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ATCC cell culture murine epithelial lung tissue cell lines
Cell Culture Murine Epithelial Lung Tissue Cell Lines, supplied by ATCC, used in various techniques. Bioz Stars score: 93/100, based on 157 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/murine+epithelial+lung+tissue+cell+lines/LA-4/pm41183169-171-0-10
Average 93 stars, based on 157 article reviews

cell culture murine epithelial lung tissue cell lines - by Bioz Stars, 2026-08

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Cell mapping of the CBN-specific course of pro-inflammatory cytokines. The scoring of the “pro-inflammatory response” pathway exhibited CBN-specific patterns in alveolar epithelial cell types (a), airway epithelial cells (b), macrophage cell types (c) and also mesenchymal cell types (d). (e). Heatmap of BAL cytokine protein level compared to relative mRNA level in defined “inflammatory niche” including alveolar and airway epithelial cells, macrophages, and mesenchymal cells. (f). The UMAPs of CBN-specific cytokines, two identified cytokines were shown for each CBN, the localization of each cytokine in cell types is circled and labeled on the plots. (g). The dotplot of specific cytokine gene induction caused by different CBN in different cell types. (h). UMAP of Cxcl2 and Cxcl5 . Experiments were performed as n = 3 for BAL cytokine measurements, n = 4 for all transcriptomics analysis. One-way ANOVA (nonparametric analysis; Kruskal–Wallis Test) followed by Dunn’s multiple comparisons test was used for statistical analysis.

Journal: ACS Nano

Article Title: Toward a ToxAtlas of Carbon-Based Nanomaterials: Single-Cell RNA Sequencing Reveals Initiating Cell Circuits in Pulmonary Inflammation

doi: 10.1021/acsnano.5c12054

Figure Lengend Snippet: Cell mapping of the CBN-specific course of pro-inflammatory cytokines. The scoring of the “pro-inflammatory response” pathway exhibited CBN-specific patterns in alveolar epithelial cell types (a), airway epithelial cells (b), macrophage cell types (c) and also mesenchymal cell types (d). (e). Heatmap of BAL cytokine protein level compared to relative mRNA level in defined “inflammatory niche” including alveolar and airway epithelial cells, macrophages, and mesenchymal cells. (f). The UMAPs of CBN-specific cytokines, two identified cytokines were shown for each CBN, the localization of each cytokine in cell types is circled and labeled on the plots. (g). The dotplot of specific cytokine gene induction caused by different CBN in different cell types. (h). UMAP of Cxcl2 and Cxcl5 . Experiments were performed as n = 3 for BAL cytokine measurements, n = 4 for all transcriptomics analysis. One-way ANOVA (nonparametric analysis; Kruskal–Wallis Test) followed by Dunn’s multiple comparisons test was used for statistical analysis.

Article Snippet: Murine epithelial lung tissue cell lines (LA-4; cat. no. ATCC CCL-196; MLE-12, cat no. CRL-2110), murine fibroblast cell line (CCL-206; cat. no. Mlg 2908), and murine macrophage cell line (J774.1; cat. no. TIB-67) were purchased from American Type Culture Collection (ATCC) instructions.

Techniques: Labeling

CNP exposure caused neutrophil attraction and formed cellular communications within the local alveolar environment (a). UMAP embedding illustrates cell types and states in the epithelial niche. (b). Treatment-dependent alteration of cell relative frequencies with activation of AT2 (AT2 activated) for CNP and DWCNT and alveolar differentiation intermediates upon MWCNT exposure. (c). Dotplots displaying the top 5 marker genes for each annotated cell type. (d). Heatmap of gene set variation analysis of hallmark signaling pathways on AT2-activated cells. (e). Matrixplot of pro-inflammatory cytokine gene expression caused by different CBN in AT2-activated cells. (f). Csf2 induction by CNP exposure in MLE12 cells after 6 and 24 h measured by qPCR. (g). Cxcl1 induction by CNP exposure in MLE12 cells after 6 and 24 h measured by qPCR. In (f, g), data are shown as mean ± SEM ( n = 3). For each time point, a Student t test was performed between two groups. P value was shown and P value <0.05 was considered statistically significant. (h). BAL CXCL1 protein level measured by ELISA. (i). The CXCL1 release into MLE-12 cell supernatant exposed to different CBN after 24 h. (j). Mouse primary epithelial cells (EpCAM+ cells) isolation and CXCL1 release into supernatants induced by different CBN. (k). Connectomes based on induced differential gene expression (DGE) analysis (treatment vs sham) show computationally inferred cellular communication strength in response to CNP. For each circle plot, edge weight and color represent the number of ligand–receptor pairs between interacting cell types. (l). The visualization of NicheNet analysis by circosplot illustrates the connectome of the situation before in (j) described prevailing interaction between different epithelial cells upon CNP exposure. The lower part of the circosplot is identified as “sender” cell types whereas the upper part draws the “receiver” cell types, signaling interaction by different genes were shown. For (h–j), data are shown as the mean ± SEM ( n = 3), one-way ANOVA followed by Dunn’s multiple comparisons test was used for statistical analysis.

Journal: ACS Nano

Article Title: Toward a ToxAtlas of Carbon-Based Nanomaterials: Single-Cell RNA Sequencing Reveals Initiating Cell Circuits in Pulmonary Inflammation

doi: 10.1021/acsnano.5c12054

Figure Lengend Snippet: CNP exposure caused neutrophil attraction and formed cellular communications within the local alveolar environment (a). UMAP embedding illustrates cell types and states in the epithelial niche. (b). Treatment-dependent alteration of cell relative frequencies with activation of AT2 (AT2 activated) for CNP and DWCNT and alveolar differentiation intermediates upon MWCNT exposure. (c). Dotplots displaying the top 5 marker genes for each annotated cell type. (d). Heatmap of gene set variation analysis of hallmark signaling pathways on AT2-activated cells. (e). Matrixplot of pro-inflammatory cytokine gene expression caused by different CBN in AT2-activated cells. (f). Csf2 induction by CNP exposure in MLE12 cells after 6 and 24 h measured by qPCR. (g). Cxcl1 induction by CNP exposure in MLE12 cells after 6 and 24 h measured by qPCR. In (f, g), data are shown as mean ± SEM ( n = 3). For each time point, a Student t test was performed between two groups. P value was shown and P value <0.05 was considered statistically significant. (h). BAL CXCL1 protein level measured by ELISA. (i). The CXCL1 release into MLE-12 cell supernatant exposed to different CBN after 24 h. (j). Mouse primary epithelial cells (EpCAM+ cells) isolation and CXCL1 release into supernatants induced by different CBN. (k). Connectomes based on induced differential gene expression (DGE) analysis (treatment vs sham) show computationally inferred cellular communication strength in response to CNP. For each circle plot, edge weight and color represent the number of ligand–receptor pairs between interacting cell types. (l). The visualization of NicheNet analysis by circosplot illustrates the connectome of the situation before in (j) described prevailing interaction between different epithelial cells upon CNP exposure. The lower part of the circosplot is identified as “sender” cell types whereas the upper part draws the “receiver” cell types, signaling interaction by different genes were shown. For (h–j), data are shown as the mean ± SEM ( n = 3), one-way ANOVA followed by Dunn’s multiple comparisons test was used for statistical analysis.

Techniques: Activation Assay, Marker, Protein-Protein interactions, Gene Expression, Enzyme-linked Immunosorbent Assay, Isolation

CNT exposure causes acute epithelial damage and DAMP release (a). BAL total protein levels detected after CBN treatment as a measurement for epithelial damage. (b). TUNEL assay of the DNA damage caused by different CBN. DAPI: blue, Phalloidin 488: green, TUNEL: red. Scale bar: 20 μm. (c). The quantification of TUNEL-positive events in mouse lung tissue at 12 h ( n = 3). (d). Double staining of TUNEL-positive cells in AT1 and AT2 cells marked by AQP5 and pro-SPC. DAPI: blue, AQP5 or pro-SPC: green, TUNEL: red. Scale bar: 20 μm. The quantification of TUNEL & APQ5 double positive events (e) and TUNEL & APQ5 double positive events (f) in mouse lung tissue at 12 h. (g). UMAP displays density and distribution of cells showing a high DAMP score in epithelial niche. (h). A matrixplot of DAMP-related gene expression caused by different CBN in AT2-activated cells. (i). IL-33 release caused by CBN into BAL fluid measured by ELISA. (j). IL-33 release into the supernatant of mouse AT2-like cells LA4 caused by CBN measured by ELISA. (k). Double staining of TUNEL-positive cells in AMs marked by CD11c. DAPI: blue, CD11c: green, TUNEL: red. Scale bar: 20 μm. (l). The quantification of TUNEL & CD11c double positive events in mouse lung tissue at 12 h. (m). IL1α release caused by CBN into BAL fluid measured by ELISA. (n). The visualization of Il1a expression and localization by UMAP. (o). IL1α release upon CBN exposure in isolated mouse primary AMs. The expression of Ccl2 (p) and Ccl3 (q) induced by CBN exposure in AM-like J774.1 cells. CNP (50 μg/mL), DWCNT (50 μg/mL), and MWCNT (30 μg/mL) were used in the in vitro study. Data were shown as the mean ± SEM ( n = 3 or 4), one-way ANOVA followed by Dunn’s multiple comparisons test was used for statistical analysis.

Journal: ACS Nano

Article Title: Toward a ToxAtlas of Carbon-Based Nanomaterials: Single-Cell RNA Sequencing Reveals Initiating Cell Circuits in Pulmonary Inflammation

doi: 10.1021/acsnano.5c12054

Figure Lengend Snippet: CNT exposure causes acute epithelial damage and DAMP release (a). BAL total protein levels detected after CBN treatment as a measurement for epithelial damage. (b). TUNEL assay of the DNA damage caused by different CBN. DAPI: blue, Phalloidin 488: green, TUNEL: red. Scale bar: 20 μm. (c). The quantification of TUNEL-positive events in mouse lung tissue at 12 h ( n = 3). (d). Double staining of TUNEL-positive cells in AT1 and AT2 cells marked by AQP5 and pro-SPC. DAPI: blue, AQP5 or pro-SPC: green, TUNEL: red. Scale bar: 20 μm. The quantification of TUNEL & APQ5 double positive events (e) and TUNEL & APQ5 double positive events (f) in mouse lung tissue at 12 h. (g). UMAP displays density and distribution of cells showing a high DAMP score in epithelial niche. (h). A matrixplot of DAMP-related gene expression caused by different CBN in AT2-activated cells. (i). IL-33 release caused by CBN into BAL fluid measured by ELISA. (j). IL-33 release into the supernatant of mouse AT2-like cells LA4 caused by CBN measured by ELISA. (k). Double staining of TUNEL-positive cells in AMs marked by CD11c. DAPI: blue, CD11c: green, TUNEL: red. Scale bar: 20 μm. (l). The quantification of TUNEL & CD11c double positive events in mouse lung tissue at 12 h. (m). IL1α release caused by CBN into BAL fluid measured by ELISA. (n). The visualization of Il1a expression and localization by UMAP. (o). IL1α release upon CBN exposure in isolated mouse primary AMs. The expression of Ccl2 (p) and Ccl3 (q) induced by CBN exposure in AM-like J774.1 cells. CNP (50 μg/mL), DWCNT (50 μg/mL), and MWCNT (30 μg/mL) were used in the in vitro study. Data were shown as the mean ± SEM ( n = 3 or 4), one-way ANOVA followed by Dunn’s multiple comparisons test was used for statistical analysis.

Techniques: TUNEL Assay, Double Staining, Gene Expression, Enzyme-linked Immunosorbent Assay, Expressing, Isolation, In Vitro

$Novel multimodal microspectroscopy-based correlative microscopy enables a comprehensive investigation of the studied nanobio interface across a broad spatial scale, from tens of micrometers down to the nanometer level. This approach provides both functional and structural insights, which in our study focus on the interface between lung epithelial cells and exposed NMs. The colored areas illustrate the typical imaging ranges for each technique, highlighting the type and extent of information obtained. * The spatial resolution extends beyond the optical limit, as FLIM and fHSI can probe molecular interactions at a subdiffraction scale.$

Journal: ACS Nano

Article Title: High-Resolution Correlative Microscopy Approach for Nanobio Interface Studies of Nanoparticle-Induced Lung Epithelial Cell Damage

doi: 10.1021/acsnano.4c17838

Figure Lengend Snippet: Novel multimodal microspectroscopy-based correlative microscopy enables a comprehensive investigation of the studied nanobio interface across a broad spatial scale, from tens of micrometers down to the nanometer level. This approach provides both functional and structural insights, which in our study focus on the interface between lung epithelial cells and exposed NMs. The colored areas illustrate the typical imaging ranges for each technique, highlighting the type and extent of information obtained. * The spatial resolution extends beyond the optical limit, as FLIM and fHSI can probe molecular interactions at a subdiffraction scale.

Article Snippet: The murine epithelial lung tissue cell line (LA-4, ATCC CCL-196), murine alveolar lung macrophage cell line (MH-S; ATCC, CRL-2019), F-12K medium (Gibco), fetal bovine serum (ATCC), 1% penicillin-streptomycin (Sigma), 1% nonessential amino acids, l -glutamine, beta-mercaptoethanol (Gibco), phosphate buffer saline (PBS), live cell imaging solution (LCIS, Invitrogen); titanium dioxide nanotubes (TiO 2 NTs) in anatase form synthesized in-house; μ-Slide 8-well (Ibidi), silicon nitride Si 3 N 4 support film (PELCO, 21509CL, Ted Pella), TEM formvar/carbon film on Au Gilder 200 F1 finder grids (FCF200F1-AU-50, EMS), ammonium acetate (Sigma-Aldrich), PTFE coated high precision and ultrafine tweezers (72919-3SATe, EMS), propane transfer system for plunge freezer (37015, Electron Microscopy Sciences); AlexaFluor 647 (Thermo Fischer Scientific), Atto 594 (ATTO-TEC), CellMask Orange (Invitrogen), SiR-actin (Spirochrome), Draq5 (Invitrogen), MitoTracker Orange CMTMRos (Invitrogen), PSM-39 (in-house).

Techniques: Microscopy, Functional Assay, Imaging

Correlative multimodal fluorescence microscopy and SEM-EDS (multimodal CLEM) applied on lung epithelial LA4 cells exposed to TiO 2 NTs for 2 days reveal physicochemical properties of the nanobio interface and the insights of DNA binding and transport during plausible cell apoptosis. (A) Low to high magnification 2D/3D CLSM showing TiO 2 -bio composites on the cell surface and the morphology of the cell nuclei, actin and TiO 2 (in red) and mitochondria (in green). (B) The same site with correlated FLIM capable of precisely distinguishing between individual labeled structures (color-coded from red to blue), using a single laser source (λ = 640 nm). Shifted distribution of τ i and τ 2 from biexponential fit (green to yellow in the chart on the left) indicate on local FRET between TiO 2 and DNA dyes, revealing plausible binding of DNA to TiO 2 surface. (C) Correlated FLIM and SEM after a successful registration and overlap of fiducials shown in (A). High magnification images reveal large EVs with different morphologies, denoted with 2 and 3. (D) Chemical characterization of the same structures performed by SEM-EDS confirms not only high accumulation of biological matter (C) on nanoparticles’ surface (Ti) but also a few times higher content of organic phosphate normalized to biological matter (P/N) (right chart and table), indicating a high but mechanistically different DNA load inside large EVs.

Journal: ACS Nano

Article Title: High-Resolution Correlative Microscopy Approach for Nanobio Interface Studies of Nanoparticle-Induced Lung Epithelial Cell Damage

doi: 10.1021/acsnano.4c17838

Figure Lengend Snippet: Correlative multimodal fluorescence microscopy and SEM-EDS (multimodal CLEM) applied on lung epithelial LA4 cells exposed to TiO 2 NTs for 2 days reveal physicochemical properties of the nanobio interface and the insights of DNA binding and transport during plausible cell apoptosis. (A) Low to high magnification 2D/3D CLSM showing TiO 2 -bio composites on the cell surface and the morphology of the cell nuclei, actin and TiO 2 (in red) and mitochondria (in green). (B) The same site with correlated FLIM capable of precisely distinguishing between individual labeled structures (color-coded from red to blue), using a single laser source (λ = 640 nm). Shifted distribution of τ i and τ 2 from biexponential fit (green to yellow in the chart on the left) indicate on local FRET between TiO 2 and DNA dyes, revealing plausible binding of DNA to TiO 2 surface. (C) Correlated FLIM and SEM after a successful registration and overlap of fiducials shown in (A). High magnification images reveal large EVs with different morphologies, denoted with 2 and 3. (D) Chemical characterization of the same structures performed by SEM-EDS confirms not only high accumulation of biological matter (C) on nanoparticles’ surface (Ti) but also a few times higher content of organic phosphate normalized to biological matter (P/N) (right chart and table), indicating a high but mechanistically different DNA load inside large EVs.

Techniques: Fluorescence, Microscopy, Binding Assay, Labeling

Novel high-resolution CLEM-μXRF confirming that changes in the physical properties of the surrounding biological environment are induced by Fe and uncovering the plausible inflammatory formation of a fibrous network that resembles the fibrin matrix formed over TiO 2 -bio composites immobilized on the plasma membrane of lung epithelial LA-4 cells. (A) Cells grown on thin Si 3 N 4 substrates (gray) with labeled cell membranes (green), actin (red), and nanoparticles (blue) acquired using 3-channel CLSM with 10× and 60× objective magnification. High-magnification 2D and 3D CLSM reveals the size, shape, and topography of a large TiO 2 -bio composite, measuring over ten microns, arrested on the surface (marked with an arrow). (B) Right: FLIM image of the investigated composite revealing significant contrast in fluorescence lifetime between local regions (from yellow to blue); Left: fluorescence decay and τ i distributions from the corresponding sites. (C) Right: correlated CLSM and SEM showing slight shrinkage and local cracks near the cell boundary after rapid freeze-drying, while preserving the investigated structures on the cellular surface; Left: high-magnification SEM revealing the local formation and the morphology of a fibrous network over the TiO 2 -bio composites on the cellular surface and its inflammatory implications, examined further in Supporting Figures S4 and S5 . (D) Left: SR μXRF elemental maps of oxygen and metals, distributed locally on the investigated cell; Right: Local molecular (physical) changes related to Fe accumulation (via τ m ) on the nanobio interface (regions within rectangles), as measured by correlated FLIM and SR μXRF and represented on top of the SEM data.

Journal: ACS Nano

Article Title: High-Resolution Correlative Microscopy Approach for Nanobio Interface Studies of Nanoparticle-Induced Lung Epithelial Cell Damage

doi: 10.1021/acsnano.4c17838

Figure Lengend Snippet: Novel high-resolution CLEM-μXRF confirming that changes in the physical properties of the surrounding biological environment are induced by Fe and uncovering the plausible inflammatory formation of a fibrous network that resembles the fibrin matrix formed over TiO 2 -bio composites immobilized on the plasma membrane of lung epithelial LA-4 cells. (A) Cells grown on thin Si 3 N 4 substrates (gray) with labeled cell membranes (green), actin (red), and nanoparticles (blue) acquired using 3-channel CLSM with 10× and 60× objective magnification. High-magnification 2D and 3D CLSM reveals the size, shape, and topography of a large TiO 2 -bio composite, measuring over ten microns, arrested on the surface (marked with an arrow). (B) Right: FLIM image of the investigated composite revealing significant contrast in fluorescence lifetime between local regions (from yellow to blue); Left: fluorescence decay and τ i distributions from the corresponding sites. (C) Right: correlated CLSM and SEM showing slight shrinkage and local cracks near the cell boundary after rapid freeze-drying, while preserving the investigated structures on the cellular surface; Left: high-magnification SEM revealing the local formation and the morphology of a fibrous network over the TiO 2 -bio composites on the cellular surface and its inflammatory implications, examined further in Supporting Figures S4 and S5 . (D) Left: SR μXRF elemental maps of oxygen and metals, distributed locally on the investigated cell; Right: Local molecular (physical) changes related to Fe accumulation (via τ m ) on the nanobio interface (regions within rectangles), as measured by correlated FLIM and SR μXRF and represented on top of the SEM data.

Techniques: Clinical Proteomics, Membrane, Labeling, Fluorescence, Preserving

Novel multimodal CLEM combined with synchrotron μXRF (CLEM-μXRF) revealing in-depth physicochemical and morpho-functional properties of inflammatory TiO 2 NPs-rich cell-excreted composites immobilized on the surface of lung epithelial LA4 cells. (A) Combined BF and wide field FM employed to visualize cell growth on 100 nm thick transparent silicon nitride (Si 3 N 4 ) films of the 100 × 100 um dimension used as fiducials and optimal substrate for the correlative microscopy both reflection and transmission mode (μXRF). (B) 2D and 3D CLSM performed on the same site to show labeled cells (in green) and cell-excreted TiO 2 composites (in orange) with an improved resolution. (C) Same site was characterized with additional FLIM and fHSI, capable of distinguishing between individual labeled structures and of inspecting local microenvironment differences, such as molecular conformations or polarity. The upper charts illustrate FLIM decay curves and fluorescence spectra for the two distinct sites. (D) Low to high magnification SEM images of the same site performed after rapid cryo-fixation of the sample to preserve distinct structural features of the TiO 2 -bio composites on the cell surface (bottom image). (E) SR μXRF elemental maps from the same site showing the extensive binding of intrinsic biomolecules (C and N) and essential minerals (Na + and Mg 2+ ) on the TiO 2 -rich local sites. (F) Left supporting atomic number (Z) and density-sensitive STXM map with the typical XRF spectra collected from the TiO 2 -bio composite site (denoted with an asterisk) and its color-coded fits for individual elements. Right – high-magnification correlated Na + map and SEM further highlighting very likely functional relationship between composition and filamentous structure with potential inflammatory implications. (G) Correlated live cell CLSM and high-vacuum SEM and μXRF revealing morpho-functional properties on the distinct sites (white arrows).

Journal: ACS Nano

Article Title: High-Resolution Correlative Microscopy Approach for Nanobio Interface Studies of Nanoparticle-Induced Lung Epithelial Cell Damage

doi: 10.1021/acsnano.4c17838

Figure Lengend Snippet: Novel multimodal CLEM combined with synchrotron μXRF (CLEM-μXRF) revealing in-depth physicochemical and morpho-functional properties of inflammatory TiO 2 NPs-rich cell-excreted composites immobilized on the surface of lung epithelial LA4 cells. (A) Combined BF and wide field FM employed to visualize cell growth on 100 nm thick transparent silicon nitride (Si 3 N 4 ) films of the 100 × 100 um dimension used as fiducials and optimal substrate for the correlative microscopy both reflection and transmission mode (μXRF). (B) 2D and 3D CLSM performed on the same site to show labeled cells (in green) and cell-excreted TiO 2 composites (in orange) with an improved resolution. (C) Same site was characterized with additional FLIM and fHSI, capable of distinguishing between individual labeled structures and of inspecting local microenvironment differences, such as molecular conformations or polarity. The upper charts illustrate FLIM decay curves and fluorescence spectra for the two distinct sites. (D) Low to high magnification SEM images of the same site performed after rapid cryo-fixation of the sample to preserve distinct structural features of the TiO 2 -bio composites on the cell surface (bottom image). (E) SR μXRF elemental maps from the same site showing the extensive binding of intrinsic biomolecules (C and N) and essential minerals (Na + and Mg 2+ ) on the TiO 2 -rich local sites. (F) Left supporting atomic number (Z) and density-sensitive STXM map with the typical XRF spectra collected from the TiO 2 -bio composite site (denoted with an asterisk) and its color-coded fits for individual elements. Right – high-magnification correlated Na + map and SEM further highlighting very likely functional relationship between composition and filamentous structure with potential inflammatory implications. (G) Correlated live cell CLSM and high-vacuum SEM and μXRF revealing morpho-functional properties on the distinct sites (white arrows).

Techniques: Functional Assay, Microscopy, Transmission Assay, Labeling, Fluorescence, Binding Assay

Novel correlated high-resolution FLIM, SR μXRF and HIM providing in-depth morpho-functional assessment of inflammatory TiO 2 -bio cell-excreted composites immobilized on the surface of lung epithelial LA4 cells. (A) Cells grown on thin Si 3 N 4 transparent substrate (in gray, BF image) with labeled cell membranes (in green), actin (in red) and nanoparticles (in light blue) acquired with 3-channel CLSM using 60× water immersion objective. 3D CLSM revealing size, shape and topography of a large, few micron-sized TiO 2 -bio composite formed on the cell surface (marked with an arrow). (B) fHSI and FLIM imaging and analysis of the investigated structure uncovering no particular spectral but significant fluorescence lifetime contrasts, respectively (see the distributions and decays on the left). (C) Correlated FLIM and HIM exhibiting colocalization of distinct fluorescence lifetime map (in orange) and nanoscale topographical features shown in the images on the left. Further ultrahigh magnification HIM reveals intriguing morpho-functional features, from the apparent multiple transport channels into the local site with an accumulated Fe (1) (marked with arrows), to a void or tunnel formed in the center of the TiO 2 -bio composite (2), which could facilitate exchange between insight and outside of the cell. (D) SR μXRF elemental maps of the investigated region showing metals and biomolecules distributed locally and more evenly, respectively. (E) Changes in the physical properties of the molecular environment at the nanobio interface plausibly caused by the high accumulation of Fe, as shown by the correlated FLIM, SR μXRF, and HIM.

Journal: ACS Nano

Article Title: High-Resolution Correlative Microscopy Approach for Nanobio Interface Studies of Nanoparticle-Induced Lung Epithelial Cell Damage

doi: 10.1021/acsnano.4c17838

Figure Lengend Snippet: Novel correlated high-resolution FLIM, SR μXRF and HIM providing in-depth morpho-functional assessment of inflammatory TiO 2 -bio cell-excreted composites immobilized on the surface of lung epithelial LA4 cells. (A) Cells grown on thin Si 3 N 4 transparent substrate (in gray, BF image) with labeled cell membranes (in green), actin (in red) and nanoparticles (in light blue) acquired with 3-channel CLSM using 60× water immersion objective. 3D CLSM revealing size, shape and topography of a large, few micron-sized TiO 2 -bio composite formed on the cell surface (marked with an arrow). (B) fHSI and FLIM imaging and analysis of the investigated structure uncovering no particular spectral but significant fluorescence lifetime contrasts, respectively (see the distributions and decays on the left). (C) Correlated FLIM and HIM exhibiting colocalization of distinct fluorescence lifetime map (in orange) and nanoscale topographical features shown in the images on the left. Further ultrahigh magnification HIM reveals intriguing morpho-functional features, from the apparent multiple transport channels into the local site with an accumulated Fe (1) (marked with arrows), to a void or tunnel formed in the center of the TiO 2 -bio composite (2), which could facilitate exchange between insight and outside of the cell. (D) SR μXRF elemental maps of the investigated region showing metals and biomolecules distributed locally and more evenly, respectively. (E) Changes in the physical properties of the molecular environment at the nanobio interface plausibly caused by the high accumulation of Fe, as shown by the correlated FLIM, SR μXRF, and HIM.

Techniques: Functional Assay, Labeling, Imaging, Fluorescence

Schematic overview of the possible modes of action of the cell response to the disruptive nature of TiO 2 NTs, toxic to lung epithelial cells, with different inflammatory and anti-inflammatory outcomes (colored from pink to green), observed at the nanobio interface. Created with BioRender.com .

Journal: ACS Nano

Article Title: High-Resolution Correlative Microscopy Approach for Nanobio Interface Studies of Nanoparticle-Induced Lung Epithelial Cell Damage

doi: 10.1021/acsnano.4c17838

Figure Lengend Snippet: Schematic overview of the possible modes of action of the cell response to the disruptive nature of TiO 2 NTs, toxic to lung epithelial cells, with different inflammatory and anti-inflammatory outcomes (colored from pink to green), observed at the nanobio interface. Created with BioRender.com .

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