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PromoCell bronchial epithelial cells hbecs

A) Immunoblot of FcRn and pIgR in hNECs and <t>hBECs.</t> B, C) Relative protein expression levels by Western blotting of FcRN, pIgR, normalized to β-tublin, n = <3. D, E) Quantification of flow cytometry cell types by percentage of total cells, values are expressed as mean ± SE, n = 1/group. F, G) Transcytosis of IgG and IgA was determined using an ELISA assay. Values are expressed as mean ± SE, n = <3well/time point. *P<0.05 **P<0.01

Bronchial Epithelial Cells Hbecs, supplied by PromoCell, used in various techniques. Bioz Stars score: 95/100, based on 94 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/bronchial+epithelial+cells/bio_rxiv__64898__2026__05__25__727697-46-6-10?v=PromoCell
Average 95 stars, based on 94 article reviews

bronchial epithelial cells hbecs - by Bioz Stars, 2026-07

95/100 stars

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1) Product Images from "Antibody Transcytosis and Neutralizing Activity in Respiratory Epithelial Cells"

Article Title: Antibody Transcytosis and Neutralizing Activity in Respiratory Epithelial Cells

Journal: bioRxiv

doi: 10.64898/2026.05.25.727697

A) Immunoblot of FcRn and pIgR in hNECs and hBECs. B, C) Relative protein expression levels by Western blotting of FcRN, pIgR, normalized to β-tublin, n = <3. D, E) Quantification of flow cytometry cell types by percentage of total cells, values are expressed as mean ± SE, n = 1/group. F, G) Transcytosis of IgG and IgA was determined using an ELISA assay. Values are expressed as mean ± SE, n = <3well/time point. *P<0.05 **P<0.01

Figure Legend Snippet: A) Immunoblot of FcRn and pIgR in hNECs and hBECs. B, C) Relative protein expression levels by Western blotting of FcRN, pIgR, normalized to β-tublin, n = <3. D, E) Quantification of flow cytometry cell types by percentage of total cells, values are expressed as mean ± SE, n = 1/group. F, G) Transcytosis of IgG and IgA was determined using an ELISA assay. Values are expressed as mean ± SE, n = <3well/time point. *P<0.05 **P<0.01

Techniques Used: Western Blot, Expressing, Flow Cytometry, Enzyme-linked Immunosorbent Assay

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Journal: bioRxiv

Article Title: Antibody Transcytosis and Neutralizing Activity in Respiratory Epithelial Cells

doi: 10.64898/2026.05.25.727697

Figure Lengend Snippet: A) Immunoblot of FcRn and pIgR in hNECs and hBECs. B, C) Relative protein expression levels by Western blotting of FcRN, pIgR, normalized to β-tublin, n = <3. D, E) Quantification of flow cytometry cell types by percentage of total cells, values are expressed as mean ± SE, n = 1/group. F, G) Transcytosis of IgG and IgA was determined using an ELISA assay. Values are expressed as mean ± SE, n = <3well/time point. *P<0.05 **P<0.01

Article Snippet: Human nasal epithelial cells (hNECs) or bronchial epithelial cells (hBECs) (Promocell) were grown to confluence in 24-well Falcon filter inserts (0.4-uM pore; 0.33cm 2 ; Becton Dickinson) using PneumaCultTM-Ex Plus Medium (Stemcell, Cat# 05001).

Techniques: Western Blot, Expressing, Flow Cytometry, Enzyme-linked Immunosorbent Assay

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.

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

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.

Journal: Toxicology Reports

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.

Techniques: Cell Culture, Control, Concentration Assay

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.

Journal: Toxicology Reports

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.

Techniques: Cell Culture, Control, Concentration Assay

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.

Journal: Toxicology Reports

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.

Techniques: Cell Culture, Staining, Control

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 .

Journal: Toxicology Reports

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 .

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

SARS-CoV-2 pseudovirus ex vivo infected nasal epithelial cells (n=3 pools). (E-H) SARS-CoV-2 pseudovirus ex vivo infected lung epithelial cells (n= 9). (I-L) SARS-CoV-2 pseudovirus ex vivo infected renal cortex cells (n=7). Flow cytometry plots showing the phenotypic comparison between GFP⁺ (infected, green) and GFP⁻ (uninfected) cells of CD45 - CD31 - EpCAM + cells from the (A) pool #NAL02 (n= 7) or (E) #HLTE197, which includes a paired sample exposed to a spike-empty pseudovirus (background). (B and F) Violin plots depicting the frequency (%) of different epithelial marker expressions within total nasal ( B ) or pulmonary ( F ) EpCAM + (grey) and EpCAM + GFP + cells (green). (C-D and G-H) Boolean pie charts displaying the proportion of nasal ( C-D ) or pulmonary ( G-H ) EpCAM + ( C-G ) and EpCAM + GFP + ( D-H ) cells expressing combinations of color code molecules according to the legend and indicated as surrounding arcs around the pie chart. (I) Flow cytometry plots showing the phenotypic comparison of CD45 - CD31 - cells from #RINN22, either infected (GFP⁺; green) or exposed to a ‘background’ pseudovirus. (J) Violin plots depicting the frequency (%) of various molecules within total CD31 - (grey) and CD31 - GFP + cells (green). (K-L) Boolean pie charts displaying the proportion of CD31 - ( K ) and CD31 - GFP + ( L ) cells expressing combinations of color code molecules according to the legend and indicated as surrounding arcs around the pie chart. For all violin plots, data are represented as median ± IQR. Statistical analyses were performed using two-sided nonparametric Wilcoxon matched-pairs signed-rank test.

Journal: bioRxiv

Article Title: Site-Specific Entry Factors Define Cellular Susceptibility to SARS-CoV-2 in Human Tissues

doi: 10.64898/2026.05.07.723425

Figure Lengend Snippet: SARS-CoV-2 pseudovirus ex vivo infected nasal epithelial cells (n=3 pools). (E-H) SARS-CoV-2 pseudovirus ex vivo infected lung epithelial cells (n= 9). (I-L) SARS-CoV-2 pseudovirus ex vivo infected renal cortex cells (n=7). Flow cytometry plots showing the phenotypic comparison between GFP⁺ (infected, green) and GFP⁻ (uninfected) cells of CD45 - CD31 - EpCAM + cells from the (A) pool #NAL02 (n= 7) or (E) #HLTE197, which includes a paired sample exposed to a spike-empty pseudovirus (background). (B and F) Violin plots depicting the frequency (%) of different epithelial marker expressions within total nasal ( B ) or pulmonary ( F ) EpCAM + (grey) and EpCAM + GFP + cells (green). (C-D and G-H) Boolean pie charts displaying the proportion of nasal ( C-D ) or pulmonary ( G-H ) EpCAM + ( C-G ) and EpCAM + GFP + ( D-H ) cells expressing combinations of color code molecules according to the legend and indicated as surrounding arcs around the pie chart. (I) Flow cytometry plots showing the phenotypic comparison of CD45 - CD31 - cells from #RINN22, either infected (GFP⁺; green) or exposed to a ‘background’ pseudovirus. (J) Violin plots depicting the frequency (%) of various molecules within total CD31 - (grey) and CD31 - GFP + cells (green). (K-L) Boolean pie charts displaying the proportion of CD31 - ( K ) and CD31 - GFP + ( L ) cells expressing combinations of color code molecules according to the legend and indicated as surrounding arcs around the pie chart. For all violin plots, data are represented as median ± IQR. Statistical analyses were performed using two-sided nonparametric Wilcoxon matched-pairs signed-rank test.

Article Snippet: Nasal epithelial cells were obtained with an ASI Rhino-Pro® nasal curette (Arlington, IL, USA) into Bronchial Epithelial Cell Medium (BEpiCM) (Innoprot) washed with PBS with 5 mM EDTA, incubated on a shaker (15 min. 30 rpm, 4°C) centrifuged, filtered and counted.

Techniques: Ex Vivo, Infection, Flow Cytometry, Comparison, Marker, Expressing

(A) UMAP projection of high-dimension single-cell flow cytometry nasal data of EpCAM + cells from ex vivo SARS-CoV-2 pseudovirus infected samples, depicting the differentiation of 8 clusters (MC) and relative abundance of each cluster across the three pools of nasal samples. (B) UMAP visualization highlighting the EpCAM + GFP + infected population (green). Adjacent heatmap displays normalized mean fluorescence intensity of epithelial markers across the 8 identified clusters as indicated in (A) . (C) UMAP-based visualization of the spatial expression of six molecules (top) and density histograms comparing EpCAM⁺ and EpCAM⁺GFP⁺ populations (bottom).

Journal: bioRxiv

Article Title: Site-Specific Entry Factors Define Cellular Susceptibility to SARS-CoV-2 in Human Tissues

doi: 10.64898/2026.05.07.723425

Figure Lengend Snippet: (A) UMAP projection of high-dimension single-cell flow cytometry nasal data of EpCAM + cells from ex vivo SARS-CoV-2 pseudovirus infected samples, depicting the differentiation of 8 clusters (MC) and relative abundance of each cluster across the three pools of nasal samples. (B) UMAP visualization highlighting the EpCAM + GFP + infected population (green). Adjacent heatmap displays normalized mean fluorescence intensity of epithelial markers across the 8 identified clusters as indicated in (A) . (C) UMAP-based visualization of the spatial expression of six molecules (top) and density histograms comparing EpCAM⁺ and EpCAM⁺GFP⁺ populations (bottom).

Techniques: Single Cell, Flow Cytometry, Ex Vivo, Infection, Fluorescence, Expressing

(A) UMAP projection of high-dimension single-cell flow cytometry data of pulmonary EpCAM + cells from uninfected or ex vivo SARS-CoV-2 pseudovirus infected samples, depicting the differentiation of 8 clusters (MC) and relative abundance of each cluster across uninfected versus infected samples (bars on top). Bars below show the percentage of less represented clusters (MC03-MC08). (B) UMAP visualization highlighting the EpCAM + GFP + infected population (green). Adjacent heatmap (bottom) displays normalized mean fluorescence intensity of epithelial markers across the 8 identified clusters as indicated in (A) highlighting the cluster representing GFP + cells (MC07). (C) Volcano plot displaying the differential cluster abundance comparing uninfected and infected samples, the green dot corresponds to MC07. (D) UMAP-based visualization of the spatial expression of six molecules (top) and density histograms comparing EpCAM⁺ and EpCAM⁺GFP⁺ populations (bottom).

Journal: bioRxiv

Article Title: Site-Specific Entry Factors Define Cellular Susceptibility to SARS-CoV-2 in Human Tissues

doi: 10.64898/2026.05.07.723425

Figure Lengend Snippet: (A) UMAP projection of high-dimension single-cell flow cytometry data of pulmonary EpCAM + cells from uninfected or ex vivo SARS-CoV-2 pseudovirus infected samples, depicting the differentiation of 8 clusters (MC) and relative abundance of each cluster across uninfected versus infected samples (bars on top). Bars below show the percentage of less represented clusters (MC03-MC08). (B) UMAP visualization highlighting the EpCAM + GFP + infected population (green). Adjacent heatmap (bottom) displays normalized mean fluorescence intensity of epithelial markers across the 8 identified clusters as indicated in (A) highlighting the cluster representing GFP + cells (MC07). (C) Volcano plot displaying the differential cluster abundance comparing uninfected and infected samples, the green dot corresponds to MC07. (D) UMAP-based visualization of the spatial expression of six molecules (top) and density histograms comparing EpCAM⁺ and EpCAM⁺GFP⁺ populations (bottom).

Techniques: Single Cell, Flow Cytometry, Ex Vivo, Infection, Fluorescence, Expressing

(A) UMAP projection of high-dimension single-cell flow cytometry data of renal CD31 - cells from uninfected or ex vivo SARS-CoV-2 pseudovirus infected samples, depicting the differentiation of 17 clusters (MC) and relative abundance of each cluster across uninfected versus infected samples. (B) UMAP visualization highlighting the CD31 - GFP + infected population (green). Adjacent heatmap displays normalized mean fluorescence intensity of epithelial markers across the 17 identified clusters as indicated in ( A ) highlighting the cluster representing GFP + cells (MC05). (C) Volcano plot displaying the differential cluster abundance comparing uninfected and infected samples, the green dot corresponds to MC05. (D) UMAP-based visualization of the spatial expression of six molecules (top) and density histograms comparing CD31 - and CD31 - GFP + populations (bottom).

Journal: bioRxiv

Article Title: Site-Specific Entry Factors Define Cellular Susceptibility to SARS-CoV-2 in Human Tissues

doi: 10.64898/2026.05.07.723425

Figure Lengend Snippet: (A) UMAP projection of high-dimension single-cell flow cytometry data of renal CD31 - cells from uninfected or ex vivo SARS-CoV-2 pseudovirus infected samples, depicting the differentiation of 17 clusters (MC) and relative abundance of each cluster across uninfected versus infected samples. (B) UMAP visualization highlighting the CD31 - GFP + infected population (green). Adjacent heatmap displays normalized mean fluorescence intensity of epithelial markers across the 17 identified clusters as indicated in ( A ) highlighting the cluster representing GFP + cells (MC05). (C) Volcano plot displaying the differential cluster abundance comparing uninfected and infected samples, the green dot corresponds to MC05. (D) UMAP-based visualization of the spatial expression of six molecules (top) and density histograms comparing CD31 - and CD31 - GFP + populations (bottom).

Techniques: Single Cell, Flow Cytometry, Ex Vivo, Infection, Fluorescence, Expressing

(A) Schematic overview of the experimental workflow. Epithelial cells were isolated from nasal, lung, and kidney tissues and infected ex vivo with SARS-CoV-2 pseudovirus. GFP⁺ (infected) and GFP⁻ (uninfected) cells were sorted and processed using Smart-seq2. After quality control, cells were clustered and analyzed by tissue. (B–D) Nasal epithelial cells. (B) UMAP embedding of five transcriptionally distinct clusters. (C) Cluster distribution across all nasal epithelial cells. (D) Cluster proportions stratified by GFP⁺ and GFP⁻ conditions. (E–G) Lung epithelial cells. (E) UMAP embedding of lung-derived cells showing the separation of three epithelial and one stromal population. (F) Cluster distribution across epithelial and stromal populations. (G) Cluster proportions by infection status. (H–J) Renal cortex epithelial cells. (H) UMAP embedding of two epithelial clusters. (I) Cluster distribution across all renal epithelial cells. (J) Cluster proportions stratified by GFP⁺ and GFP⁻ conditions.

Journal: bioRxiv

Article Title: Site-Specific Entry Factors Define Cellular Susceptibility to SARS-CoV-2 in Human Tissues

doi: 10.64898/2026.05.07.723425

Figure Lengend Snippet: (A) Schematic overview of the experimental workflow. Epithelial cells were isolated from nasal, lung, and kidney tissues and infected ex vivo with SARS-CoV-2 pseudovirus. GFP⁺ (infected) and GFP⁻ (uninfected) cells were sorted and processed using Smart-seq2. After quality control, cells were clustered and analyzed by tissue. (B–D) Nasal epithelial cells. (B) UMAP embedding of five transcriptionally distinct clusters. (C) Cluster distribution across all nasal epithelial cells. (D) Cluster proportions stratified by GFP⁺ and GFP⁻ conditions. (E–G) Lung epithelial cells. (E) UMAP embedding of lung-derived cells showing the separation of three epithelial and one stromal population. (F) Cluster distribution across epithelial and stromal populations. (G) Cluster proportions by infection status. (H–J) Renal cortex epithelial cells. (H) UMAP embedding of two epithelial clusters. (I) Cluster distribution across all renal epithelial cells. (J) Cluster proportions stratified by GFP⁺ and GFP⁻ conditions.

Techniques: Isolation, Infection, Ex Vivo, Control, Derivative Assay

(A) Violin plots showing distributions of standard single-cell RNA-seq quality control metrics across all cells, including the number of detected genes (nFeature_RNA), total UMI counts (nCount_RNA), and the percentage of mitochondrial transcripts (percent.mt). ( B ) Heatmap of the top 10 differentially expressed genes for each identified cluster. Genes are ranked by average log-normalized expression within each cluster relative to others. Color scale indicates scaled expression levels. ( C ) Violin plots depicting normalized expression levels of selected epithelial marker genes ( EPCAM, ELF3, CLDN4 , and CDH1 ) across the indicated clusters, highlighting cluster-specific expression patterns. ( D ) Dot plot summarizing the expression of representative marker genes across clusters, based on Ahn, J.H., et al. (2021. J. Clin. Invest). Dot size reflects the percentage of cells expressing each gene, and color intensity represents the average expression level within each cluster

Journal: bioRxiv

Article Title: Site-Specific Entry Factors Define Cellular Susceptibility to SARS-CoV-2 in Human Tissues

doi: 10.64898/2026.05.07.723425

Figure Lengend Snippet: (A) Violin plots showing distributions of standard single-cell RNA-seq quality control metrics across all cells, including the number of detected genes (nFeature_RNA), total UMI counts (nCount_RNA), and the percentage of mitochondrial transcripts (percent.mt). ( B ) Heatmap of the top 10 differentially expressed genes for each identified cluster. Genes are ranked by average log-normalized expression within each cluster relative to others. Color scale indicates scaled expression levels. ( C ) Violin plots depicting normalized expression levels of selected epithelial marker genes ( EPCAM, ELF3, CLDN4 , and CDH1 ) across the indicated clusters, highlighting cluster-specific expression patterns. ( D ) Dot plot summarizing the expression of representative marker genes across clusters, based on Ahn, J.H., et al. (2021. J. Clin. Invest). Dot size reflects the percentage of cells expressing each gene, and color intensity represents the average expression level within each cluster

Techniques: Single Cell, RNA Sequencing, Control, Expressing, Marker

Journal: bioRxiv

Article Title: Site-Specific Entry Factors Define Cellular Susceptibility to SARS-CoV-2 in Human Tissues

doi: 10.64898/2026.05.07.723425

Figure Lengend Snippet: (A) Violin plots showing distributions of standard single-cell RNA-seq quality control metrics across all cells, including the number of detected genes (nFeature_RNA), total UMI counts (nCount_RNA), and the percentage of mitochondrial transcripts (percent.mt). (B) Heatmap of the top 10 differentially expressed genes per cluster, highlighting transcriptionally distinct epithelial and stromal compartments. Genes are ranked by average log-normalized expression within each cluster relative to others. Color scale indicates scaled expression levels. (C) Violin plots depicting normalized expression levels of representative markers: epithelial markers EPCAM and ELF3 enriched in epithelial groups, and stromal/extracellular matrix markers DCN and MFAP4 enriched in fibroblasts.

Techniques: Single Cell, RNA Sequencing, Control, Expressing

Journal: bioRxiv

Article Title: Site-Specific Entry Factors Define Cellular Susceptibility to SARS-CoV-2 in Human Tissues

doi: 10.64898/2026.05.07.723425

Figure Lengend Snippet: (A) Violin plots showing distributions of standard single-cell RNA-seq quality control metrics across all cells, including the number of detected genes (nFeature_RNA), total UMI counts (nCount_RNA), and the percentage of mitochondrial transcripts (percent.mt). (B) Heatmap of the top 10 differentially expressed genes per cluster, separating proximal tubular epithelial cells from broader epithelial populations. Genes are ranked by average log-normalized expression within each cluster relative to others. Color scale indicates scaled expression levels. (C) Violin plots depicting normalized expression levels of representative markers: epithelial marker EPCAM enriched in epithelial cells, proximal-tubule markers AQP1 and CUBN enriched in the proximal tubular epithelial cluster and SLC12A3 , expressed in the distal convoluted tubule.

Techniques: Single Cell, RNA Sequencing, Control, Expressing, Marker

Volcano plots showing differentially expressed genes between GFP⁺ and GFP⁻ in overall epithelial cells from the (A) nasal mucosa, (B) lung parenchyma and (C) renal cortex; or in individual clusters from a given tissue: (D) epithelial cluster 0 from the nasal mucosa; (F) alveolar type 2 (AT2) cells from the lung; and (G) general epithelial cluster from renal cortex. The horizontal axis shows log₂ fold change, and the vertical axis shows –log₁₀ adjusted p values. Selected significantly upregulated genes (in red) are highlighted in bigger dots.

Journal: bioRxiv

Article Title: Site-Specific Entry Factors Define Cellular Susceptibility to SARS-CoV-2 in Human Tissues

doi: 10.64898/2026.05.07.723425

Figure Lengend Snippet: Volcano plots showing differentially expressed genes between GFP⁺ and GFP⁻ in overall epithelial cells from the (A) nasal mucosa, (B) lung parenchyma and (C) renal cortex; or in individual clusters from a given tissue: (D) epithelial cluster 0 from the nasal mucosa; (F) alveolar type 2 (AT2) cells from the lung; and (G) general epithelial cluster from renal cortex. The horizontal axis shows log₂ fold change, and the vertical axis shows –log₁₀ adjusted p values. Selected significantly upregulated genes (in red) are highlighted in bigger dots.

Techniques:

( A–B ) SARS-CoV-2 pseudovirus entry in lung ( A ) and kidney ( B ) epithelial cells following treatment with inhibitors. Lung or renal cortex-derived cells were exposed to pseudovirus in the presence of anti-ACE2 (25 µg/ml), Camostat (100 µM), KP-457 (ADAM17 inhibitor, 100 µM), anti-IL1R1 (100 µM), Ruxolitinib (JAK1/2 inhibitor, 100 µM), anti-ADAMTSL3 (250 ng/ml), anti-CADM1 (625 ng/ml), anti-GULP1 (625 ng/ml), anti-MDGA2 (62.5 ng/ml), anti-PILRα (1.25 µg/ml) or anti-PTPRK (1.25 µg/ml). Infection levels, quantified by luciferase activity, are expressed relative to untreated controls (100% infection). Each color-coded dot indicates an individual tissue with median and interquartile range indicated for each treatment with dotted lines. Statistical significance was assessed using a Kruskal–Wallis test for multiple comparisons (****P < 0.0001, ***P < 0.001, **P < 0.01, *P < 0.05). ( C ) Plots showing Spearman correlation coefficients and associated significant P values comparing inhibitor effects across lung and kidney tissues.

Journal: bioRxiv

Article Title: Site-Specific Entry Factors Define Cellular Susceptibility to SARS-CoV-2 in Human Tissues

doi: 10.64898/2026.05.07.723425

Figure Lengend Snippet: ( A–B ) SARS-CoV-2 pseudovirus entry in lung ( A ) and kidney ( B ) epithelial cells following treatment with inhibitors. Lung or renal cortex-derived cells were exposed to pseudovirus in the presence of anti-ACE2 (25 µg/ml), Camostat (100 µM), KP-457 (ADAM17 inhibitor, 100 µM), anti-IL1R1 (100 µM), Ruxolitinib (JAK1/2 inhibitor, 100 µM), anti-ADAMTSL3 (250 ng/ml), anti-CADM1 (625 ng/ml), anti-GULP1 (625 ng/ml), anti-MDGA2 (62.5 ng/ml), anti-PILRα (1.25 µg/ml) or anti-PTPRK (1.25 µg/ml). Infection levels, quantified by luciferase activity, are expressed relative to untreated controls (100% infection). Each color-coded dot indicates an individual tissue with median and interquartile range indicated for each treatment with dotted lines. Statistical significance was assessed using a Kruskal–Wallis test for multiple comparisons (****P < 0.0001, ***P < 0.001, **P < 0.01, *P < 0.05). ( C ) Plots showing Spearman correlation coefficients and associated significant P values comparing inhibitor effects across lung and kidney tissues.

Techniques: Derivative Assay, Infection, Luciferase, Activity Assay

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Images

1) Product Images from "Antibody Transcytosis and Neutralizing Activity in Respiratory Epithelial Cells"

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