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Biology subjects

Li, F.-J.

Publications and source records attributed to Li, F.-J..

4 recordsLinked to original sources

Superior batch alignment and hyper-dimensional cytometry representations allow ultra-sensitive classification of disease phenotypes

Analysis of cytometry data predominantly relies on clustering and dimensionality reduction approaches for computational tractability. This is particularly relevant for modern spectral flow cytometers, which can simultaneously measure an increasingly large number of antibody marker channels. While dimensionality reduction provides for more efficient data processing, this comes at the expense of data loss that may miss subtle patterns among rare cell types that may be critical for disease detection. Maintaining analysis at full dimensions presents opportunities to preserve resolution and provides complete downstream data interpretability. However, a significant obstacle to analysis of cytometry data without dimensionality reduction is the significant batch effects observed in this data between experiment days, operators and equipment types. Here we show a new strategy to denoise batch variation from both flow- and mass-cytometry datasets using an autoencoder neural network architecture. We generated a benchmark flow cytometry dataset in mice to compare this approach to current toolsets and find our approach shows superior preservation of biological signals, whilst also performing batch correction equal to current best methodology. Our batch alignment approach works to such an extent that it becomes practically possible to project batch aligned data into multidimensional space to generate a novel representation of cellular phenotype for downstream model building. This hyperdimensional approach maintains original data resolution without requiring dimensionality reduction, and thus any resultant cell populations that differentiate phenotypes remain fully interpretable. We show with two large clinical datasets that our batch-alignment approach coupled with the multi-dimensional representation successfully detects meaningful patterns in cases where the original analysis methods struggled. This new framework removes some of the inherent technical limitations encountered in the integration of large, multi-batch cytometry datasets and provides a framework for machine learning model building from this modality. An implementation of this framework and an associated web application accompanies this manuscript at http://voxelcoder.cloud. Significance StatementThis work addresses a critical bottleneck in cytometry analysis by introducing a neural network-based approach that effectively removes technical batch variation while preserving biological signals. The novel hyperdimensional representation maintains full data resolution without dimensionality reduction, enabling more sensitive detection of disease-associated cellular signatures than current methods. Importantly, this framework enables reliable batch normalization of fresh samples processed at different times and locations, overcoming the practical constraints of clinical sample collection where simultaneous processing is often impossible. The enhanced sensitivity for identifying pathogenic cellular patterns has immediate implications for biomarker discovery and personalized medicine applications.

systems biology↗

Rab2B promotes chaperonin-mediated actin folding and prevents developmental transcription reprogramming and quiescence in trypanosomes

The Rab family of small GTPases are regulators of intracellular membrane trafficking. Rab2B, a Golgi-resident Rab GTPase, has been shown to function in ER-Golgi transport and autophagosome-lysosome fusion in mammalian cells and Drosophila. In Trypanosoma brucei, the autophagy-related function of Rab2B was conserved and depletion of Rab2B blocked autophagosome-lysosome fusion. Intriguingly, depletion of Rab2B induced differentiation of T. brucei from a proliferative slender form to a quiescent stumpy form, a step crucial for parasite transmission. Chaperonin CCT/TRiC was identified as an effector of Rab2B. Depletion of CCT/TRiC subunits or actin (a known CCT/TRiC substrate), or blocking actin polymerisation with Latrunculin A all triggered differentiation, suggesting a role of Rab2B on CCT/TRiC-mediated actin folding. Using an actin chromobody, we identified a pool of nuclear actin that is crucial for transcription reprogramming and life cycle differentiation in T. brucei. The study revealed a function of Rab2B and actin in T. brucei transcription reprogramming leading to cell differentiation, and an unexpected role of Rab2B and CCT/TRiC mediated actin folding.

cell biology↗

GBP1 promotes killing of multidrug-resistant Acinetobacter baumannii and promotes host protection via interferon signalling and inflammasome activation.

Multidrug resistant (MDR) Acinetobacter baumannii are of major concern worldwide due to their resistance to last resort carbapenem and polymyxin antibiotics. To develop an effective treatment strategy, it is critical to better understand how an A. baumannii MDR bacterium interacts with its mammalian host. Pattern-recognition receptors sense microbes, and activate the inflammasome pathway, leading to pro-inflammatory cytokine production and programmed cell death. Here, we found that MDR A. baumannii activate the NLRP3 inflammasome complex predominantly via the non-canonical caspase-11-dependent pathway. We show that caspase-11-deficient mice are protected from a virulent MDR A. baumannii strain by maintaining a balance between protective and deleterious inflammation via IL-1. Caspase-11-deficient mice also compromise between effector cell recruitment, phagocytosis, and programmed cell death in the lung during infection. Importantly, we found that cytosolic immunity - mediated by guanylate-binding protein 1 (GBP1) and type I interferon signalling - orchestrates caspase-11-dependent inflammasome activation. This exerts a bactericidal activity against carbapenem- and colistin-resistant, lipooligosaccharide (LOS)- deficient bacteria. Together, our results suggest that developing therapeutic strategies targeting GBP1 might pave the way as a host-directed therapy to overcome multidrug resistance in A. baumannii infection.

microbiology↗

Differential activation of NLRP3 inflammasome by Acinetobacter baumannii strains

Acinetobacter baumannii is an emerging nosocomial, opportunistic pathogen with growing clinical significance globally. A. baumannii has an exceptional ability to rapidly develop drug resistance. It is frequently responsible for ventilator-associated pneumonia in clinical settings and inflammation resulting in severe sepsis. The inflammatory response is mediated by host pattern-recognition receptors and the inflammasomes. Inflammasome activation triggers inflammatory responses, including the secretion of the pro-inflammatory cytokines IL-1{beta} and IL-18, the recruitment of innate immune effectors against A. baumannii infection, and the induction programmed cell death by pyroptosis. An important knowledge gap is how variation among clinical isolates affects the hosts innate response and activation of the inflammasome during A. baumannii infection. In this study, we compared nine A. baumannii strains, including clinical locally-acquired isolates, in their ability to induce activation of the inflammasome and programmed cell death pathway in primary macrophages and mice. We found a striking variability in survival outcomes of mice and bacterial dissemination in organs among three ATCC A. baumannii strains, likely due to the differences in virulence between strains. Interestingly, we found a stark contrast in activation of the NLRP3 inflammasome pathway, the non-canonical caspase-11 pathway, plasmatic secretion of the pro-inflammatory cytokines IL-1{beta} and IL-18 between A. baumannii strains. Our study highlights the importance of utilising multiple bacterial strains and clinical isolates with differential virulence to investigate the innate immune response to A. baumannii infection.

microbiology↗