bronchial epithelial cells  (PromoCell)

Journal: bioRxiv

Article Title: The Joubert syndrome protein CSPP1 is a conserved regulator of vertebrate multiciliogenesis and motile cilia function

doi: 10.64898/2026.03.20.713242

Figure Lengend Snippet: (A) Schematic illustration of multiciliated cell (MCC) differentiation in mouse tracheal epithelial cells (MTECs) and Xenopus embryonic epidermis. Key stages include cell cycle exit, centriole amplification (fibrous granules and deuterosomes), basal body docking, and ciliary axoneme elongation. ( B–F) CSPP1 localization in Mouse Tracheal Epithelial Cells (MTECs). Representative immunofluorescence images of MTECs at different air-liquid interface (ALI) culture days. Scale bars: 5 μm. (B) Centrioles. Cells were stained for CSPP1 (green), Centrin (magenta; centrioles), and ZO-1 (yellow; tight junctions) across differentiation stages. (C) Fibrous granules. MTECs at ALI2 (amplification) stained for CSPP1 (green), PCM1 (magenta; fibrous granules), and Centrin (yellow). (D) Deuterosomes. At ALI2, CSPP1 (green) associates with deuterosome cores marked by DEUP1 (magenta), surrounded by Centrin-positive nascent centrioles (yellow). Inset in ALI2 is 2.5X zoom. (E) Proximal-distal orientation at the centrioles. Top (ALI2) and Bottom (ALI8): CSPP1 (green) localizes relative to ODF2 (magenta; mother centriole appendage) and gamma-tubulin (yellow). Cyan arrowheads indicate the mother centriole (MC); DC indicates daughter centriole. Inset in ciliary plane is 2.5X zoom. (F) Basal bodies and cilia (ALI8). Orthogonal views show CSPP1 (green) localizing to the basal body plane (co-stained with Centrin, yellow) and extending into the ciliary plane (co-stained with Acetylated Tubulin, magenta). Inset in ciliary plane is 3X zoom. (G–J) Cspp1–mCherry localization in Xenopus epidermal MCCs. Representative immunofluorescence images of Xenopus MCCs at different differentiation stages. Scale bars: 10 μm (main panels), 0.1 μm (insets). (G) Fibrous granules. During early amplification, Cspp1–mCherry (magenta) co-localizes with PCM1 (green) and Centrin (yellow) within fibrous granules. Intercalating cell is outlined by dashed lines. Insets are 10X zoom. (H) Deuterosomes. During active amplification, Cspp1–mCherry (magenta) associates with deuterosomes marked by Deup1 (top, green) and PCNT (bottom, green), surrounded by Centrin-positive nascent centrioles (yellow). Intercalating cells are outlined by dashed lines. Inset is 10X zoom. (I) Basal bodies. In differentiated MCCs, Cspp1–mCherry (magenta) localizes to basal bodies marked by PCNT (top, green) and gamma-tubulin (bottom, green), occupying a region partially distinct from the Centrin core (yellow). Inset is 10X zoom. (J) Cilia. Cspp1–mCherry (magenta) localizes to the ciliary axoneme marked by Acetylated Tubulin (green) with enrichment at the distal tips, while maintaining basal body localization (bottom panels; Centrin in yellow).

Article Snippet: Cryopreserved human bronchial epithelial cells (HBEpC, C-12640, PromoCell, maximum passage 3) were thawed in T75 flasks in complete PneumaCult-Ex Plus medium and cultured at 37°C with 5% CO2.

Techniques: Amplification, Immunofluorescence, Staining

Journal: Toxicology Reports

Article Title: Comparative toxicity of menthol- and tobacco-flavored electronic cigarette constituents inducing inflammation, epithelial barrier dysfunction, and nicotinic acetylcholine receptor modulation in the absence of nicotine

doi: 10.1016/j.toxrep.2026.102224

Figure Lengend Snippet: Menthol and tobacco flavoring chemicals caused BEAS-2B epithelial cell barrier dysfunction. BEAS-2B cells were grown in transwell inserts in complete medium. Once reached a monolayer and 80–85 % confluency, cells were serum deprived overnight. Around 90–95 % confluency, cells were treated with 100 μM (A) 98 % Menthone. (B) L -Menthone, (C). Carvone (D) WS-23 (E) Acetoin, (F) Vanillin, (G) PG/VG, and (H) Benzoic Acid. Transepithelial electrical resistance (TEER) and voltage (mV) data were collected pretreatment (0 hr), 6, 8, 20, and 24 hrs. following the treatments and the correlation of TEER and mV vs. time ± SEM are represented. *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001 vs. untreated control., two-way ANOVA. N = 3 wells per chemical treatment.

Article Snippet: Human bronchial epithelial cells (BEAS-2B) (ATCC) were seeded on the apical side of 12 mm diameter polyester membrane transwell inserts with 0.4 μM pore size and 1.12 cm 2 surface area (Corning #3460) in Dulbecco's Modified Eagle Medium/Nutrient Mixture F-12 1:1 (Gibco, Cat# 11320033) supplemented with 5 % fetal bovine serum (FBS), 15 mM HEPES, 1 % L -glutamine, and 1 % antibiotic-antimycotic.

Techniques: Control

Journal: Toxicology Reports

Article Title: Comparative toxicity of menthol- and tobacco-flavored electronic cigarette constituents inducing inflammation, epithelial barrier dysfunction, and nicotinic acetylcholine receptor modulation in the absence of nicotine

doi: 10.1016/j.toxrep.2026.102224

Figure Lengend Snippet: Menthol and tobacco flavoring constituents elicited an interleukin 6 cytokine response in lung epithelial cells. BEAS-2B cells cultured in transwells in complete media, 80–85 % confluency, and serum deprived overnight. Around 90–95 % confluency, cells were treated with 100µM L -Menthone, 98 % Menthone, Carvone, WS-23, Vanillin, Acetoin, Benzoic Acid, and PG/VG. Apical conditioned media was collected after the 24-h time point and IL-6 was quantified. (A) control, PG/VG, and Benzoic Acid-induced response, and (B) L -Menthone, 98 % Menthone, Carvone, WS-23, Vanillin, and Acetoin response compared to untreated control. IL-6 concentration in pg/mL ± SEM is represented, *p < 0.05. vs. control, one-way ANOVA. N = 3 wells per treatment.

Article Snippet: Human bronchial epithelial cells (BEAS-2B) (ATCC) were seeded on the apical side of 12 mm diameter polyester membrane transwell inserts with 0.4 μM pore size and 1.12 cm 2 surface area (Corning #3460) in Dulbecco's Modified Eagle Medium/Nutrient Mixture F-12 1:1 (Gibco, Cat# 11320033) supplemented with 5 % fetal bovine serum (FBS), 15 mM HEPES, 1 % L -glutamine, and 1 % antibiotic-antimycotic.

Techniques: Cell Culture, Control, Concentration Assay

Journal: Toxicology Reports

Article Title: Comparative toxicity of menthol- and tobacco-flavored electronic cigarette constituents inducing inflammation, epithelial barrier dysfunction, and nicotinic acetylcholine receptor modulation in the absence of nicotine

doi: 10.1016/j.toxrep.2026.102224

Figure Lengend Snippet: Menthol and tobacco flavoring constituents elicited an interleukin-8 cytokine response in lung epithelial cells. BEAS-2B cells cultured in transwells in complete media, 80–85 % confluency, and serum deprived overnight. Around 90–95 % confluency, cells were treated with 100 μM l-menthone, 98 % menthone, carvone, WS-23, vanillin, acetoin, benzoic acid, and PG/VG. Apical conditioned media was collected after the 24-h time point and IL6 was quantified. (A) control, PG/VG, and Benzoic Acid-induced response, and (B) l-menthone, 98 % menthone, carvone, WS-23, vanillin, and acetoin response compared to untreated control. IL-8 concentration in pg/mL ± SEM is represented, *p < 0.05, and **p < 0.01 vs. untreated control. one-way ANOVA. N = 3 wells per treatment.

Article Snippet: Human bronchial epithelial cells (BEAS-2B) (ATCC) were seeded on the apical side of 12 mm diameter polyester membrane transwell inserts with 0.4 μM pore size and 1.12 cm 2 surface area (Corning #3460) in Dulbecco's Modified Eagle Medium/Nutrient Mixture F-12 1:1 (Gibco, Cat# 11320033) supplemented with 5 % fetal bovine serum (FBS), 15 mM HEPES, 1 % L -glutamine, and 1 % antibiotic-antimycotic.

Techniques: Cell Culture, Control, Concentration Assay

Journal: Toxicology Reports

Article Title: Comparative toxicity of menthol- and tobacco-flavored electronic cigarette constituents inducing inflammation, epithelial barrier dysfunction, and nicotinic acetylcholine receptor modulation in the absence of nicotine

doi: 10.1016/j.toxrep.2026.102224

Figure Lengend Snippet: Menthol and tobacco flavoring constituents caused minimum cytotoxicity in BEAS-2B cells. BEAS-2B cells cultured in transwells in complete media, at 80–85 % confluency, and serum deprived overnight. Around 90–95 % confluency, Cells were treated with 100 μM l-menthone, 98 % menthone, carvone, WS-23, vanillin, acetoin, benzoic acid, and PG/VG. At the 24-h time point, cells were collected and stained with acridine orange and propidium iodide and the live, cell, and total cells were counted using CellDrop automatic cell counter. Cytotoxicity ± SEM is represented. *p < 0.05 vs. control, one-way ANOVA, N = 3 wells per treatment.

Article Snippet: Human bronchial epithelial cells (BEAS-2B) (ATCC) were seeded on the apical side of 12 mm diameter polyester membrane transwell inserts with 0.4 μM pore size and 1.12 cm 2 surface area (Corning #3460) in Dulbecco's Modified Eagle Medium/Nutrient Mixture F-12 1:1 (Gibco, Cat# 11320033) supplemented with 5 % fetal bovine serum (FBS), 15 mM HEPES, 1 % L -glutamine, and 1 % antibiotic-antimycotic.

Techniques: Cell Culture, Staining, Control

Journal: Toxicology Reports

Article Title: Comparative toxicity of menthol- and tobacco-flavored electronic cigarette constituents inducing inflammation, epithelial barrier dysfunction, and nicotinic acetylcholine receptor modulation in the absence of nicotine

doi: 10.1016/j.toxrep.2026.102224

Figure Lengend Snippet: Menthol and tobacco flavoring constituents caused nicotinic acetylcholine receptor (nAchR) modulation in BEAS-2B lung epithelial cells. BEAS-2B cells cultured in transwells in complete media, 80–85 % confluency, and serum deprived overnight. Around 90–95 % confluency, cells were treated with 100 μM l-menthone, 98 % menthone, carvone, WS-23, vanillin, acetoin, benzoic acid, and PG/VG. At the 24-h time point, cells were collected, lysed, and after BCA protein estimation, 5 μg of protein were loaded to 10-well gel for SDS-gel electrophoresis. After cellulose membrane transfer and blocking, the membranes were probed with primary antibodies for nAchR1,4,5, and 7, with ß-actin loading control for normalization. The same membrane was sometimes re-probed up to 3 times with a different CHRNA. The blots with (A) Nicotinic Acetylcholine Receptors α1 expression with acetoin and PG/VG. (B) Nicotinic Acetylcholine Receptors α4 expression with carvone and WS-23. (C) Nicotinic Acetylcholine Receptors α5 expression with acetoin and PG/VG. (D) Nicotinic Acetylcholine Receptors α5 expression with l-menthone and 98 % menthone. (E) Nicotinic Acetylcholine Receptors α7 expression with carvone and WS-23. All respective CHRNA bands ß-actin are shown with their densitometry fold-change ± SEM. *p < 0.05 and ****p < 0.0001 vs. control, one-way ANOVA. N = 3 wells per chemical. Full blots are shown in the .

Article Snippet: Human bronchial epithelial cells (BEAS-2B) (ATCC) were seeded on the apical side of 12 mm diameter polyester membrane transwell inserts with 0.4 μM pore size and 1.12 cm 2 surface area (Corning #3460) in Dulbecco's Modified Eagle Medium/Nutrient Mixture F-12 1:1 (Gibco, Cat# 11320033) supplemented with 5 % fetal bovine serum (FBS), 15 mM HEPES, 1 % L -glutamine, and 1 % antibiotic-antimycotic.

Techniques: Cell Culture, SDS-Gel, Electrophoresis, Membrane, Blocking Assay, Control, Expressing

Journal: Redox Biology

Article Title: Prophylactic C-terminal occludin–derived peptide attenuates LPS-induced airway inflammation via barrier preservation and mitochondrial ROS regulation

doi: 10.1016/j.redox.2026.104119

Figure Lengend Snippet: Occludin modulates LPS-induced IL-8 secretion, barrier integrity, and cytoskeletal remodeling in human bronchial epithelial cells. (A) The BEAS-2b cells were transfected and were then incubated with LPS in a time-dependent manner before the generation of total cell lysates, and occludin transcripts were assessed by qRT-PCR. ∗ p < 0.05 compared to the control. (B) The cells were treated with LPS in a time-dependent manner. The occludin-specific antibody was assessed by Western blot analysis. β-actin was used as a loading control. (C) A construct expressing wild-type occludin or siRNA-occludin was transiently transfected into BEAS-2b cells. The cells were washed and serum-starved overnight. They were subsequently treated with LPS for 2 h and a cytokine assay was performed with cultured media and cell lysates were harvested for qRT-PCR of IL-8 (D) . The density of the resulting spots of IL-8 was measured using a densitometric analysis. ∗ p < 0.05 compared with control; ∗∗ p < 0.05 compared with LPS treatment; ∗∗∗ p < 0.05 compared with WT occludin-treated transfectants. (E) The cells were transfected with either the wild-type occludin construct or siRNA-occuldin before incubation with LPS for various times, and then TEER testing was performed. Error bars represent the SEM of at least three independent experiments. (F) Cells were then treated with LPS for 2 h. F-actin staining was performed using ActinRed 555 ReadyProbe reagent (Molecular Probes) following the manufacturer's instructions. Cell nuclei were stained with diluted Deep Red (1:300). The fluorescence intensity was analyzed and statistically evaluated (right panel). ∗ p < 0.05 compared with control; ∗∗ p < 0.05 compared with LPS treatment; ∗∗∗ p < 0.05 compared with WT occludin-treated transfectants. All data are representative of at least three independent experiments.

Article Snippet: Human bronchial epithelial (BEAS-2b) cells were purchase from ATCC (CRL-9609), and cells were cultured in BEBM (Lonza, Basel, Switzerland) with a BEGM kit at 37 °C in a humidified incubation with 5% CO 2 .

Techniques: Transfection, Incubation, Quantitative RT-PCR, Control, Western Blot, Construct, Expressing, Cytokine Assay, Cell Culture, Staining, Fluorescence

Journal: Redox Biology

Article Title: Prophylactic C-terminal occludin–derived peptide attenuates LPS-induced airway inflammation via barrier preservation and mitochondrial ROS regulation

doi: 10.1016/j.redox.2026.104119

Figure Lengend Snippet: The C-terminal domain of occludin reduces IL-8 expression and F-actin formation in BEAS-2b cells (A) The occludin deletion mutants were imaged. (B) The cells were transfected with each occludin deletion mutant construct and treated with LPS for 2 h, the IL-8 transcripts were assessed by qRT-PCR and TEER testing was performed (C) . ∗ p < 0.05 compared with control; ∗∗ p < 0.05 compared with LPS treatment; ∗∗∗ p < 0.05 compared with other deletion mutant construct-treated transfectants. (D) After transfected with deletion mutant construct, cells were then treated with LPS for 2 h. F-actin staining was performed using ActinRed 555 ReadyProbe reagent (Molecular Probes) following the manufacturer's instructions. Cell nuclei were stained with diluted Deep Red (1:300). The fluorescence intensity was analyzed and statistically evaluated (lower panel). ∗ p < 0.05 compared with control; ∗∗ p < 0.05 compared with LPS treatment; ∗∗∗ p < 0.05 compared with WT occludin-treated transfectants. All data are representative of at least three independent experiments.

Article Snippet: Human bronchial epithelial (BEAS-2b) cells were purchase from ATCC (CRL-9609), and cells were cultured in BEBM (Lonza, Basel, Switzerland) with a BEGM kit at 37 °C in a humidified incubation with 5% CO 2 .

Techniques: Expressing, Transfection, Mutagenesis, Construct, Quantitative RT-PCR, Control, Staining, Fluorescence

Journal: Redox Biology

Article Title: Prophylactic C-terminal occludin–derived peptide attenuates LPS-induced airway inflammation via barrier preservation and mitochondrial ROS regulation

doi: 10.1016/j.redox.2026.104119

Figure Lengend Snippet: A peptide based on the core sequence of the occludin C-terminal domain modulates LPS-induced inflammatory responses. (A) Peptides were synthesized with a Tat region (italic amino acids) based on the C-terminal domain core sequence of occludin and also tagged with FITC for tracing. A mutant peptide was synthesized by substituting the core sequence YTT with AAA. (B) The BEAS-2b cells were treated with wild-type occludin peptide (pepWT OCLN) or mutant occludin peptide (pepMut OCLN) for 30 h and incubated with LPS for 2 h. The occludin transcripts were assessed by qRT-PCR (B) , TEER testing (C) , and F-actin formation (D) were performed (C) . ∗ p < 0.05 compared with control; ∗∗ p < 0.05 compared with LPS treatment; ∗∗∗ p < 0.05 compared with wild-type occludin peptide-treated cells. The fluorescence intensity was analyzed and statistically evaluated (right panel). All data are representative of at least three independent experiments.

Article Snippet: Human bronchial epithelial (BEAS-2b) cells were purchase from ATCC (CRL-9609), and cells were cultured in BEBM (Lonza, Basel, Switzerland) with a BEGM kit at 37 °C in a humidified incubation with 5% CO 2 .

Techniques: Sequencing, Synthesized, Mutagenesis, Incubation, Quantitative RT-PCR, Control, Fluorescence

Journal: Redox Biology

Article Title: Prophylactic C-terminal occludin–derived peptide attenuates LPS-induced airway inflammation via barrier preservation and mitochondrial ROS regulation

doi: 10.1016/j.redox.2026.104119

Figure Lengend Snippet: Comparison of mRNA expression in the BEAS-2b cells overexpressed occludin. BEAS-2B cells were transfected with wild-type occludin or siRNA-occludin for 24 h and then incubated with LPS for 2 h, after which RNA sequencing analysis was performed. (A) The heat map shows the general regulation pattern of inflammation-related genes that are differentially expressed when WT occludin and siRNA-occludin were treated with LPS, an inflammatory substance. Each row represents a gene, and the columns represent the values of the control group treated only with LPS and the WT occludin and siRNA-occludin groups with LPS. This was used by converting each log value into a fold change value. All genes were adjusted to have the same mean and standard deviation, the unit of change is the standard deviation from the mean, and the color value range of each row is the same. (B) Significant genes were selected using Gene category chat (Fold change value of 2.00 and normalized data (log2) value of 4.00). The above pie chart shows the distribution of four gene categories when comparing LPS versus control, WT occludin + LPS/LPS, and siRNA-occludin + LPS/control. The bar graph below shows RED = upregulated, GREEN = downregulated for each gene category, and shows the number of upregulated and downregulated genes in each gene category. (C) The most markedly altered categories were summarized based on the results shown in panel B. (D) The protein-protein interaction network constructed by the STRING database differentially displays commonly occurring genes by comparing WT occludin + LPS/LPS, siRNA-occludin + LPS/LPS, and LPS/control. These nodes represent proteins associated with inflammation, and these connecting lines denote interactions between two proteins. Different line thicknesses indicate types of evidence used in predicting the associations.

Article Snippet: Human bronchial epithelial (BEAS-2b) cells were purchase from ATCC (CRL-9609), and cells were cultured in BEBM (Lonza, Basel, Switzerland) with a BEGM kit at 37 °C in a humidified incubation with 5% CO 2 .

Techniques: Comparison, Expressing, Transfection, Incubation, RNA Sequencing, Control, Standard Deviation, Construct

Journal: Redox Biology

Article Title: Prophylactic C-terminal occludin–derived peptide attenuates LPS-induced airway inflammation via barrier preservation and mitochondrial ROS regulation

doi: 10.1016/j.redox.2026.104119

Figure Lengend Snippet: The peptide regulates mitochondrial dysfunction and ROS production by inhibiting LPS-induced p38 activation. (A) The BEAS-2b cells were treated with wild-type occludin peptide (pepWT OCLN) or mutant occludin peptide (pepMut OCLN) and incubated with LPS for 15, 30 min. The phospho-specific and total antibodies were assessed by Western blot analysis. β-actin was used as a loading control. (B) The BEAS-2b cells were transfected with p38 overexpression construct (WT p38) or siRNA-p38 for 24 h and incubated with LPS for 4 h siRNA-scramble was used as a negative control. The proinflammatory cytokine transcripts were assessed by qRT-PCR. ∗ p < 0.05 compared with control; ∗∗ p < 0.05 compared with LPS treatment; ∗∗∗ p < 0.05 compared with WT p38-transfected cells. (C) The mitochondrial membrane potential of LPS-induced BEAS-2b cells treated with either WT OCLN peptide or mut peptide was stained with JC-1 dye. Images are representative results of 3 independent experiments. (D) The mitochondria fission was stained using phospho-Drp1 antibody and visualized. The fluorescence intensity was analyzed and statistically evaluated (right panel). ∗ p < 0.05 compared with control; ∗∗ p < 0.05 compared with LPS treatment; ∗∗∗ p < 0.05 compared with WT OCLN peptide-treated transfectants. (E) After the BEAS-2b cells were harvested, cell lysates were used for MTT assay. (F) After mitochondria from the cells was isolated, the mitochondria lysates were used for mtROS measurement. ∗ p < 0.05 compared with control; ∗∗ p < 0.05 compared with LPS only; ∗∗∗ p < 0.05 compared with LPS- and WT occludin peptide-treated cells. All data shown are representative of three independent experiments.

Article Snippet: Human bronchial epithelial (BEAS-2b) cells were purchase from ATCC (CRL-9609), and cells were cultured in BEBM (Lonza, Basel, Switzerland) with a BEGM kit at 37 °C in a humidified incubation with 5% CO 2 .

Techniques: Activation Assay, Mutagenesis, Incubation, Western Blot, Control, Transfection, Over Expression, Construct, Negative Control, Quantitative RT-PCR, Membrane, Staining, Fluorescence, MTT Assay, Isolation

Journal: bioRxiv

Article Title: Anti-oxidant and anti-inflammatory Effects of Aerosolised microalgal-derived extracellular vesicles in Bronchial Epithelial–Macrophage Co-cultures at the Air-Liquid Interface

doi: 10.64898/2026.03.19.712886

Figure Lengend Snippet: Cytotoxicity of co-cultured CALU-3 and dTHP-1 cells as determined by LDH release following oxidative stimuli (1mM TBHP) for 4 hours ( A ), 24 hours ( B ), or following inflammatory stimuli (125 and 250 µg/mL LPS) for 24 hours ( C ). Data are expressed as mean ± SEM of at least three independent experiments. One-way ANOVA was used to determine statistically significant differences among the tested groups. (*p < 0.05).

Article Snippet: A bronchial epithelial–macrophage co-culture model was established using the human bronchial epithelial cell line Calu-3 (ATCC, HTB-55) and differentiated macrophages derived from the human monocytic cell line THP-1 (ATCC, TIB-202) to investigate the anti-inflammatory and antioxidant properties of nanoalgosomes.

Techniques: Cell Culture

Journal: bioRxiv

Article Title: Anti-oxidant and anti-inflammatory Effects of Aerosolised microalgal-derived extracellular vesicles in Bronchial Epithelial–Macrophage Co-cultures at the Air-Liquid Interface

doi: 10.64898/2026.03.19.712886

Figure Lengend Snippet: Effect of nanoalgosome priming on epithelial barrier integrity in CALU-3/dTHP-1 coculture. TEER values after 1mM TBHP treatment for 4 hours ( A ) and 24 hours ( B ), and in response to nebulized LPS (125 and 250 µg/mL) after 24 hours ( C ). Data are presented as mean ± SEM of four independent experiments. Statistical significance was determined using one-way ANOVA (**p < 0.01, ****p < 0.0001).

Article Snippet: A bronchial epithelial–macrophage co-culture model was established using the human bronchial epithelial cell line Calu-3 (ATCC, HTB-55) and differentiated macrophages derived from the human monocytic cell line THP-1 (ATCC, TIB-202) to investigate the anti-inflammatory and antioxidant properties of nanoalgosomes.

Techniques:

Journal: bioRxiv

Article Title: Anti-oxidant and anti-inflammatory Effects of Aerosolised microalgal-derived extracellular vesicles in Bronchial Epithelial–Macrophage Co-cultures at the Air-Liquid Interface

doi: 10.64898/2026.03.19.712886

Figure Lengend Snippet: Cytokine secretion profile of CALU-3/dTHP-1 coculture following exposure to nebulized LPS. ( A ) IL-6, ( B ) IL-8, ( C ) IL-1β, ( D ) IL-18, (E) TNF-α, and ( F ) IL-10 were quantified after exposure to 125 and 250 µg/mL nebulized LPS solution for 24 hours. Data are presented as mean ± SEM from three independent experiments. Statistical significance was determined using one-way ANOVA (*p< 0.5, **p < 0.01).

Article Snippet: A bronchial epithelial–macrophage co-culture model was established using the human bronchial epithelial cell line Calu-3 (ATCC, HTB-55) and differentiated macrophages derived from the human monocytic cell line THP-1 (ATCC, TIB-202) to investigate the anti-inflammatory and antioxidant properties of nanoalgosomes.

Techniques:

Journal: International Journal of Nanomedicine

Article Title: Exploring the Potential Role of Manganese-Based Zeolitic Imidazolate Framework Nanoparticles in Cancer Therapy: In vitro Studies Using Lung Cancer Cells

doi: 10.2147/IJN.S578869

Figure Lengend Snippet: Dose-dependent effect of Mn-rods on the cell viability of ( A ) A549 and ( B ) Calu-3 cells after 24 and 48 h incubation at 37 °C. Cell viability was assessed using Alamar Blue metabolic assay and expressed as percentage relative to untreated cells (normalized to 100%). Data are shown as means ± SD. n=3. The statistical analysis was conducted using two-way ANOVA, p<0.05 (*), p<0.01 (**) and p<0.001 (***) compared to negative control (untreated cells) for each time point.

Article Snippet: Human alveolar epithelial type II cells (A549) and human bronchial epithelial cells (Calu-3) (passages 4–22) from the American Tissue Type Culture Collection (ATCC) were cultured at 37 °C in 5% CO 2 and 95% humidity.

Techniques: Incubation, Metabolic Assay, Negative Control

Journal: International Journal of Nanomedicine

Article Title: Exploring the Potential Role of Manganese-Based Zeolitic Imidazolate Framework Nanoparticles in Cancer Therapy: In vitro Studies Using Lung Cancer Cells

doi: 10.2147/IJN.S578869

Figure Lengend Snippet: TEM images showing the cellular uptake of Mn-rods (10 µg/mL) by A549 and Calu-3 cells. Panels ( A – C ) correspond to A549 cells: ( A and B ) after 24 and 48 h of exposure to Mn-rods, respectively. ( C ) corresponds to untreated A549 cells. Panels ( D – F ) correspond to Calu-3 cells: ( D and E ) show Mn-rods internalization after 24 and 48 h of exposure, respectively. ( F ) corresponds to untreated Calu-3 cells. Yellow dashed circles highlight internalized Mn-rods, and yellow dashed lines mark the areas shown at higher magnification.

Article Snippet: Human alveolar epithelial type II cells (A549) and human bronchial epithelial cells (Calu-3) (passages 4–22) from the American Tissue Type Culture Collection (ATCC) were cultured at 37 °C in 5% CO 2 and 95% humidity.

Techniques: