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Weaver, A.

Publications and source records attributed to Weaver, A..

17 recordsLinked to original sources

Extracellular vesicle cross-linking coupled with solid-phase purification facilitates discovery of ribonucleoprotein complexes assembled on EV RNAs.

Extracellular vesicles (EVs) are fundamental mediators of intercellular communication that transfer macromolecular cargo, including proteins and RNAs, to functionally reprogram recipient cells. However, the molecular processes by which transferred ribonucleoprotein (RNP) complexes engage recipient host machinery to influence cellular behavior are poorly understood, primarily due to a dearth of methods capable of tracking these post-transfer interactions. To address this gap, we developed two complementary chemical biology platforms: EV-CLASP and EV(r)-CLASP. While EV-CLASP maps the native, intra-vesicular RNP landscape packaged within the EV, EV(r)-CLASP captures post-transfer dynamics by identifying the host proteins that directly associate with EV-derived RNAs following cellular uptake. Both approaches leverage metabolic labeling and photo-crosslinking for high-specificity recovery. Donor cells are cultured with 4-thiouridine (4SU) to biosynthetically label newly synthesized RNAs during EV biogenesis. Purified EVs can be crosslinked using 365 nm UV light to capture intra-vesicular RNP composition. Alternatively, 4SU-labeled EVs can be delivered to recipient cells and subsequently crosslinked to identify the primary physical interactions formed within the recipient-cell environment. Crosslinked RNP complexes are isolated under stringent conditions using solid-phase reversible beads to minimize background, followed by quantitative mass spectrometry for protein identification. Together, EV-CLASP and EV(r)-CLASP provide a robust, versatile framework for defining the dynamic RNP assemblies that facilitate extracellular RNA communication, offering a powerful toolkit to uncover novel RNA-associated regulatory networks, therapeutic targets, and biomarkers across diverse biological and disease contexts.

cancer biology↗

Fluid shear stress modulates endocytic pathways and junctional targeting of tumor-derived extracellular vesicles in endothelial cells

Breast cancer is the most common malignancy in women, with triple-negative breast cancer (TNBC) representing the most aggressive subtype and carrying a poor metastatic prognosis. Metastasis requires tumor cells to cross the endothelial barrier, a process facilitated by tumor-derived extracellular vesicles (EVs), which can disrupt vascular integrity. Fluid shear stress (FSS), generated by blood flow, shapes endothelial physiology and may influence EV uptake, yet the mechanisms underlying TNBC-derived small EV (sEV) internalization remain unclear. Here, we investigated TNBC sEV-endothelial interactions using combined in silico and in vitro approaches. Human umbilical vein endothelial cells (HUVECs) were cultured under static or FSS conditions (20 dyn/cm{superscript 2}), followed by proteomic profiling and protein-protein interaction analyses with sEV proteomes. Uptake assays employed pharmacological inhibition (Dynasore, M{beta}CD, Pitstop2), Caveolin-1 (CAV-1) and Clathrin Heavy Chain (CLHC), siRNA-mediated knockdown, and junctional interaction analyses via confocal microscopy and co-immunoprecipitation. FSS downregulated proliferation- and angiogenesis-associated proteins while upregulating adhesion and cytoskeletal regulators assessed by proteomics. Network analysis identified clathrin- and caveolin-mediated endocytosis (CME and CavME), integrins, and early endosomes as central mediators of sEV uptake. Functionally, uptake was reduced by Pitstop2, M{beta}CD, and CAV-1/CLHC knockdown under static conditions, but silencing paradoxically enhanced uptake under FSS, suggesting compensatory flow-dependent pathways. Notably, under FSS, sEVs accumulated at endothelial junctions, colocalizing with VE-CAD and associating with CLDN5, indicating a potential disruption mechanism of adherens and tight junctions and consequent endothelial permeability. These findings identify CME and CavME as key uptake routes while underscoring FSS as a critical determinant of endothelial-tumor EV interactions. By revealing junctional targeting of sEVs, this work provides new mechanistic insight into vascular remodeling during metastasis and highlights EV pathways as potential therapeutic targets in TNBC. Graphical Abstract O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=104 SRC="FIGDIR/small/721946v1_ufig1.gif" ALT="Figure 1"> View larger version (25K): org.highwire.dtl.DTLVardef@f91c5org.highwire.dtl.DTLVardef@2b4dc8org.highwire.dtl.DTLVardef@ff94f1org.highwire.dtl.DTLVardef@18b714b_HPS_FORMAT_FIGEXP M_FIG C_FIG Uptake and localization of sEVs on HUVEC under (a) static and (b) fluid shear-stress conditions. sEVs: Small Extracellular Vesicles. CME: Clathrin-mediated Endocytosis. CavME: Caveolin-mediated Endocytosis. CLDN5: Claudin-5. VE-CAD: Vascular Endothelial Cadherin. FSS: Fluid shear-stress.

cancer biology↗

Cardiac PIEZO 1 Channels Modulate Anxiety

Increases in conscious cardiac interoception explain the ability of some individuals with anxiety to "feel" their heartbeat without taking their pulse. Subconscious cardiac interoception is the detection of heart signals from baroreceptors without subjective awareness. We tested our hypothesis that contrasting sensitivity of PIEZO 1 stretch channels mediates both forms of cardiac interoception and feelings of anxiety. In healthy volunteers, we found conscious cardiac interoception assessed by measuring heartbeat detection accuracy was increased with lower heart rates and greater stroke volumes and cardiac stretch but not associated with anxiety. Disruption of Piezo 1 in cardiac sensory neurons enhanced anxiety in rodents. Accordingly, we used an ex vivo assay of PIEZO 1 sensitivity to correlate subconscious cardiac interoception with anxiety in men and women. When compared to healthy individuals with lower PIEZO 1 sensitivity, men and women with higher PIEZO 1 activity had marked diminution in state anxiety. Those with lower anxiety also had enhanced variability in their instantaneous baroreceptor sensitivity at rest and reduced cardiac rate pressure products following stress. We propose that a reduction in PIEZO 1 sensitivity causes errors in "predictive coding;" the imbalance between expected and actual heart rate responses to changes in blood pressure leads to anxiety and increased cardiac workloads. We also report testosterone, which is anxiolytic, enhanced, whereas the stress hormone corticosterone, decreased Piezo 1 gene transcription. Selectively enhancing subconscious interoception by increasing PIEZO 1 sensitivity may improve predictive coding, cardiovascular outcomes, and ameliorate the subjective manifestations of anxiety.

physiology↗

Identification and inhibition of the Cyclin D Rb-docking interface that drives cell division

The animal cell division cycle is initiated by the cyclin-dependent kinases CDK4 and CDK6 in complex with D-type cyclins. Cyclin D-CDK4/6 complex formation is promoted by the assembly factors p21 and p27, which bind both subunits. p27 binds the hydrophobic patch on cyclin D that is similar to the patch used by other cell cycle cyclins to dock their substrates. This raised the question as to how cyclin D could find its substrates if its hydrophobic patch were already occupied? Here, we show that D-type cyclins use their A2 helix to dock the retinoblastoma protein Rb, a key substrate regulating cell cycle progression. The specific interface of cyclin Ds A2 helix is unique among cyclins and its mutation slows proliferation. Taken together, our work identifies a cyclin D-substrate docking mechanism that can be targeted by novel cancer therapeutics.

biochemistry↗

Small Extracellular Vesicle Cargoes Associated with Lymph Node Metastasis in Head and Neck Cancer

Head and neck squamous cell carcinoma (HNSCC) is a highly aggressive malignancy in which cervical lymph node metastasis critically determines patient prognosis. Despite advances in clinical staging based on tumor size, depth of invasion, and nodal status, these parameters fail to capture the biological heterogeneity of HNSCC, leading to overtreatment or undertreatment, and significant morbidity. Emerging evidence implicates small extracellular vesicles (SEVs) as key mediators of tumor progression and promising biomarkers for metastatic potential. In this study, we performed iTRAQ-based proteomic profiling of SEVs from metastatic (MOC2) and nonmetastatic (MOC1) HNSCC mouse cell lines and identified multiple cargoes associated with metastatic processes, including angiogenesis, extracellular matrix remodeling, immune modulation, and perineural invasion. Further, we employed an immune-competent orthotopic mouse oral carcinoma (MOC) model to investigate how exosome biogenesis affects HNSCC metastasis. Loss of the exosome/SEV biogenesis protein HRS in MOC2 HNSCC cells impaired SEV formation in vitro and tumor growth and metastasis in vivo. Consistent with the SEV cargoes enriched in MOC2 EVs, immunohistochemical analyses of MOC2 tumors revealed reduced blood vessel and nerve density in HRS-deficient tumors. Analysis of candidate biomarker SEV cargoes in the circulating EVs from HPV-negative HNSCC patients revealed significant correlations of these proteins with metastatic status. Collectively, these findings identify SEV cargoes as potential functional mediators of metastasis and liquid biopsy biomarkers in HNSCC.

cancer biology↗

Exosomes are specialized vehicles to induce fibronectin assembly

Fibronectin is a key stromal matrix molecule whose assembly into fibrils is thought to require cells. In contrast, we find that small exosome-type extracellular vesicles (EVs) are critical initiators of fibronectin assembly. Fibroblasts engineered to be deficient in exosome secretion showed greatly reduced assembly of fibronectin and other stromal matrix molecules in 2D, 3D, and in vivo environments, and led to reduced tumor growth and lung metastasis by breast cancer cells. Furthermore, transgenic mice with defects in exosome secretion had greatly reduced lung fibrosis after treatment with bleomycin. In a direct test of exosome function, we find that the addition of purified small EVs to purified soluble fibronectin in a cell-free system is sufficient to induce fibronectin assembly. The EV-induced fibronectin assembly requires the presence of fibronectin-binding integrins and Syndecan-1 in the EVs. We propose a new model in which secreted exosomes directly drive stromal matrix assembly and tissue fibrosis.

cell biology↗

Macromolecular Diamidobenzimidazole Conjugates Activate STING

Pharmacologic activation of the stimulator of interferon genes (STING) pathway has broad potential applications, including the treatment of cancer and viral infections, which has motivated the synthesis and testing of a diversity of STING agonists as next generation immunotherapeutics. A promising class of STING agonists are the non-nucleotide, small molecule, dimeric-amidobenzimidazoles (diABZI), which have been recently used in the synthesis of polymer- and antibody-drug conjugates to improve pharmacokinetics, modulate biodistribution, and to confer other favorable properties for specific disease applications. These approaches have leveraged diABZI variants functionalized with reactive handles and enzyme-cleavable linkers at the 7-position of the benzimidazole for conjugation to and tunable drug release from carriers. However, since this position does not interact with STING and is exposed from the binding pocket when bound in an "open lid" configuration, we sought to evaluate the activity of macromolecular diABZI conjugates that lack enzymatic release and are instead conjugated to polymers via a stable linker. By covalently ligating diABZI to 5 or 20 kDa mPEG chains via an amide bond, we surprisingly found that these conjugates could activate STING in vitro. To further evaluate this phenomenon, we designed a diABZI-functionalized RAFT chain transfer agent that provided an enabling tool for synthesis of large, hydrophilic, dimethylacrylamide (DMA) polymers directly from a single agonist and we found that these conjugates also elicited STING activation in vitro with similar kinetics to highly potent small molecule analogs. We further demonstrated the in vivo activity of these macromolecular diABZI platforms, which inhibited tumor growth to a similar extent as small molecule variants. Using flow cytometry and fluorescence microscopy to evaluate intracellular uptake and distribution of Cy5-labeled analogs, our data indicate that although diABZI-DMA conjugates enter cells via endocytosis, they can still colocalize with the ER, suggesting that intracellular trafficking processes can promote delivery of endocytosed macromolecular diABZI compounds to STING. In conclusion, we have described new chemical strategies for the synthesis of stable macromolecular diABZI conjugates with unexpectedly high immunostimulatory potency, findings with potential implications for the design of polymer-drug conjugates for STING agonist delivery that also further motivate investigation of endosomal and intracellular trafficking as an alternative route for achieving STING activation.

bioengineering↗

Human and Mouse Models for Kabuki Syndrome Reveal Increase in Inhibitory Synapse Development.

Intellectual disability, affecting 2-3% of the general population, often co-occurs with neurodevelopmental disorders and is frequently caused by mutations that impair synaptic function. Kabuki syndrome (KS), a rare multisystem disorder associated with developmental delay and intellectual disability, results from mutations in either KMT2D (KS1) or KDM6A (KS2), encoding a histone methyltransferase and demethylase, respectively. The mechanisms underlying intellectual disability in KS remain poorly understood. Here, we generated human iPS cells carrying conditional Cre/lox-dependent loss-of-function mutations in KMT2D or KDM6A and differentiated them into excitatory or inhibitory neurons. Analysis revealed that KS1 and KS2 inhibitory neurons unexpectedly showed increased GABAergic synapse formation, whereas excitatory neurons displayed reduced synapse development and impaired synaptic transmission. We confirmed these findings in hippocampal neurons in vitro and in vivo using a mouse model for KS1 demonstrating a bidirectional shift: increase in inhibition and decrease in excitation. Synapse numbers and synaptic transmission in brain slices were shifted to increased inhibition/excitation ratio. Mechanistically, KS1 mutations activated neuroinflammatory signaling, impaired astrocytic function, and promoted glia-driven inhibitory synapse formation in human neurons. By integrating human neuron models with conditional KMT2D/KDM6A deletions and a Kmt2d-mutant mouse model, we identify a novel synaptic disease mechanism in KS that links chromatin remodeling defects to disrupted information transfer in neural circuits, providing a mechanistic explanation for intellectual disability. Significance StatementKabuki syndrome, a rare disorder with intellectual disability, is caused by mutations in the chromatin regulators KMT2D and KDM6A, yet its cellular pathophysiology has remained unclear. Using new Cre/lox-inducible human neuron models together with a mouse model, we reveal a conserved excitation-inhibition imbalance characterized by increased inhibitory and decreased excitatory synapse formation. Our findings establish the first mechanistic framework linking KMT2D/KDM6A mutations to synaptic dysfunction, uncover glial contributions to disease pathogenesis, and suggest potential therapeutic avenues for restoring synaptic balance. HighlightsO_LIKS1 and KS2 mutations cause decrease in excitatory synapses in human neurons C_LIO_LIKS1 and KS2 mutations cause increase in inhibitory synapses in human neurons C_LIO_LIKS1 mutation causes decrease in excitatory and increase in inhibitory synapses in mice C_LIO_LIKS1 mutant mouse astrocytes facilitate increase in inhibitory synapses in human neurons C_LI

neuroscience↗

A Drosophila holidic diet optimised for growthand development

Diets composed of chemically pure components (holidic diets) are useful for determining the metabolic roles of individual nutrients. For the model organism Drosophila melanogaster, existing holidic diets are unable to support rapid growth characteristic of the larval stage. Here, we use a nutrient co-optimisation strategy across more than 50 diet variants to design HoldFast, a holidic medium tailored to fast larval growth and development. We identify dietary amino acid ratios optimal for developmental speed but show that they compromise survival unless vitamins and sterols are co-optimised. Rapid development on HoldFast is not improved by adding fatty acids but it is dependent upon their de novo synthesis in the fat body via fatty acid synthase (FASN). HoldFast outperforms other holidic diets, supporting rates of growth and development close to those of yeast-based diets and, under germ-free conditions, identical. HoldFast provides new opportunities for studying growth and metabolism during Drosophila development.

developmental biology↗

Synthesis and in vitro evaluation shows disquaramide compounds are a promising class of anti-leishmanial drugs

An increasing number of treatment failures with current pharmaceutics, as well as a lack of a vaccine, demonstrates the need to develop new treatment options for leishmaniasis. Herein, we describe the synthesis and in vitro analysis of 24 disquaramide compounds targeting the Leishmania major parasite. Of the compounds that were evaluated, six of them (13, 19, 20, 22, 24, and 26) were capable of significantly decreasing the number of parasites by up to 42% compared to the control by day four. This demonstrates that disquaramides either impair parasite replication or have leishmancidal effects. Additionally, none of the disquaramide compounds tested displayed host cell cytotoxicity. These experiments provide evidence that disquaramides have the potential to be effective anti-leishmanial therapeutics.

microbiology↗

Enhanced translational activity is linked to lymphatic endothelial cell activation in cutaneous leishmaniasis

Cutaneous leishmaniasis (CL) is a significant public health problem leading to permanently disfiguring skin lesions caused by Leishmania parasites. Lesion severity stems from an excessive host inflammatory response that prevents healing. Here, we characterized the transcriptional and translational responses of lymphatic endothelial cells (LECs) during murine CL using historical single-cell RNA sequencing data combined with flow cytometry and in vivo puromycin incorporation to assess translational activity. We identified upregulation of antigen presentation pathways including MHC-I, MHC-II, and immunoproteasome transcripts in dermal LECs from Leishmania major-infected mice compared to naive controls. LECs also exhibited increased expression of guanylate binding proteins and interferon-inducible genes, indicative of immune activation. Moreover, our findings demonstrate that LECs in leishmanial lesions displayed heightened translational activity relative to LECs from uninflamed ears, and LEC translational activity was highest in activated LECs. Furthermore, LEC translational activity exceeded that of other cell types within the lesion microenvironment. Validating the transcriptomic data, LECs in lesions expressed elevated MHC-II and programmed death-ligand 1 (PDL-1), supporting their potential role in antigen presentation. Functional assays using DQ-OVA confirmed that LECs from leishmanial lesions efficiently uptake and process antigens, highlighting their capability as antigen presenting cells in the inflamed dermal microenvironment. Overall, our study reveals the activation status of LECs in leishmanial lesions, shedding light on their potential role in shaping local immunity and inflammation in a variety of skin diseases.

microbiology↗

miR-100 and miR-125b Contribute to Enhanced Growth and Invasiveness

Extracellular communication via the transfer of vesicles and nanoparticles is now recognized to play an important role in tumor microenvironment interactions. Cancer cells upregulate and secrete abundant levels of miR-100 and miR-125b that can alter gene expression by both cell- and non-cell-autonomous mechanisms. We previously showed that these miRNAs activate Wnt signaling in colorectal cancer (CRC) through noncanonical pairing with 5 negative regulators of Wnt signaling. To identify additional targets of miR-100 and miR-125b, we used bioinformatic approaches comparing multiple CRC cell lines, including knockout lines lacking one or both of these miRNAs. From an initial list of 96 potential mRNA targets, we tested 15 targets with 8 showing significant downregulation in the presence of miR-100 and miR-125b. Among these, Cingulin (CGN) and Protein tyrosine phosphatase receptor type-R (PTPRR) are downregulated in multiple cancers, consistent with regulation by increased levels of miR-100 and miR-125b. We also show that increased cellular levels of miR-100 and miR-125b enhance 3D growth and invasiveness in CRC and glioblastoma cell lines. Lastly, we demonstrate that extracellular transfer of miR-100 and miR-125b can silence both reporter and endogenous mRNA targets in recipient cells and also increase the invasiveness of recipient spheroid colonies when grown under 3D conditions in type I collagen.

cancer biology↗

Analysis of small EV proteomes reveals unique functional protein networks regulated by VAP-A

Extracellular vesicles (EVs) influence cell phenotypes and functions via protein, nucleic acid and lipid cargoes. EVs are heterogeneous, due to diverse biogenesis mechanisms that remain poorly understood. Our previous study revealed that the endoplasmic rectiulum (ER) membrane contact site (MCS) linker protein VAP-A drives biogenesis of a subset of RNA-enriched EVs. Here, we examine the protein content of VAP-A-regulated EVs. Using label-free proteomics, we identified down- and up-regulated proteins in sEVs purified from VAP-A knockdown (KD) colon cancer cells. Gene set enrichment analysis (GSEA) of the data revealed protein classes that are differentially sorted to SEVs dependent on VAP-A. STRING protein-protein interaction network analysis of the RNA-binding protein (RBP) gene set identified several RNA functional machineries that are downregulated in VAP-A KD EVs, including ribosome, spliceosome, mRNA surveillance, and RNA transport proteins. We also observed downregulation of other functionally interacting protein networks, including cadherin-binding, unfolded protein binding, and ATP-dependent proteins. Significance of the studyLittle is known about biogenesis mechanisms that underlie EV heterogeneity. This study explores the protein repertoire of a specific subset of EVs that we recently identified to be generated at ER MCS and that are highly enriched in RNAs. We find that proteins from several classes of RNA machineries, including spliceosomes, are downregulated in EVs purified from cells knocked down for the ER MCS linker protein VAP-A. These data suggest that dynamic regulation of these protein machineries at ER MCS are involved in the sorting of RNA-RBP complexes into EVs.

cell biology↗

EV Fingerprinting: Resolving extracellular vesicle heterogeneity using multi-parametric flow cytometry

Mammalian cells release a heterogeneous array of extracellular vesicles (EVs) that impact human biology by contributing to intercellular communication. To resolve EV heterogeneity and define the EV populations associated with specific biological processes, we developed a method named "EV Fingerprinting" that discerns distinct vesicle populations using dimensional reduction of multi-parametric data collected by quantitative single-EV flow cytometry. After validating this method against synthetic standards, the EV Fingerprinting analysis of highly purified EVs enabled a much more granular resolution of biochemically distinct EV populations than previously established methods. The analysis of EVs produced after molecular perturbation of EV biogenesis through ablation of the GTPase Rab27a and overexpression of the tetraspanin CD63 revealed that EV Fingerprinting reflects the molecular state of a cell. Subsequent analysis of human plasma demonstrates the capacity of EV Fingerprinting to resolve EV populations in complex biological samples and detect tumor-cell derived EVs.

cell biology↗

Extracellular vesicles from non-neuroendocrine SCLC cells promote adhesion and survival of neuroendocrine SCLC cells

Small Cell Lung Cancer (SCLC) tumors are made up of distinct cell subpopulations, including neuroendocrine (NE) and non-NE cells. While secreted factors from non-NE SCLC cells have been shown to support the growth of the NE cells, the underlying molecular factors are not well understood. Here, we show that exosome-type small extracellular vesicles (SEVs) secreted from non-NE SCLC cells promote adhesion and survival of NE SCLC cells. Proteomic analysis of purified small EVs revealed that extracellular matrix (ECM) proteins and integrins are highly enriched in small EVs of non-NE cells whereas nucleic acid-binding proteins are enriched in small EVs purified from NE cells. Addition of select purified ECM proteins identified in purified EVs, specifically fibronectin, laminin 411, and laminin 511, were able to substitute for the role of non-NE-derived SEVs in promoting adhesion, survival, and tumorigenicity of NE SCLC cells. Those same proteins were differentially expressed by human SCLC subtypes. These data suggest that ECM-carrying SEVs secreted by non-NE cells play a key role in supporting SCLC tumor growth and survival.

cancer biology↗

Dynamic Laser Speckle Imaging meets Machine Learning to enable Rapid Antibacterial Susceptibility Testing (DyRAST)

Rapid antibacterial susceptibility testing (RAST) methods which measure change of a bacterial phenotype in response to a given treatment are of significant importance in healthcare, as they can assist care-givers in timely administration of the right treatment. Various RAST techniques have been reported for tracking bacterial phenotypes, such as size, shape, motion, and metabolic activity. However, they still require bulky and expensive instruments (which hinders their application in resource-limited environments) and/or utilize labeling reagents (which can interfere with antibiotics and add to cost). Furthermore, the existing ultra-rapid methods do not address possible adaptation of gradual adaptation of bacteria to antibiotics, which can lead to false interpretation of resistance when using ultra-rapid methods. In this work, we present a RAST approach leveraging machine learning analysis of time-resolved dynamic laser speckle imaging (DLSI) results to accurately predict the minimum inhibitory concentration (MIC) of a model strain of Escherichia coli in 60 minutes, compared to 6 hours using the currently FDA-approved phenotype-based RAST technique. To demonstrate the DLSI performance, we studied the effect of a {beta}-lactam ampicillin and an aminoglycoside gentamicin on Escherichia coli strain K-12. DLSI captures change of bacterial motion/division in response to treatment. The machine learning algorithm was trained and validated using the overnight results of gold standard, broth microdilution method. Empowered by machine learning, DyRAST can predict MIC with high accuracy comparable to gold standard methods through a voting strategy.

microbiology↗

Spheroplast-mediated carbapenem tolerance in Gram-negative pathogens

Antibiotic tolerance, the ability to temporarily sustain viability in the presence of bactericidal antibiotics, constitutes an understudied, yet likely widespread cause of antibiotic treatment failure. We have previously shown that the Gram-negative pathogen Vibrio cholerae is able to tolerate exposure to the typically bactericidal {beta}-lactam antibiotics by assuming a spherical morphotype devoid of detectable cell wall material. However, it is unclear how widespread tolerance is. Here, we have tested a panel of clinically significant Gram-negative pathogens for their response to the potent, broad-spectrum carbapenem antibiotic meropenem. We show that clinical isolates of Enterobacter cloacae, Klebsiella pneumoniae, and Klebsiella aerogenes, but not Escherichia coli, exhibit moderate to high levels of tolerance to meropenem, both in laboratory growth medium and in human serum. Importantly, tolerance was mediated by cell wall-deficient spheroplasts, which readily recovered to wild-type morphology and exponential growth upon removal of antibiotic. Our results suggest that carbapenem tolerance is prevalent in clinically significant bacterial species, and we suggest that this could contribute to treatment failure associated with these organisms.

microbiology↗