Biology subjects

An, H.

Publications and source records attributed to An, H..

At least 19 recordsLinked to original sources

bioRxiv2026

Longitudinal imaging of single cells in opaque tissue with cell chirp ultrasound

Small numbers of cells can determine the fate of an entire organism. For example, metastatic cancer cells seed distant organs, therapy-resistant clones repopulate tumors, and T cells infiltrate and expand in tissues with matching antigens. Visualizing the activity of such cells in living organisms requires highly sensitive, specific and repeatable imaging in optically opaque tissues. Here we introduce cell chirp, an ultrasound imaging method for real-time imaging of single cells in living organs inaccessible to light. Cell chirp exploits the harmonic response of genetically encoded gas vesicles to frequency-coded ultrasound to sensitively and specifically visualize single cells in scattering background. We first develop this method in tissue-mimicking phantoms, demonstrating the ability to quantitatively detect single cells as validated by optical cell counts. We then establish the ability of cell chirp to image thousands of genetically labeled cells within a million-cell background tissue, track reporter gene expression over days, and suppress background signals by more than two orders of magnitude. Finally, we use cell chirp to track the fate of antigen-positive or antigen-negative tumor-cell minorities during weeks-long T-cell engager treatments. Cell chirp reveals the dynamics of sparsely distributed, genetically defined cells in opaque tissues.

bioengineering↗

bioRxiv2026

Cytosolic MagLOV Magnetofluorescence in Mammalian Cell Lines and Primary Neurons

Magnetic fields can influence the outcome of photochemical reactions through the radical pair mechanism, but whether this sensitivity extends to standard experimental conditions in mammalian cells has remained unclear. Here, we quantify the cytosolic magnetofluorescence of MagLOV, a genetically encoded, flavin-binding fluorescent protein, in mammalian cells, validated against extensive artifact controls. Excitation intensity and magnetic field strength differentially tune response kinetics and amplitude, respectively, with amplitude saturating above approximately 8 mT. Magnetic field-effect amplitude is further modulated by cellular culture state. This response generalizes across HEK293T, HeLa, U2OS, and A549 cells and primary mouse cortical neurons, with plateau amplitudes ranging from 1.4% to 2.7%. Together, these results establish that genetically encoded spin-dependent photochemistry can be quantitatively interrogated under standard mammalian live-cell imaging conditions, and generalizes across mammalian cell types.

biophysics↗

bioRxiv2026

Task-evoked deactivations: dissociation between BOLD fMRI and FDG

Task-evoked decreases in blood-oxygenation-level-dependent (BOLD) signals are a well-recognized phenomenon in functional magnetic resonance imaging (fMRI) studies. These deactivations are most prominent in the default mode network (DMN), a set of regions most active at rest. The metabolic basis of task-induced BOLD fMRI deactivations remains unclear. To address this question, we used PET/MRI to simultaneously measure BOLD fMRI and cerebral glucose consumption (CMRglc) during visuomotor and language tasks in 22 cognitively unimpaired older adults (15 female, 7 male). Task performance increased BOLD signals in task-relevant regions and decreased BOLD signals in the DMN. Positive BOLD responses generally coincided with increases in CMRglc. In contrast, CMRglc did not decrease in regions showing negative BOLD responses; instead, it typically increased. In particular, the posterior cingulate cortex showed significant CMRglc elevations in conjunction with negative BOLD responses. Whole-brain intensity normalization partially restored task-induced decreases in CMRglc, indicating that relative reductions appear in regions in which CMRglc increases are smaller than the global average. Overall, our results imply that BOLD fMRI deactivations can occur in conjunction with stable or even increased glucose consumption.

neuroscience↗

bioRxiv2026

Astrocytes mediate the pro-cognitive value of α7nAChRs and of α7nAChR-targeting therapeutics

The 7-nicotinic acetylcholine receptor (7nAChR) has driven extensive research over the past three decades for its pro-cognitive potential. It is the leading druggable target for the cognitive deficits associated with schizophrenia and has motivated major pharmaceutical and clinical efforts to ameliorate similar impairments in other neurological disorders, such as Alzheimers disease (AD). Yet, a systematic evaluation of the role played by 7nAChR in cognition, and its mechanistic underpinnings, is still lacking. Here we report that 7nAChRs on principal and inhibitory forebrain neurons are largely inconsequential to mouse behavior, including in domains that are most sensitive to schizophrenia-related cognitive impairments. By contrast, loss of 7nAChR from astrocytes produces profound behavioral alterations that are cognitive domain-specific, are time-of-day dependent, coincide with reduced levels of the N-methyl D-aspartate receptor (NMDAR) co-agonist D-serine, and are fully restored by D-serine supplementation. Further, an 7nAChR partial agonist previously evaluated in Phase III trials for cognitive enhancement in schizophrenia and AD fails to augment behavior in mice lacking astrocytic 7nAChRs. Together, these findings identify astrocytes and D-serine/NMDAR signaling as a central mechanism through which 7nAChR, a major drug target, promotes cognitive behavior.

neuroscience↗

bioRxiv2026

Coexistent PTEN and PIK3CA alterations hyperactivate mTORC1 signaling in endometrial cancers and cause their selective sensitivity to mTORC1 inhibition

In approximately half of endometrial carcinoma (EC), PTEN loss-of-function and activating PI3K mutants coexist. Unlike cells with either single mutation, PTEN/PIK3CA coexistent alterations result in elevated membrane phosphatidylinositol (3,4,5)-trisphosphate (PIP3) levels and mTORC1 hyperactivation, rendering PI3K or AKT inhibition ineffective in blocking mTORC1 activity and tumor growth. The bi-steric mTORC1 kinase inhibitor, RMC-6272, suppresses mTORC1 activity and cell growth by reducing protein translation and cell cycle progression. In vivo, RMC-6272, but not PI3K inhibitors, effectively suppressed mTORC1 and growth of EC PDXs with coexistent PTEN/PIK3CA lesions. These findings are consistent with a phase I trial of bi-steric mTORC1 inhibitor RMC-5552, showing anti-tumor activity in patients with EC. PDXs with KRAS co-mutations regrew after RMC-6272 treatment, which was prevented by the addition of the RAS(ON) multi-selective inhibitor RMC-7977. Overall, these data suggest that mTORC1 hyperactivation drives ECs with coexistent PTEN/PIK3CA mutations, explain the limited antitumor activity of PI3K and AKT inhibitors, and support clinical evaluation of mTORC1 inhibitors as potential therapy for EC. SignificanceWe have found the mechanistic consequences of PTEN/PIK3CA co-alterations in endometrial tumors and that these mutations result in a profound hyperactivation of mTORC1 signaling. Single mutant tumors are sensitive to PI3K inhibition but those with both mutations are insensitive to PI3K or AKT inhibition but are exquisitely dependent on mTORC1 kinase. This provides strong preclinical rationale for targeting mTORC1, alone or combined with RAS inhibition (in RAS co-mutant tumors), as an effective therapeutic strategy.

cancer biology↗

bioRxiv2025

Plasma Ficolins Enable Liver Macrophages to Capture Blood-Borne Bacteria by Recognizing Capsular Polysaccharides

Ficolins are evolutionarily conserved glycan-binding lectins in plasma or on cell membranes of immune cells, yet their physiological functions remain to be defined. Here we demonstrate that plasma ficolins drives the capture of diverse encapsulated bacteria in the blood circulation by the liver resident macrophages (Kupffer cells). Ficolin-activated immunity in the liver sinusoids provides swift and sterilizing immunity in mice. Mice lacking ficolin-A (the only plasma ficolin) became hypersusceptible to the blood infections of the ficolin-A-recognizable bacterial serotypes. Mechanistically, plasma ficolins activate complement C3 on bacterial surfaces by pattern recognition of acetylated monosaccharides on polysaccharide capsules, and thereby deliver the opsonized bacteria to C3 receptors on Kupffer cells for phagocytic elimination. These findings reveal that plasma ficolins serve as pattern-recognition receptors that are essential for maintaining the bloodstream sterile.

microbiology↗

bioRxiv2025

Identification of a putative RBOHD-FERONIA-CRK10-PIP2;6 plasma membrane complex that interacts with phyB to regulate ROS production in Arabidopsis thaliana

O_LIReactive oxygen species (ROS) regulate plant growth, development, and responses to the environment. ROS production by the RESPIRATORY BURST OXIDASE PROTEIN D (RBOHD) protein was recently shown to be regulated by PHYTOCHROME B (phyB), and phyB was found to be phosphorylated by FERONIA, highlighting the possibility that these three proteins interact to regulate ROS levels during stress. C_LIO_LIImmunoprecipitation and proximity labelling, followed by split-luciferase and functional validation assays, were used to study the interactions between FERONIA, phyB, and RBOHD during excess light (EL) stress in Arabidopsis thaliana. C_LIO_LIWe reveal that phyB and FERONIA interact with RBOHD, that phosphorylation of phyB by FERONIA, as well as the kinase activity of FERONIA, are required for RBOHD-driven ROS production in response to EL stress, and that CYSTEINE-RICH RECEPTOR LIKE KINASE 10 (CRK10) and PLASMA MEMBRANE INTRINSIC PROTEIN 2;6 (PIP2;6) interact with RBOHD and phyB and are also required for EL-driven RBOHD ROS production. C_LIO_LIOur findings uncover the existence of a putative plasma membrane complex between FERONIA, RBOHD, CRK10, and PIP2;6 that interacts with phyB to regulate ROS production in Arabidopsis in response to stress. This complex could play a canonical role in the integration and regulation of multiple signaling pathways in plants. C_LI Plain Language SummaryWe identified a complex between several different proteins at the plasma membrane that interacts with the light and temperature receptor protein phytochrome B to regulate reactive oxygen species formation during stress in plants. This complex could be involved in the regulation and integration of multiple abiotic and biotic signals in plants. tenten

plant biology↗

bioRxiv2025

Activity-based probes and chemical proteomics reveal the potential of targeting HMGCS1 for cancer therapy

Mevalonate is a precursor for essential metabolites, such as isoprenoids and sterols. Its synthesis starts with HMGCS1 producing HMG-CoA, which is then converted to mevalonate by HMGCR, a target of statins. Cancer cells often upregulate enzymes in the mevalonate pathway (MVP) to meet their metabolic demands, leading to the development of inhibitors targeting several enzymes in this pathway. However, current inhibitors have not yet shown significant anti-cancer activity. While HMGCS1 has unique biochemical properties that distinguish it from other MVP enzymes, the effects of inhibiting HMGCS1 have not been thoroughly investigated. Here, we present a set of chemical probes that enable us to systematically assess the proteome-wide selectivity and potency of Hymeglusin, the primary inhibitor of HMGCS1 used in the field, confirming it as a useful tool for short-term HMGCS1 inhibition. Inhibiting HMGCS1 with Hymeglusin causes proteome changes that are nearly identical to those caused by inhibiting HMGCR or degrading HMGCS1. Accordingly, simultaneously targeting HMGCS1 and HMGCR effectively suppresses the growth of statin-resistant cells and xenograft models, without increasing the risk of side effects. Finally, we find that while Hymeglusin is a valuable tool for short-term mechanistic studies, its usefulness is limited for long-term efficacy studies due to its poor stability in serum. Together, this study highlights the biological implications of targeting HMGCS1 as monotherapy or in combination with statins, and caution is required when using Hymeglusin as a tool.

biochemistry↗

bioRxiv2025

Astrocytic MAOB-GABA axis as a molecular brake on repair following spinal cord injury

Neuroregeneration and remyelination rarely occur in the adult mammalian brain and spinal cord following central nervous system (CNS) injury. The glial scar has been proposed as a major contributor to this failure in the regenerative process. However, its underlying molecular and cellular mechanisms remain unclear. Here, we report that monoamine oxidase B (MAOB)-dependent excessive GABA release from reactive astrocytes suppresses CNS repair system by reducing BDNF and TrkB expression in severe spinal cord injury (SCI) animal models. Genetic deletion of MAOB in a mouse SCI model promotes both functional and tissue recovery. Notably, the selective MAOB inhibitor, KDS2010, facilitates recovery and regeneration by disinhibiting the BDNF-TrkB axis in a rat SCI model. Its dose-dependent effects were further validated in a monkey SCI model. Moreover, KDS2010 demonstrates a tolerable safety profile and dose-proportional pharmacokinetics in healthy humans during a phase 1 clinical trial. Our findings identify the astrocytic MAOB-GABA axis as a crucial molecular and cellular brake on CNS repair system following SCI and highlight translational potential of KDS2010 as a promising therapeutic candidate for SCI treatment.

neuroscience↗

bioRxiv2025

FUS post-transcriptional splicing is autoregulated via RNA condensation with therapeutic potential for ALS-FUS

Mutations in the FUS gene cause aggressive and often juvenile forms of amyotrophic lateral sclerosis (ALS-FUS). In addition to mRNA, the FUS gene gives rise to a partially processed RNA with retained introns 6 and 7. We demonstrate that these FUSint6&7-RNAs form nuclear condensates scaffolded by the highly structured intron 7 and associated with nuclear speckles. Using hybridization-proximity labelling proteomics, we show that the FUSint6&7-RNA condensates are enriched in splicing factors and the m6A reader YTHDC1. These ribonucleoprotein structures facilitate post-transcriptional FUS splicing and depend on m6A/YTHDC1 for their maintenance. FUSint6&7-RNAs become hypermethylated in cells expressing mutant FUS, leading to their enhanced condensation and consequently, splicing. We further demonstrate that FUS protein is repelled by m6A. Thus, ALS-FUS mutations may cause an abnormal activation of FUS post-transcriptional splicing via altered RNA methylation. Strikingly, ectopic expression of FUS intron 6&7 sequences dissolves the endogenous FUSint6&7-RNA condensates, downregulating FUS mRNA and protein. Overall, we describe an RNA condensation-dependent mechanism regulating FUS splicing that can be harnessed for developing new therapies.

cell biology↗

bioRxiv2025

Mouse Single-Cell Long-Read Splicing Atlas by Ouro-Seq

Alternative splicing creates cellular and phenotypic diversity; thus, characterizing splicing patterns across diverse cell types is essential for a comprehensive understanding of these cell types. However, existing full-length single-cell RNA-sequencing methods suffer from multiple technical limitations, such as the pervasive presence of reverse transcription artifacts across genes. Here, we introduce Ouro-Seq, a novel single-cell long-read sequencing framework with a versatile artifact removal mechanism for characterizing full-length mRNA species expressed by individual cells. We also developed a computational pipeline that identifies genuine full-length cDNAs and normalizes full-length mRNA size distributions for integration. Using Ouro-Seq, we constructed the Mouse Single-Cell Long-Read Splicing Atlas by collecting full-length transcriptomes of 103,304 nuclei or cells from 12 major organs and tissues of adult mice. Our atlas comprehensively characterizes alternative splicing, alternative promoter usage, and alternative polyadenylation events across cell types, revealing previously unappreciated functional heterogeneity among individual cells. Different cell types exhibit largely distinct expression patterns of various isoforms, corresponding to their specific morphologies and biological functions. Our splicing atlas and generalized long-read frameworks will empower researchers to fully interpret biological variation across full-length transcriptomes of single cells.

genomics↗

bioRxiv2024

Effects of Age and Cognitive Functions on the Neural Tracking of Speech in Noise

Older adults often struggle to comprehend speech in noisy environments, a challenge influenced by declines in both auditory processing and cognitive functions. This study examines age-related differences in speech recognition in noise, focusing on the roles of delta (1-4 Hz) and theta (4-8 Hz) neural oscillations and their relationship with cognitive function, particularly working memory. Electroencephalography (EEG) was used to collect data from 23 young adults (20-35 years) and 23 older adults (65-80 years) with normal hearing. Cognitive assessments were administered to older adults, and both groups completed an EEG task involving speech recognition in Speech-Shaped Noise (SSN) at individualized noise levels based on their Sentence Recognition Scores (SRS). Results showed that age significantly impacted hit rates and reaction times in noisy speech recognition tasks. Theta-band neural tracking was notably stronger in older adults, while delta-band tracking showed no age-related difference. Pearsons correlations indicated significant associations between age-related cognitive decline, reduced hearing sensitivity, and Mini-Mental State Examination (MMSE) scores. Regression analyses showed that theta-band neural tracking at specific SRS levels significantly predicted word list recognition in the higher SRT group, while constructional recall was strongly predicted in the lower SRT group. The findings suggest that older adults may rely on theta-band neural tracking as a compensatory mechanism to support speech perception in noise, with indirect links between working memory and speech perception. Further research is needed to explore the causal relationship between cognitive function and hearing.

neuroscience↗

bioRxiv2024

Influenza Virus Enhances Bacterial Growth in the Lungs through Weakening Capsule Receptor-Mediated Bacterial Capture by Neutrophils

Certain serotypes of encapsulated bacteria are more associated with severe pneumonia than others, but the biological reason behind this association has remained largely unknown. This study has uncovered a causal relationship between capsule serotype and virulence phenotype of Streptococcus pneumoniae, a leading cause of community-acquired pneumonia, in mice using isogenic bacteria. Certain high-virulence (HV) serotypes persist in the lungs and lead to severe pneumonia, whereas the low-virulence (LV) serotypes are effectively cleared. The capsule type-dependent difference in virulence is determined by the capsule-binding receptors, which recognize the capsular polysaccharides of the LV serotypes (but not the HV serotypes) and enable pathogen capture by neutrophils through complement activation. The capsule receptor-driven immunity of lung neutrophils is significantly compromised by pre-infection of influenza virus, which enhances the survival and virulence of the LV S. pneumoniae serotypes, and recurs in the heightened pathogenicity of Haemophilus influenzae. This study not only unravels the long-sought mechanistic mystery of serotype-dependent virulence in bacterial lung infections, but also provides an explanation for the well-known pathogenesis synergism between influenza virus and respiratory bacteria. Graphical abstract O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=160 SRC="FIGDIR/small/622589v1_ufig1.gif" ALT="Figure 1"> View larger version (49K): org.highwire.dtl.DTLVardef@1464164org.highwire.dtl.DTLVardef@16f34e5org.highwire.dtl.DTLVardef@1f9ad46org.highwire.dtl.DTLVardef@df104d_HPS_FORMAT_FIGEXP M_FIG C_FIG

microbiology↗

bioRxiv2024

Multi-Omics Single-Cell Analysis Reveals Key Regulators of HIV-1 Persistence and Aberrant Host Immune Responses in Early Infection

The clearance of human immunodeficiency virus-1 (HIV-1) remains a significant public health challenge due to impaired cellular immune responses and HIV-1 maintenance during acute infection. However, the genetic and epigenetic changes influencing the immune response on host infected cells remain unclear. Here, this study analyzes HIV-1 infected CD4+ T cells from peripheral blood mononuclear cells from people living with HIV-1 (PLWH) during early infection (<6 months) using single-cell RNA and ATAC sequencing. It is observed that HIV-1 hinders the antiviral response, particularly by interfering with the interferon signaling pathway. Multimodal analysis identifies KLF2 as a key transcription factor in infected CD4+ T cells. Moreover, cells harboring HIV-1 provirus are predominantly identified as Th17 cells, which exhibit elevated KLF2 activity. This suggests an increased susceptibility to HIV-1 infection and a constrained immune response due to the quiescent characteristics of these cells. The finding provides insights into the immune mechanisms and key regulators of HIV-1 maintenance in CD4+ T cells during the early stages of infection.

microbiology↗

bioRxiv2024

C-Reactive Protein Drives Potent Clearance of Blood Bacteria in the Liver by Activating the Complement System

Plasma C-reactive protein (CRP) is widely used as a biomarker for bacterial infections due to its massive induction during infections, however, the precise function of CRP in bacterial infections remains undefined. Here we show that CRP enables Kupffer cells (liver macrophages) to capture and eliminate a wide range of encapsulated bacteria from the bloodstream of mice and thereby provides rapid and effective immunity. Mechanistically, CRP binds to the structurally diverse capsular polysaccharides of major Gram-positive and -negative pathogens, and thereby activates complement C3 at the bacterial surface. The C3-opsonized microbes are in turn captured by C3 receptors on the surface of Kupffer cells, and eliminated in the liver sinusoids. Since CRP principally shares the functional features of antibodies in pathogen recognition/execution, CRP-based defense combines the broad spectrum of the innate immunity with the swiftness, potency and specificity of the adaptive immunity, which helps explain massive rise of CRP during systemic bacterial infections.

immunology↗

bioRxiv2024

Trem2 deficiency attenuates breast cancer tumor growth in lean, but not obese or weight loss, mice and is associated with alterations of clonal T cell populations

AbstractObesity is an established risk factor for breast cancer development and worsened prognosis; however, the mechanisms for this association - and the potential benefits of weight loss - have not been fully explored. The adipose environment surrounding breast tumors, which is inflamed in obesity, has been implicated in tumor progression. An emerging therapeutic target for cancer is TREM2, a transmembrane receptor of the immunoglobulin superfamily that is expressed on macrophages in adipose tissue and tumors. We utilized genetic loss of function (Trem2+/+ and Trem2-/-) models and dietary (lean, obese, and weight loss) intervention approaches to examine impacts on postmenopausal breast cancer. Remarkably, Trem2 deficiency ameliorated tumor growth in lean, but not obese or weight loss mice. Single-cell RNA sequencing, in conjunction with VDJ sequencing of tumor and tumor-adjacent mammary adipose tissue (mATTum-adj) immune cells, revealed that tumors of lean Trem2-/- mice exhibited a shift in clonal CD8+ T cells from an exhausted to an effector memory state, accompanied with increased clonality of CD4+ Th1 cells, that was not observed in any other diet-genotype group. Notably, identical T cell clonotypes were identified in the tumor and mATTum-adj of the same mouse. Finally, an immune checkpoint study demonstrated that PD-1 therapy restricted tumor growth in lean and weight loss, but not obese mice. We conclude that weight history is relevant when considering potential efficacy of TREM2 inhibition in postmenopausal breast cancer. This work reveals immunological interactions between tumors and surrounding adipose tissue, highlighting significant differences under obese and weight loss conditions.

cancer biology↗

bioRxiv2024

Splenic red pulp macrophages eliminate the liver-resistant Streptococcus pneumoniae during bloodstream infection

The spleen is well-known for defense against invasive infections of encapsulated bacteria, particularly Streptococcus pneumoniae (pneumococcus). However, the precise mechanism of the splenic anti-bacterial immunity remains elusive. Here we report that red pulp (RP) macrophages execute the splenic defense against S. pneumoniae in mice, with the help of natural antibodies (nAbs) and complement system. The spleen slowly but substantially cleared encapsulated pneumococci from the bloodstream in the early phase of blood infection, especially the serotypes that resist to liver filtration. Among splenic macrophage subpopulations, only the lack of RP macrophages led to the complete loss of the splenic immunity. Intravital microscopy detected direct capture and phagocytic killing of circulating pneumococci by RP macrophages in the absence of neutrophils and inflammatory monocytes. Likewise, plasma nAbs targeting pneumococcal cell wall phosphocholine and complement protein C3 were essential for RP macrophage-mediated immune clearance. Our findings have thus uncovered the long-sought immune pathway against invasive pneumococcal infections in the spleen. Short summaryThe spleen plays a crucial role in defending against invasive infections caused by Streptococcus pneumoniae (pneumococcus) and other encapsulated bacteria in humans, but the mechanisms underlying this organ-specific immunity remain largely elusive. This study has revealed that the spleen eliminates pneumococci through a coordinated interplay among red pulp macrophages, serum nAbs targeting phosphocholine and the complement system.

microbiology↗

bioRxiv2024

Natural antibodies to polysaccharide capsules enable Kupffer cells to capture invading bacteria in the liver sinusoids

The interception of blood-borne bacteria in the liver defines the outcomes of invasive bacterial infections, but the mechanisms of this anti-bacterial immunity are largely speculative. This study shows that natural antibodies (nAbs) to capsules enable liver macrophage Kupffer cells (KCs) to rapidly capture and kill blood-borne encapsulated bacteria in mice. Affinity pulldown with serotype-10A capsular polysaccharides (CPS10A) of S. pneumoniae (Spn10A) led to the identification of CPS10A-binding nAbs in serum. The CPS10A-antibody interaction enabled KCs to capture Spn10A bacteria from the bloodstream, in part through complement receptors on KCs. The nAbs were found to recognize the {beta}1-6-linked galactose branch of CPS10A, and similar moieties of serotype-39 S. pneumoniae and serotype-K50 Klebsiella pneumoniae capsules. More importantly, the nAbs empowered KCs to capture serotype-39 S. pneumoniae and serotype-K50 K. pneumoniae in the liver. Collectively, our data have revealed a highly effective immune function of nAb against encapsulated bacteria, and provided a proof of concept for treating septic bacterial diseases with monoclonal antibodies. Short summaryRapid capture of potentially harmful bacteria in blood by liver macrophages are vital for the blood sterility and health. This work reports how naturally occurring antibodies in the plasma enable macrophages to capture and kill blood-borne bacteria in the liver.

microbiology↗