lymphoid Immune Organization in Clear Cell Renal Cell Carcinoma

Clear cell renal cell carcinoma (ccRCC) exhibits heterogeneity in immune infiltration and clinical outcomes, but the mechanisms governing recruitment and organization of tumor-reactive CD8 T cells remain incompletely defined. We investigated the role of the CXCL13-CXCR5 axis in shaping CD8 T cell recruitment, differentiation, and immune organization in high-risk, non-metastatic ccRCC. Human tumor, plasma, and matched adjacent kidney specimens were analyzed using ELISA, quantitative PCR, migration assays, multiplex immunofluorescence, single-cell RNA sequencing, spatial transcriptomics, and a syngeneic mouse model. CXCL13 was among the most upregulated chemokines in ccRCC relative to matched normal kidney and was embedded within a CD8 T cell-associated inflammatory transcriptional program. In transwell and microphysiological system (MPS) assays, CXCL13 promoted CD8 T cell migration, enriched CXCR5 cells among migrating CD8 T cells and showed reduced migration after CXCL13 or CXCR5 blockade. Single-cell analyses identified CXCR5 expression within stem-like CD8 T cell states associated with TCF7 and IL7R, whereas CXCL13 associated with later cytotoxic/exhausted states along a continuous differentiation landscape. Spatial transcriptomics demonstrated that stem-like CD8 T cells localized within structured lymphoid aggregates enriched for B cells, coordinated CXCL13/CXCR5 expression, and signaling programs. In vivo, tumor-derived CXCL13 suppressed tumor growth, increased intratumoral CD8 T cell infiltration, and enriched CXCR5TCF1CD8 stem-like T cells. In human tumors, higher CXCL13 expression correlated with increased CXCR5CD8 T cell infiltration and improved recurrence-free survival. These findings identify CXCL13 as a regulator of immune recruitment and niche organization and support the CXCL13-CXCR5 axis as a biomarker and possible therapeutic target in ccRCC.

cancer biology↗

A Head and Neck Cancer Patient-Specific Microphysiological System for Predicting Response to Chemoradiation

Head and neck cancer (HNC) is the 6th most common malignancy worldwide. 60% of patients present with advanced disease and approximately 50% of patients recur following primary treatment. Chemoradiation remains a standard of care for most patients. However, clinicians lack functional tools to predict which patients will respond to chemoradiation prior to treatment and current models, including organoids and animal model systems, fail to capture either full complexity or patient-to-patient heterogeneity of the individual HNC tumor and microenvironment (TME). Here, we have developed, characterized, and tested a patient-specific microphysiological system (MPS) that reconstructs the HNC TME in a vascularized 3D environment. This MPS was constructed from malignant cells, fibroblasts, and immune cells from a patients surgically resected tumor, seeded within a 3D hydrogel with molded endothelial lumens. Single-cell RNA sequencing confirmed that the MPS preserved 12 transcriptionally distinct cell populations found in matched native tissue. The platform recapitulated tumor hypoxia, with a 12-fold increase in hypoxic marker expression that altered radiation response, consistent with clinical HNC biology. Compartment-resolved imaging revealed distinct treatment dynamics in tumor, stromal, and vascular regions, and individual patients exhibited divergent responses to chemoradiation in spheroid morphology, cell viability, and migration. We found the slope of spheroid area change with treatment tracked with tumor recurrence, suggesting this metric could serve as a functional predictor of therapeutic response.

bioengineering↗

Lymphatic endothelial cells regulate neutrophil phenotypes and function in a microphysiological model of infection

Early skin inflammation requires coordinated immune regulation, with neutrophils acting as first-line responders. While the blood vasculature and its role in neutrophil recruitment during infection has been extensively studied, the lymphatic system remains comparatively understudied despite its known role in immune cell trafficking. Growing evidence suggests lymphatic vessels actively participate in regulating inflammatory responses, yet whether they coordinate neutrophil behavior during skin infection remains unclear. Staphylococcus aureus is particularly problematic in this context, employing multiple immune evasion strategies and representing a major driver of antibiotic-resistant skin and soft tissue infections worldwide. To address this gap, we developed a human-based 3D microphysiological system incorporating luminal lymphatic endothelial vessels, a collagen matrix and bacteria to model an infected microenvironment. We evaluated neutrophil migration, phagocytosis and NETosis in response to Escherichia coli and S. aureus. Lymphatic endothelium amplified neutrophil migration in a bacterial-dependent manner, with E. coli promoting directional migration toward the vessel while S. aureus suppressed migration and directionality despite increased phagocytic uptake. S. aureus also induced myeloperoxidase-positive NETs with nuclear morphology consistent with vital NETosis, rescued by DNase treatment. To our knowledge, this is the first demonstration that lymphatic endothelium directly drives neutrophil behavior during skin infection.

immunology↗

A microphysiological system of sterile injury demonstrates neutrophil reverse migration via macrophage-derived extracellular vesicle crosstalk.

Persistent neutrophilic inflammation can lead to tissue damage and chronic inflammation, contributing to non-healing wounds. The resolution phase of neutrophilic inflammation is critical to preventing tissue damage, as observed in diseases characterized by influx of neutrophils such as atherosclerosis and non-healing wounds. Animal models have provided insight into resolution of neutrophilic inflammation via efferocytosis and reverse migration (rM); however, species-specific differences and complexity of innate immune responses make translation to humans challenging. Thus, there is a need for in vitro systems that can elucidate mechanisms of resolution of human neutrophilic inflammation. Here, we developed a human microphysiological system (MPS) to mimic an inflammatory sterile injury (SI) microenvironment to study the role of macrophage derived extracellular vesicles (M-EVs) in determining the resolution of inflammation via neutrophil rM. The MPS integrates a human umbilical vein endothelial cell (HUVEC) lined lumen, injury site spheroid, human neutrophils, macrophages and macrophage derived EVs to investigate the role of M-EVs in neutrophil rM in vitro. The key features of the MPS enabled us to demonstrate that EVs derived from macrophage subsets modulate migratory behavior in primary neutrophils differently in specific inflammatory microenvironments. Importantly, we identified a new mechanism underlying neutrophil rM via M-EV, where neutrophils exposed to M2-EV-derived IL-8 migrate away from the SI site upon reaching the site, using the SI MPS. Overall, our SI MPS system demonstrates a reverse migratory pattern in human primary neutrophils, advancing the study of the resolution of inflammation via M-EVs.

immunology↗

Co-zorbs: Motile, multispecies biofilms aid transport of diverse bacterial species

Biofilms are three-dimensional structures containing one or more bacterial species embedded in extracellular polymeric substances. Although most biofilms are stationary, Flavobacterium johnsoniae forms a motile spherical biofilm called a zorb, which is propelled by its base cells and contains a polysaccharide core. Here, we report formation of spatially organized, motile, multispecies biofilms, designated "co-zorbs," that are distinguished by a core-shell structure. F. johnsoniae forms zorbs whose cells collect other bacterial species and transport them to the zorb core, forming a co-zorb. Live imaging revealed that co-zorbs also form in zebrafish, thereby demonstrating a new type of bacterial movement in vivo. This discovery opens new avenues for understanding community behaviors, the role of biofilms in bulk bacterial transport, and collective strategies for microbial success in various environments. Significance StatementThis paper reports the discovery of co-zorbs, which are spherical aggregates of bacteria that move and transport other bacteria. Zorbs move toward other bacteria and collect them in a manner reminiscent of phagocytes. Once inside the zorb, the new species form a striking, organized core. The discovery of co-zorbs introduces an entirely new type of bacterial movement and transport involving cooperation among bacterial species. Co-zorbs have potential for engineering microbial systems for biotechnology applications and for managing spread of bacterial pathogens in their hosts.

microbiology↗

Surface colonization by Flavobacterium johnsoniae promotes its survival in a model microbial community

Flavobacterium johnsoniae is a ubiquitous soil and rhizosphere bacterium, but despite its abundance, the factors contributing to its success in communities are poorly understood. Using a model microbial community, The Hitchhikers Of the Rhizosphere (THOR), we determined the effects of colonization on fitness of F. johnsoniae in the community. Insertion sequencing (INSeq), a massively parallel transposon mutant screen, on sterile sand identified 25 genes likely to be important for surface colonization. We constructed in-frame deletions of nine candidate genes predicted to be involved in cell membrane biogenesis, motility, signal transduction, and transport of amino acids and lipids. All mutants poorly colonized sand, glass, and polystyrene and produced less biofilm than the wild type, indicating the importance of the targeted genes in surface colonization. Eight of the nine colonization-defective mutants were also unable to form motile biofilms, or zorbs, thereby suggesting that the affected genes play a role in group movement and linking stationary and motile biofilm formation genetically. Furthermore, we showed that deletion of colonization genes in F. johnsoniae affected its behavior and survival in THOR on surfaces, suggesting that the same traits are required for success in a multispecies microbial community. Our results provide insight into the mechanisms of surface colonization by F. johnsoniae and form the basis for further understanding its ecology in the rhizosphere. IMPORTANCEMicrobial communities direct key environmental processes through multispecies interactions. Understanding these interactions is vital for manipulating microbiomes to promote health in human, environmental, and agricultural systems. However, microbiome complexity can hinder our understanding of the underlying mechanisms in microbial community interactions. As a first step towards unraveling these interactions, we explored the role of surface colonization in microbial community interactions using THOR, a genetically tractable model community of three bacterial species, Flavobacterium johnsoniae, Pseudomonas koreensis, and Bacillus cereus. We identified F. johnsoniae genes important for surface colonization in solitary conditions and in the THOR community. Understanding the mechanisms that promote success of bacteria in microbial communities brings us closer to targeted manipulations to achieve outcomes that benefit agriculture, the environment, and human health.

microbiology↗

Neutrophil motility is regulated by both cell intrinsic and endothelial cell ARPC1B

Neutrophil directed motility is necessary for host defense, but its dysregulation can also cause collateral tissue damage. Actinopathies are monogenic disorders that affect the actin cytoskeleton and lead to immune dysregulation. Deficiency in ARPC1B, a component of the ARP2/3 complex, results in vascular neutrophilic inflammation; however, the mechanism remains unclear. Here we generated ARPC1B-deficient human iPSC-derived iNeutrophils that show impaired migration and a switch from pseudopodia to the formation of elongated filopodia. We show, using a blood vessel on a chip model, that primary human neutrophils have impaired movement across an endothelium deficient in APRC1B. We also show that the combined deficiency of ARPC1B in iNeutrophils and endothelium results in further reduction in neutrophil migration. Taken together, these results suggest that ARPC1B in endothelium is sufficient to drive neutrophil behavior. Summary statementThe actin regulator ARPC1B in both neutrophils and endothelium drives neutrophil motility.

cell biology↗

Modeling Sepsis-Associated ARDS Using a Lung Endothelial Microphysiological System

Acute respiratory distress syndrome due to non-pulmonary causes exhibits prominent endothelial activation which is challenging to assess in critically ill patients. Preclinical in vivo models of sepsis and ARDS have failed to yield useful therapies in humans, perhaps due to interspecies differences in inflammatory responses. Use of microphysiological systems (MPS) offer improved fidelity to human biological responses and better predict pharmacological responses than traditional culture. We adapted a lung endothelial MPS based on the LumeNEXT platform to evaluate the effect of plasma from critically ill sepsis patients on endothelial permeability, adhesion molecule expression and inflammatory cytokine production. Lumens incubated with sepsis plasma exhibited areas of contraction, loss of cellular coverage, and luminal defects. Sepsis plasma-incubated lumens had significantly increased permeability compared to lumens incubated with healthy donor plasma. ICAM-1 expression increased significantly in lumens incubated with sepsis plasma compared with those incubated with healthy control plasma, while concentrations of IL-6, IL-18, and soluble VEGF-R1 increased in sepsis plasma before and after incubation in the MPS compared with healthy control plasma. Use of the lung endothelial MPS may enable interrogation of specific mechanisms of endothelial dysfunction that promote ARDS in sepsis patients.

cell biology↗

Immune Cells and Inflammatory mediators cause endothelial dysfunction in a vascular microphysiological system

Functional assessment of endothelium serves as an important indicator of vascular health and is compromised in vascular disorders including hypertension, atherosclerosis, and preeclampsia. Endothelial dysfunction in these cases is linked to dysregulation of the immune system involving both changes to immune cells and increased secretion of inflammatory cytokines. Herein, we utilize a well-established microfluidic device to generate a 3-dimensional vascular Microphysiological System (MPS) consisting of a tubular blood vessel lined with Human Umbilical Vein Endothelial Cells (HUVECs) to evaluate endothelial function measured via endothelial permeability and Ca2+ signaling. We evaluated the effect of a mixture of factors associated with inflammation and cardiovascular disease (TNF, VEGF-A, IL-6 at 10ng/ml each) on vascular MPS and inferred that inflammatory mediators contribute to endothelial dysfunction by disrupting the endothelial barrier over a 48-hour treatment and by diminishing coordinated Ca2+ activity over a 1-hour treatment. We also evaluated the effect of peripheral blood mononuclear cells (PBMCs) on endothelial permeability and Ca2+ signaling in the HUVEC MPS. HUVECs were co-cultured with PBMCs either directly wherein PBMCs passed through the lumen or embedded in the supporting collagen hydrogel. We revealed that Phytohemagglutinin (PHA)-M activated PBMCs cause endothelial dysfunction in MPS both through increased permeability and decreased coordinated Ca2+ activity compared to non-activated PBMCs. Our MPS has potential applications in modeling cardiovascular disorders and screening for potential treatments using measures of endothelial function.

bioengineering↗

Naive primary neutrophils play a dual role in the tumor microenvironment

The tumor microenvironment (TME) is characterized by a network of cancer cells, recruited immune cells and extracellular matrix (ECM) in a hypoxic microenvironment. However, the specific role of neutrophils during tumor development, and their interactions with other immune cells is still not well understood. Thus, there is a need to investigate the interaction between primary neutrophils and natural killer cells and the resulting effects on tumor development. Here we use both standard well plate culture and an under oil microfluidic (UOM) assay with an integrated extracellular cell matrix (ECM) bridge to elucidate how naive primary neutrophils respond to both patient derived tumor cells and tumor cell lines. Our data demonstrated that both patient derived head and neck squamous cell carcinoma (HNSCC) tumor cells and MDA-MB-231 breast cancer cells trigger cluster formation in neutrophils, and the swarm of neutrophils restricts tumor invasion through the generation of reactive oxygen species (ROS) and neutrophil extracellular trap (NETs) release within the neutrophil cluster. However, we also observed that the presence of neutrophils downregulates granzyme B in NK-92 cells and the resulting NETs can obstruct NK cells from penetrating the tumor mass in vitro suggesting a dual role for neutrophils in the TME. Further, using label-free optical metabolic imaging (OMI) we observed changes in the metabolic activities of primary neutrophils during the different swarming phases when challenged with tumor cells. Finally, our data demonstrates that neutrophils in direct contact, or in close proximity, with tumor cells exhibit greater metabolic activities (lower nicotinamide adenine dinucleotide phosphate (NAD(P)H) mean lifetime) compared to non-contact neutrophils.

cell biology↗

A high-throughput nematode sensory assay reveals an inhibitory effect of ivermectin on parasite gustation

Sensory pathways first elucidated in Caenorhabditis elegans are conserved across free-living and parasitic nematodes, even though each species responds to a diverse array of compounds. Most nematode sensory assays are performed by tallying observations of worm behavior on two-dimensional planes using agarose plates. These assays have been successful in the study of volatile sensation but are poorly suited for investigation of water-soluble gustation or parasitic nematodes without a free-living stage. In contrast, gustatory assays tend to be tedious, often limited to the manipulation of a single individual at a time. We have designed a nematode sensory assay using a microfluidics device that allows for the study of gustation in a 96-well, three-dimensional environment. This device is suited for free-living worms and parasitic worms that spend their lives in an aqueous environment, and we have used it to show that ivermectin inhibits the gustatory ability of vector-borne parasitic nematodes.

molecular biology↗

Microbial Community Interactions on a Chip

Multispecies microbial communities drive most ecosystems on Earth. Chemical and biological interactions within these communities can affect survival of individual members and the entire community. However, the prohibitively high number of possible interactions within a microbial community has made the characterization of factors that influence community development challenging. Here we report a Microbial Community Interaction (CI) device to advance the systematic study of chemical and biological interactions within a microbial community. The CI creates a combinatorial landscape made up of an array of triangular wells interconnected with circular wells, which each contains either a different chemical or microbial strain, generating chemical gradients and revealing biological interactions. Bacillus cereus UW85 containing GFP provided the "target" readout in the triangular wells, and antibiotics or microorganisms in adjacent circular wells are designated the "variables". The CI device revealed that gentamicin and vancomycin are antagonistic to each other in inhibiting the target B. cereus UW85, displaying weaker inhibitory activity when used in combination than alone. We identified three-member communities constructed with isolates from the plant rhizosphere that increased or decreased growth of B. cereus. The CI device enables both strain-level and community-level insight. The scalable geometric design of the CI device enables experiments with high combinatorial efficiency, thereby providing a simple, scalable platform for systematic interrogation of three-factor interactions that influence microorganisms in solitary or community life.

microbiology↗

Transendothelial migration induces differential migration dynamics of leukocytes in tissue matrix

Leukocyte extravasation into inflamed tissue is a complex process that is difficult to capture as a whole in vitro. We employed a blood-vessel-on-a-chip model in which endothelial cells were cultured in a tube-like lumen in a collagen-1 matrix. The vessels are leak-tight, creating a barrier for molecules and leukocytes. Addition of inflammatory cytokine TNF- caused vasoconstriction, actin remodelling and upregulation of ICAM-1. Introducing leukocytes into the vessels allowed real-time visualisation of all different steps of the leukocyte transmigration cascade including migration into the extracellular matrix. Individual cell tracking over time distinguished striking differences in migratory behaviour between T-cells and neutrophils. Neutrophils cross the endothelial layer more efficiently than T-cells, but upon entering the matrix, neutrophils display high speed but low persistence, whereas T-cells migrate with low speed and rather linear migration. In conclusion, 3D imaging in real-time of leukocyte extravasation in a vessel-on-a-chip enables detailed qualitative and quantitative analysis of different stages of the full leukocyte extravasation process in a single assay. SummaryA functional hydrogel-based blood-vessel-on-a-chip model is used to study the complete leukocyte transendothelial migration process in real time. T-lymphocytes and neutrophils exhibit distinct migration dynamics in the extravascular matrix after transendothelial migration, which can be altered using a chemotactic gradient.

cell biology↗

Enhanced Immunoprecipitation Techniques for the Identification of RNA Binding Protein Partners: CRD-BP interactions in mammary epithelial cells

RNA binding proteins (RBPs) regulate expression of large cohorts of RNA species to affect programmatic changes in cellular phenotypes. In order to describe the function of RBPs within a cell, it is key to identify their mRNA binding partners. This is often done by cross-linking nucleic acids to RBPs, followed by chemical release of the nucleic acid fragments for analysis. However, this methodology is lengthy, involves complex processing leading to extraordinary losses, requires large amounts of starting materials, and is prone to artifacts due to the labile nature of mRNA. To evaluate potential alternative technologies, we tested "exclusion-based" purification of immunoprecipitates (oil-based IFAST or air-based SLIDE), and report here that these methods can efficiently, rapidly and specifically isolate RBP-RNA complexes with minimal handling. The analysis starts with >100x less material than for techniques that include cross-linking. Depending on the specific antibody used, 50-100% of starting protein is retrieved, allowing the assay of endogenous levels of RBP instead of tagged and over-expressed ectopic proteins. Isolated protein and nucleic acid components are purified and analyzed using standard techniques to provide a comprehensive portrait of RBP complexes. Using exclusion-based techniques, we show that the mRNA binding partners for CRD-BP/IMP1/IGF2BP1/ZBP1 in cultured mammary epithelial cells are enriched in mRNAs important for de-toxifying superoxides (glutathione metabolic enzymes) and other mRNAs encoding mitochondrial proteins.

molecular biology↗

Under-oil autonomously regulated oxygen microenvironments for cell culture

Oxygen levels in vivo are autonomously regulated by a supply-demand balance, which can be altered in disease states. However, the oxygen levels of in vitro cell culture systems, particularly microscale cell culture, are typically dominated by either supply or demand. Further, the oxygen microenvironment in these systems are rarely monitored or reported. Here, we present a method to establish and dynamically monitor autonomously regulated oxygen microenvironments (AROM) using an oil overlay in an open microscale cell culture system. Using this method, the oxygen microenvironment is dynamically regulated via a supply-demand balance of the system. We simulate the kinetics of oxygen diffusion in multiliquid-phase microsystems on COMSOL Multiphysics and experimentally validate the method using a variety of cell types including mammalian, fungal and bacterial cells. Finally, we demonstrate the utility of this method to establish a co-culture between primary intestinal epithelial cells and a highly prevalent human gut species Bacteroides uniformis.

bioengineering↗

Autofluorescence imaging of 3D tumor-macrophage microscale cultures resolves spatial and temporal dynamics of macrophage metabolism

Macrophages within the tumor microenvironment (TME) exhibit a spectrum of pro-tumor and anti-tumor functions, yet it is unclear how the TME regulates this macrophage heterogeneity. Standard methods to measure macrophage heterogeneity require destructive processing, limiting spatiotemporal studies of function within the live, intact 3D TME. Here, we demonstrate two-photon autofluorescence imaging of NAD(P)H and FAD to non-destructively resolve spatiotemporal metabolic heterogeneity of individual macrophages within 3D microscale TME models. Fluorescence lifetimes and intensities of NAD(P)H and FAD were acquired at 24, 48, and 72 hours post-stimulation for mouse macrophages (RAW 264.7) stimulated with IFN-{gamma} or IL-4 plus IL-13 in 2D culture, validating that autofluorescence measurements capture known metabolic phenotypes. To quantify metabolic dynamics of macrophages within the TME, mouse macrophages or human monocytes (RAW264.7 or THP-1) were cultured alone or with breast cancer cells (mouse PyVMT or primary human IDC) in 3D microfluidic platforms. Human monocytes and mouse macrophages in tumor co-cultures exhibited significantly different FAD mean lifetimes and greater migration than mono-cultures at 24, 48, and 72 hours post-seeding. In co-cultures with primary human cancer cells, actively-migrating monocyte-derived macrophages had greater redox ratios (NAD(P)H/FAD intensity) compared to passively-migrating monocytes at 24 and 48 hours post-seeding, reflecting metabolic heterogeneity in this sub-population of monocytes. Genetic analyses further confirmed this metabolic heterogeneity. These results establish label-free autofluorescence imaging to quantify dynamic metabolism, polarization, and migration of macrophages at single-cell resolution within 3D microscale models. This combined culture and imaging system provides unique insights into spatiotemporal tumor-immune crosstalk within the 3D TME.

bioengineering↗