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Biology subjects

Guerra, N.

Publications and source records attributed to Guerra, N..

7 recordsLinked to original sources

Different data analysis models for detecting miRNAs using nanopores

Nanopore sensors offer exceptional sensitivity for detecting single molecules, making them ideal for early disease diagnostics. In this study, we present a multiplexed nanopore-based assay that combines DNA-barcoded probes with advanced computational analysis to detect microRNAs (miRNAs) with high specificity and quantitative accuracy. Each probe binds selectively to its target biomarker and generates a characteristic delay in the ionic current signal upon translocation through the nanopore, enabling label-free detection. We evaluated three analytical strategies for classifying delayed versus non-delayed events: (1) moving standard deviation (MSD), (2) spectral entropy (SE), and (3) a convolutional neural network (CNN). While MSD and SE rely on manually defined thresholds and exhibit limited sensitivity, the CNN model, trained on image representations of raw current traces, achieved near-perfect classification performance across all metrics. Grad-CAM visualisation confirmed that the CNN focused on biophysically relevant signal regions, enhancing interpretability and generalisability. All methods produced sigmoidal concentration-response curves consistent with expected binding kinetics, and nanopore-derived delay metrics closely matched RT-qPCR validation data. All three methods were capable of distinguishing between signal classes; however, the CNN model demonstrated superior sensitivity and robustness. This work highlights the importance of data interpretation in nanopore sensing and presents a comparative framework for binary event classification. The findings pave the way for the development of machine learning-driven nanopore diagnostics capable of detecting diverse biomarker types at the single-molecule level.

biophysics↗

Evaluating the potential of cross-species neutralization of anti-PfCyRPA and anti-PfRIPR Monoclonal Antibodies

PfCyRPA and PfRIPR are promising next-generation malaria blood-stage vaccine candidate antigens that play an essential role in erythrocyte invasion of Plasmodium falciparum. CyRPA and RIPR orthologs are present in all human-infecting Plasmodium species, suggesting the potential for a cross-species vaccine. Using Growth Inhibition Assays (GIA), this study investigates seven anti-PfCyRPA and three anti-PfRIPR monoclonal antibodies targeting P. falciparum for their inhibitory activity against P. knowlesi, a non-falciparum species that contributes to a significant burden of zoonotic disease in South-East Asia, shares some biological features with Plasmodium vivax, and has a robust in vitro culture system. Despite their efficacy against P. falciparum and partially conserved epitopes, these antibodies exhibited minimal inhibition of P. knowlesi. Understanding the antigenic diversity and immune mechanisms across Plasmodium species is critical for advancing pan-species vaccine strategies.

immunology↗

Tyramine promotes colon cancer risk and development by inducing DNA damage and inflammation

High dietary consumption of processed meat is associated with increased colorectal cancer (CRC) risk, but mechanistic links remain largely unknown. Tyramine is a biogenic amine found in processed food and a gut bacterial product from tyrosine. However, the impact of tyramine on gut health has not been studied. We found that tyramine induced necrosis and promoted cell proliferation and DNA damage in HCT116 cells. Ingestion of tyramine increased colonic tumor size, intestinal cell proliferation and inflammation (e.g., increased mRNA expression of IL-17A and a higher number of Ly6G+ neutrophils) in ApcMin/+ mice. Furthermore, tyramine-treated wild-type mice exhibited visible adenomas and significantly enhanced intestinal tissue DNA damage, together with altered gene pathways involved in epithelial barrier function. In addition, natural killer cell numbers were lower and polymorphonuclear-myeloid derived suppressor cells were higher in tumors from tyramine-treated ApcMin/+ mice, suggesting a suppressive anti-tumor immune response. Thus, tyramine not only increases CRC risk, but also facilitates tumor development. Modulating the levels of tyramine in food and monitoring high-risk individuals could aid in better prognosis and management of CRC.

cancer biology↗

NKG2D signaling regulates IL-17A-producing γδT cells to promote cancer progression

{gamma}{delta}T cells are unconventional T cells particularly abundant in mucosal tissues that play an important role in tissue surveillance and homeostasis. {gamma}{delta}T cell activation is mediated by the T cell receptor composed of {gamma} and {delta} chains, as well as activating receptors for stress-induced ligands, such as NKG2D. Contrary to the well-established anti-tumor function of {gamma}{delta}T cells, recent studies have shown that {gamma}{delta}T cells can promote tumor development in certain contexts. However, the mechanisms leading to this diseasepromoting role remain poorly understood. Here, we show that mice lacking {gamma}{delta}T cells survive longer in a mouse model of intestinal cancer, further supporting their pro-tumoral role. In a surprising conceptual twist, we found that these pro-tumor {gamma}{delta}T cells are regulated by NKG2D signaling, a receptor normally associated with cancer cell killing. Germline deletion of Klrk1, the gene encoding NKG2D, reduced the frequency of {gamma}{delta}T cells in the tumor microenvironment and delayed tumor progression. We further show that blocking NKG2D reduces the capability of {gamma}{delta}T cells to produce IL-17A in the pre-metastatic lung and that co-culture of lung T cells with NKG2D ligand-expressing tumor cells specifically increases the frequency of {gamma}{delta}T cells. Together, these data support the hypothesis that in a tumor microenvironment where NKG2D ligands are constitutively expressed, {gamma}{delta}T cells accumulate in an NKG2D-dependent manner and drive tumor progression by secreting pro-inflammatory cytokines, such as IL-17A.

immunology↗

Pulmonary natural killer cells control neutrophil intravascular motility and response to acute inflammation

The pulmonary immune system defends a huge surface area directly in contact with the contents of the air we breathe. Neutrophils, the most abundant immune cell in the pulmonary vasculature, are critical to immunity but they are also capable of generating life-threatening pathology. Natural Killer cells are the most highly represented lymphocyte subset in the lung, but relatively little is known about their localization, motility or the specific mechanisms by which they contribute to local homeostasis. Here, we used lung-intravital microscopy to directly visualise and quantify neutrophil and natural killer cell dynamics in the pulmonary vasculature of live mice. This approach revealed unexpected sessile behaviour by intravascular natural killer cells. Interactions with natural killer cells made neutrophils scan the endothelium more slowly over larger distances and reduced the number of neutrophils that accumulated in an LPS-triggered inflammatory challenge. This represents a new paradigm by which natural killer cells contribute to lung physiology by diminishing potentially pathogenic neutrophil accumulation.

immunology↗

Nanoscale colocalization of NK cell activating and inhibitory receptors controls signal integration

NK cell responses depend on the balance of signals from inhibitory and activating receptors. However, how the integration of antagonistic signals occurs upon NK cell-target cell interaction is not fully understood. Here, we provide evidence that NK cell inhibition via the inhibitory receptor Ly49A is dependent on its relative colocalization at the nanometer scale with the activating receptor NKG2D upon immune synapse (IS) formation. NKG2D and Ly49A signal integration and colocalization was studied using NKG2D-GFP and Ly49A-RFP-expressing primary NK cells, forming ISs with NIH3T3 target cells, with or without expression of single chain trimer (SCT) H2-Dd and an extended form of SCT H2-Dd-CD4 MHC-I molecules. Nanoscale colocalization was assessed by Forster resonance energy transfer (FRET) between NKG2D-GFP and Ly49A-RFP and measured for each synapse. In the presence of their respective cognate ligands, NKG2D and Ly49A colocalize at a nanometer scale leading to NK cell inhibition. However, increasing the size of the Ly49A ligand reduced the nanoscale colocalization with NKG2D consequently impairing Ly49A-mediated inhibition. Thus, our data shows NK cell signal integration is critically dependent on the dimensions of NK cell ligand-receptor pairs by affecting their relative nanometer-scale colocalization at the IS. Together, our results suggest the balance of NK cell signals, and NK cell responses, are determined by the relative nanoscale colocalization of activating and inhibitory receptors in the immune synapse.

immunology↗

Failure of in vitro differentiation of Plasmodium falciparum gametocytes into ookinetes arises because of poor gamete fertilisation

A critical step towards malaria elimination will be the interruption of Plasmodium transmission from the human host to the mosquito. At the core of the transmission cycle lies Plasmodium sexual reproduction leading to zygote formation and mosquito midgut colonisation by ookinetes. Whilst in vitro ookinete culture from the murine and avian malaria parasites, Plasmodium berghei and P. gallinaceum, has greatly increased our knowledge of transmission biology; efforts to mimic the process in the human parasite P. falciparum have, to date, had only limited success. Using fluorescence microscopy and flow cytometry with antibodies specific to the male gametocyte and developing ookinetes, we sought to evaluate P. falciparum ookinete production using previously published in vitro protocols. We then compared in vitro versus in vivo ookinete production in both P. falciparum and P. berghei parasites, exploring potential barriers to complete development. Finally, we sought to test a wide range of literature-led culture conditions towards further optimisation of in vitro P. falciparum ookinete production. Despite extensive testing, our efforts to replicate published methods did not produce appreciable quantities of fully formed P. falciparum ookinetes in vitro. In parallel, however, gametocyte cultures that failed to differentiate fully in vitro successfully developed into ookinetes in vivo with an efficiency approximating that of P. berghei. Flow cytometry analysis showed that this disparity likely lies with the poor fertilization of P. falciparum gametes in vitro. Attempts to improve gametocyte fertility or define conditions more permissive to fertilisation/ookinete survival in vitro were also unsuccessful. Current in vitro conditions for P. falciparum ookinete production are not optimal for gamete fertilisation either due to the lack of parasite-species-specific mosquito factors missing from in vitro culture, or non-permissive cues contaminating culture preparations.

microbiology↗