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Dhaliwal, K.

Publications and source records attributed to Dhaliwal, K..

6 recordsLinked to original sources

Beyond Navigation - Tissue-contacting Fluorescent Lifetime Imaging reveals a pathology-linked lung cancer phenotype at the point of biopsy

Background: Accurate sampling of suspected peripheral lung cancers depends on access to the lesion and confirmation that the biopsy tool is in contact with target tissue. Current bronchoscopic navigation and imaging techniques can guide instruments to a target but do not provide real-time biological confirmation at the point of sampling. Fluorescence lifetime imaging microscopy (FLIM) provides molecular contrast by measuring fluorescence decay - how long photons continue to be emitted from fluorescent molecules. In the Precision Lung clinical study (ISRCTN15093468), the Prothea Imaging System (Generation 1) identified a candidate tumour-associated phenotype of spatially overlapped low fluorescence lifetime and low intensity (LLLI) from in-vivo imaging. We used this observation as the basis for a reverse-translational study to determine whether the LLLI phenotype is linked to cancer pathology; reproducible with the Imaging System (Generation 2); and distinguishable from normal lung tissue. Methods: Previously reported Precision Lung findings were used as the clinical starting observation and were not re-analysed. Validation was then performed using: (i) pathology linked benchtop FLIM of early-stage non-small-cell lung tissue microarrays encompassing malignant cell clusters of approximately 300 um2, matched to the EoT imaging scale; (ii) five sequential fresh lung-cancer resections imaged at tumour and comparator regions, including visibly blood-rich contact sites, using the (Generation 2) Imaging System; and (iii) systematic mapping of two ventilated non-cancer donor lungs, one from a smoker and one from a non-smoker, across all available lobes. The LLLI phenotype was defined as spatial co-localisation of low intensity and short lifetime. Results: Using a real time fibre based FLIM system, capable of deployment through a working channel of a bronchoscope, the LLLI tumour phenotype was optically identified in freshly resected tumour tissue. The same phenotype was identified in fixed tissue samples with known pathology, and with images taken in the Precision Lung clinical study. Whole human lung controls did not show evidence of the tumour phenotype. Conclusions: This evidence forms a reverse-translational chain that supports the concept of the Prothea Imaging System - as a platform that confirms that the tool is in contact with a region of cancer in the lesion, while preserving continuous access for biopsy or intervention.

cancer biology↗

Therapeutic signature mapping of paired direct and indirect LPS injury in an ex vivo human lung perfusion platform reveals injury-specific druggable programs

Acute Respiratory Distress Syndrome (ARDS) remains highly morbid and lacks approved disease-modifying pharmacotherapies. Direct (pulmonary) and indirect (extrapulmonary) insults may initiate biologically distinct early injury programs, but human tissue-level evidence from the first hours is scarce. Here we establish a paired, acellular ex vivo lung perfusion (EVLP) platform using human donor lungs unsuitable for transplantation to model direct (endobronchial) and indirect (perfusate) lipopolysaccharide (LPS) injury within the same donor. We profiled lung tissue proteomes at 4 h post-insult and performed therapeutic nomination by querying proteomics-derived injury signatures against the CLUE L1000 perturbational compendium with independent cross-platform validation. Both models developed histological injury and robust cytokine release. Direct injury preferentially enriched neutrophil degranulation, extracellular matrix remodelling and metabolic reprogramming modules, whereas indirect injury showed prominent complement/coagulation perturbation with greater endothelial activation markers in perfusate. Cross-platform prioritisation converged on tractable signalling and epigenetic axes, including JAK/STAT, PI3K/AKT/mTOR, SYK, CDK and HDAC inhibitor classes - yielding a tiered shortlist for EVLP intervention testing. This intact human lung perturbation platform enables injury-stratified mechanistic inference and therapeutic prioritisation in early lung injury relevant to ARDS.

immunology↗

Endomicroscopic fluorescence lifetime imaging enables molecular detection and targeted sampling in the distal human lung

PurposeAccurate molecular characterisation of infection and inflammation within the distal human lung remains challenging, particularly in critically ill patients, due to limited access to the alveolar space and delayed diagnostic workflows. Molecular imaging approaches capable of real-time detection and targeted sampling could substantially improve diagnostic precision and the future translational development of molecular imaging probes and therapeutics. MethodsIn a preclinical setting, we evaluated a clinic-ready endomicroscopic fluorescence lifetime imaging microscopy (eFLIM) platform combined with molecularly targeted SmartProbes for in situ detection of bacteria and activated neutrophils in the distal human lung. A multifunctional 1.9-mm diameter imaging and sampling catheter (Eyes on Target; EoT) enabled real-time fluorescence intensity and lifetime imaging alongside directed alveolar microlavage via a 1.2-mm working channel. Fluorescence intensity and lifetime signatures of Gram-negative bacteria, Gram-positive bacteria, and activated neutrophils were characterised using three wash-free SmartProbes: NBD-PMX, Merocy-Van, and a neutrophil activation probe (NAP). Imaging and sampling performance were assessed in ventilated ex vivo human lungs. ResultsEoT reliably navigated to alveolar regions across all lung lobes in both phantom and ventilated human lung models. eFLIM distinguished alveolar microanatomy and enabled probe-specific molecular detection within the distal lung. Increased NBD-PMX signal was detected in Escherichia coli-instilled lobes, while Merocy-Van lifetime signatures selectively identified Staphylococcus aureus-instilled regions. Activated neutrophils were detected throughout lung tissue following NAP administration. Directed alveolar microlavage enabled recovery of cellular material and bacterial DNA from imaged regions for downstream analysis. ConclusioneFLIM using EoT combined with molecular SmartProbes enables real-time molecular imaging and targeted sampling within the distal human lung. This platform provides a translatable approach for evaluating infection and inflammation at the alveolar level and supports the clinical development of molecular imaging probes for pulmonary disease.

microbiology↗

Far-Ultraviolet Light Causes Direct DNA Damage in Human Lung Cells and Tissues

Far-ultraviolet C (Far-UVC) radiation, with a wavelength range from 200 to 235 nm, is germicidal and holds potential for clinical applications. However, its use against deep-seated and internal infections, such as those affecting the lungs, remains less well established. The safety profile of Far-UVC irradiation requires further investigation across different human tissues. In this study, we utilised a krypton-chloride (KrCl) excimer lamp and a pulsed laser system to examine the effects of Far-UVC irradiation on human lung cells in vitro and primary human tracheal tissue. Primary human tracheal tissue and cells exposed to continuous wave (222 nm) and pulsed 206 nm and 222 nm light at doses of 5, 25, and 50 mJ/cm2 exhibited Deoxyribonucleic acid (DNA) damage, including phosphorylation of {gamma}H2AX (Ser139). The continuous wave and pulsed 222 nm irradiation caused the formation of pyrimidine-pyrimidone (6-4) photoproducts. Irradiated human lung cells demonstrated reduced viability in vitro, and increased lactate dehydrogenase release into the culture medium 48 hours post-irradiation. Our findings reveal that even low doses of Far-UVC (206 nm, 222 nm) light can penetrate monolayers of human lung epithelial cells, causing direct DNA damage in the form of (6-4) photoproducts and DNA double-strand breaks, ultimately leading to cell death.

cell biology↗

Quantitative proteomics identifies tumour matrisome signatures in patients with non-small cell lung cancer

The composition and remodelling of the extracellular matrix (ECM) are important factors in the development and progression of cancers, and the ECM is implicated in promoting tumour growth and restricting anti-tumour therapies through multiple mechanisms. The characterisation of differences in ECM composition between normal and diseased tissues may aid in identifying novel diagnostic markers, prognostic indicators and therapeutic targets for drug development. Using tissue from non-small cell lung cancer (NSCLC) patients undergoing curative intent surgery, we characterised quantitative tumour-specific ECM proteome signatures by mass spectrometry, identifying 161 matrisome proteins differentially regulated between tumour tissue and nearby non-malignant lung tissue. We defined a collagen hydroxylation functional protein network that is enriched in the lung tumour microenvironment. We validated two novel putative extracellular markers of NSCLC, the collagen cross-linking enzyme peroxidasin and a disintegrin and metalloproteinase with thrombospondin motifs 16 (ADAMTS16), for discrimination of malignant and non-malignant lung tissue. These proteins were up-regulated in lung tumour samples, and high PXDN and ADAMTS16 gene expression was associated with shorter survival of lung adenocarcinoma and squamous cell carcinoma patients, respectively. These data reveal tumour matrisome signatures in human NSCLC. O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=19 SRC="FIGDIR/small/510064v1_ufig1.gif" ALT="Figure 1"> View larger version (8K): org.highwire.dtl.DTLVardef@b34045org.highwire.dtl.DTLVardef@40a5a9org.highwire.dtl.DTLVardef@3c150corg.highwire.dtl.DTLVardef@89c6f2_HPS_FORMAT_FIGEXP M_FIG C_FIG

cancer biology↗

Evaluation of intranasal nafamostat or camostat for SARS-CoV-2 chemoprophylaxis in Syrian golden hamsters

Successful development of a chemoprophylaxis against SARS-CoV-2 could provide a tool for infection prevention implementable alongside vaccination programmes. Camostat and nafamostat are serine protease inhibitors that inhibit SARS-CoV-2 viral entry in vitro but have not been characterised for chemoprophylaxis in animal models. Clinically, nafamostat is limited to intravenous delivery and while camostat is orally available, both drugs have extremely short plasma half-lives. This study sought to determine whether intranasal dosing at 5 mg/kg twice daily was able to prevent airborne transmission of SARS-CoV-2 from infected to uninfected Syrian golden hamsters. SARS-CoV-2 viral RNA was above the limits of quantification in both saline- and camostat-treated hamsters 5 days after cohabitation with a SARS-CoV-2 inoculated hamster. However, intranasal nafamostat-treated hamsters remained RNA negative for the full 7 days of cohabitation. Changes in body weight over the course of the experiment were supportive of a lack of clinical symptomology in nafamostat-treated but not saline- or camostat-treated animals. These data are strongly supportive of the utility of intranasally delivered nafamostat for prevention of SARS-CoV-2 infection and further studies are underway to confirm absence of pulmonary infection and pathological changes.

pharmacology and toxicology↗