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Human Leukemia 60 Hl60 Cells, supplied by ATCC, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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In vitro validation of the Pep@MNP platform for specific capture and identification of thyroid cancer cells. A and B, Immunofluorescence staining of the capture marker EpCAM ( A ) and the identification marker CKmix ( B ) in thyroid cancer cell lines (BHT101 and BCPAP) and a negative control cell line <t>(HL60).</t> Nuclei were counterstained with DAPI. Scale bars, 10 μm. C, Quantitative analysis of the MFI of CKmix in BHT101, BCPAP, and HL60 cells, demonstrating significantly higher expression in thyroid cancer cells. D and E, FCM analysis confirming the surface expression of EpCAM ( D ) and high intracellular expression of CKmix ( E ) in BHT101 and BCPAP cells but not in HL60 cells. F, Scanning electron microscopy images showing the specific binding of Pep@MNPs to target BCPAP cells, whereas bare MNPs show minimal interaction. Both nanoparticle types show negligible binding to the negative control HL60 cells. Scale bars, 5 μm (top row) and 3 μm (bottom row). G, Representative immunofluorescence images defining the criteria for identifying a captured BCPAP cell (CTCs-like phenotype: DAPI+/CKmix+/CD45 − ) and distinguishing it from a co-captured white blood cell (WBC; DAPI+/CKmix − /CD45 + ). H, Capture sensitivity analysis. The graph shows the capture efficiency of the platform for varying numbers of BCPAP cells spiked into a solution. I, Capture specificity analysis. The graph compares the capture efficiency of the platform for cells with high EpCAM expression (BCPAP), low EpCAM expression (BHT101), and negative EpCAM expression (HL60). ****, P value < 0.0001.
Promyelocytic Leukemia Cell Line Hl60, supplied by Procell Inc, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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In vitro validation of the Pep@MNP platform for specific capture and identification of thyroid cancer cells. A and B, Immunofluorescence staining of the capture marker EpCAM ( A ) and the identification marker CKmix ( B ) in thyroid cancer cell lines (BHT101 and BCPAP) and a negative control cell line <t>(HL60).</t> Nuclei were counterstained with DAPI. Scale bars, 10 μm. C, Quantitative analysis of the MFI of CKmix in BHT101, BCPAP, and HL60 cells, demonstrating significantly higher expression in thyroid cancer cells. D and E, FCM analysis confirming the surface expression of EpCAM ( D ) and high intracellular expression of CKmix ( E ) in BHT101 and BCPAP cells but not in HL60 cells. F, Scanning electron microscopy images showing the specific binding of Pep@MNPs to target BCPAP cells, whereas bare MNPs show minimal interaction. Both nanoparticle types show negligible binding to the negative control HL60 cells. Scale bars, 5 μm (top row) and 3 μm (bottom row). G, Representative immunofluorescence images defining the criteria for identifying a captured BCPAP cell (CTCs-like phenotype: DAPI+/CKmix+/CD45 − ) and distinguishing it from a co-captured white blood cell (WBC; DAPI+/CKmix − /CD45 + ). H, Capture sensitivity analysis. The graph shows the capture efficiency of the platform for varying numbers of BCPAP cells spiked into a solution. I, Capture specificity analysis. The graph compares the capture efficiency of the platform for cells with high EpCAM expression (BCPAP), low EpCAM expression (BHT101), and negative EpCAM expression (HL60). ****, P value < 0.0001.
Acute Promyelocytic Leukemia Cell Line Hl60, supplied by ATCC, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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In vitro validation of the Pep@MNP platform for specific capture and identification of thyroid cancer cells. A and B, Immunofluorescence staining of the capture marker EpCAM ( A ) and the identification marker CKmix ( B ) in thyroid cancer cell lines (BHT101 and BCPAP) and a negative control cell line <t>(HL60).</t> Nuclei were counterstained with DAPI. Scale bars, 10 μm. C, Quantitative analysis of the MFI of CKmix in BHT101, BCPAP, and HL60 cells, demonstrating significantly higher expression in thyroid cancer cells. D and E, FCM analysis confirming the surface expression of EpCAM ( D ) and high intracellular expression of CKmix ( E ) in BHT101 and BCPAP cells but not in HL60 cells. F, Scanning electron microscopy images showing the specific binding of Pep@MNPs to target BCPAP cells, whereas bare MNPs show minimal interaction. Both nanoparticle types show negligible binding to the negative control HL60 cells. Scale bars, 5 μm (top row) and 3 μm (bottom row). G, Representative immunofluorescence images defining the criteria for identifying a captured BCPAP cell (CTCs-like phenotype: DAPI+/CKmix+/CD45 − ) and distinguishing it from a co-captured white blood cell (WBC; DAPI+/CKmix − /CD45 + ). H, Capture sensitivity analysis. The graph shows the capture efficiency of the platform for varying numbers of BCPAP cells spiked into a solution. I, Capture specificity analysis. The graph compares the capture efficiency of the platform for cells with high EpCAM expression (BCPAP), low EpCAM expression (BHT101), and negative EpCAM expression (HL60). ****, P value < 0.0001.
Human Acute Myeloid Leukemia Aml Cell Line Hl60, supplied by ATCC, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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a , Bacterial burden one day after UTI89 infection (200 CFUs intraperitoneal inoculation) in 3-day old pups administered sera from control mice without EcN colonization (n=8) compared with sera from EcN colonized WT (n=5) or EcN colonized μMT −/− (n=8) donors. b , Bacterial burden one day after UTI89 infection in 3-day old pup or 8-week old adult FcγR null , C3 −/−, C1q −/− or Cd22 −/− recipients administered sera from EcN colonized WT donor mice (n=6–8 mice/group, with each dot representing the data from an individual animal) compared with sera from control mice without E. coli colonization (n=6–8 mice/group, with each dot representing the data from an individual animal). c , EcN opsonization by sera from control mice without EcN colonization (n=7) compared with sera from WT (n=7), μMT −/− (n=7) or C3 −/− (n=7) EcN colonized donors in RAW264.7 murine macrophage cells. d , EcN opsonization by sera from control mice without E. coli colonization (n=6) compared with sera from EcN colonized donors (n=6) with anti-CD16/32 Fc blockade or rat IgG2b isotype control antibody in RAW264.7 murine macrophage cells. e, Opsonization of E. coli (pooled mix of neonatal clinical isolates RS218, SCB12, SCB29, SCB61, SCB34, SCB58, SCB37, SCB60) by cord blood sera from term pregnancy after heat-inactivation, supplementation with IgG-depleted human sera, or with anti-human Fc block compared with goat polyclonal IgG isotype control antibody in human THP1 activated macrophage cells (left) or <t>HL60</t> differentiated neutrophil cells (right) (n=8 unique cord blood specimens/group [THP1 cells]; n=6 unique cord blood specimens/group [HL60 cells]). Data are presented as mean values (bar) ± one standard deviation. Differences between groups analyzed using one-way ANOVA (panels a, c-e) or unpaired Student’s t test (panel b). LOD, limits of detection.
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ATCC promyelocytic leukemia hl60 line
a , Bacterial burden one day after UTI89 infection (200 CFUs intraperitoneal inoculation) in 3-day old pups administered sera from control mice without EcN colonization (n=8) compared with sera from EcN colonized WT (n=5) or EcN colonized μMT −/− (n=8) donors. b , Bacterial burden one day after UTI89 infection in 3-day old pup or 8-week old adult FcγR null , C3 −/−, C1q −/− or Cd22 −/− recipients administered sera from EcN colonized WT donor mice (n=6–8 mice/group, with each dot representing the data from an individual animal) compared with sera from control mice without E. coli colonization (n=6–8 mice/group, with each dot representing the data from an individual animal). c , EcN opsonization by sera from control mice without EcN colonization (n=7) compared with sera from WT (n=7), μMT −/− (n=7) or C3 −/− (n=7) EcN colonized donors in RAW264.7 murine macrophage cells. d , EcN opsonization by sera from control mice without E. coli colonization (n=6) compared with sera from EcN colonized donors (n=6) with anti-CD16/32 Fc blockade or rat IgG2b isotype control antibody in RAW264.7 murine macrophage cells. e, Opsonization of E. coli (pooled mix of neonatal clinical isolates RS218, SCB12, SCB29, SCB61, SCB34, SCB58, SCB37, SCB60) by cord blood sera from term pregnancy after heat-inactivation, supplementation with IgG-depleted human sera, or with anti-human Fc block compared with goat polyclonal IgG isotype control antibody in human THP1 activated macrophage cells (left) or <t>HL60</t> differentiated neutrophil cells (right) (n=8 unique cord blood specimens/group [THP1 cells]; n=6 unique cord blood specimens/group [HL60 cells]). Data are presented as mean values (bar) ± one standard deviation. Differences between groups analyzed using one-way ANOVA (panels a, c-e) or unpaired Student’s t test (panel b). LOD, limits of detection.
Promyelocytic Leukemia Hl60 Line, supplied by ATCC, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Image Search Results


In vitro validation of the Pep@MNP platform for specific capture and identification of thyroid cancer cells. A and B, Immunofluorescence staining of the capture marker EpCAM ( A ) and the identification marker CKmix ( B ) in thyroid cancer cell lines (BHT101 and BCPAP) and a negative control cell line (HL60). Nuclei were counterstained with DAPI. Scale bars, 10 μm. C, Quantitative analysis of the MFI of CKmix in BHT101, BCPAP, and HL60 cells, demonstrating significantly higher expression in thyroid cancer cells. D and E, FCM analysis confirming the surface expression of EpCAM ( D ) and high intracellular expression of CKmix ( E ) in BHT101 and BCPAP cells but not in HL60 cells. F, Scanning electron microscopy images showing the specific binding of Pep@MNPs to target BCPAP cells, whereas bare MNPs show minimal interaction. Both nanoparticle types show negligible binding to the negative control HL60 cells. Scale bars, 5 μm (top row) and 3 μm (bottom row). G, Representative immunofluorescence images defining the criteria for identifying a captured BCPAP cell (CTCs-like phenotype: DAPI+/CKmix+/CD45 − ) and distinguishing it from a co-captured white blood cell (WBC; DAPI+/CKmix − /CD45 + ). H, Capture sensitivity analysis. The graph shows the capture efficiency of the platform for varying numbers of BCPAP cells spiked into a solution. I, Capture specificity analysis. The graph compares the capture efficiency of the platform for cells with high EpCAM expression (BCPAP), low EpCAM expression (BHT101), and negative EpCAM expression (HL60). ****, P value < 0.0001.

Journal: Clinical Cancer Research

Article Title: Clinical Significance for Risk Stratification of Papillary Thyroid Cancer by TUMORFISHER Circulating Tumor Cell Technique

doi: 10.1158/1078-0432.CCR-25-2694

Figure Lengend Snippet: In vitro validation of the Pep@MNP platform for specific capture and identification of thyroid cancer cells. A and B, Immunofluorescence staining of the capture marker EpCAM ( A ) and the identification marker CKmix ( B ) in thyroid cancer cell lines (BHT101 and BCPAP) and a negative control cell line (HL60). Nuclei were counterstained with DAPI. Scale bars, 10 μm. C, Quantitative analysis of the MFI of CKmix in BHT101, BCPAP, and HL60 cells, demonstrating significantly higher expression in thyroid cancer cells. D and E, FCM analysis confirming the surface expression of EpCAM ( D ) and high intracellular expression of CKmix ( E ) in BHT101 and BCPAP cells but not in HL60 cells. F, Scanning electron microscopy images showing the specific binding of Pep@MNPs to target BCPAP cells, whereas bare MNPs show minimal interaction. Both nanoparticle types show negligible binding to the negative control HL60 cells. Scale bars, 5 μm (top row) and 3 μm (bottom row). G, Representative immunofluorescence images defining the criteria for identifying a captured BCPAP cell (CTCs-like phenotype: DAPI+/CKmix+/CD45 − ) and distinguishing it from a co-captured white blood cell (WBC; DAPI+/CKmix − /CD45 + ). H, Capture sensitivity analysis. The graph shows the capture efficiency of the platform for varying numbers of BCPAP cells spiked into a solution. I, Capture specificity analysis. The graph compares the capture efficiency of the platform for cells with high EpCAM expression (BCPAP), low EpCAM expression (BHT101), and negative EpCAM expression (HL60). ****, P value < 0.0001.

Article Snippet: The human thyroid cancer cell lines BCPAP (RRID: CVCL_0153) and BHT101 (RRID: CVCL_1085), and the human promyelocytic leukemia cell line HL60 (RRID: CVCL_0002), were obtained from Procell Life Science & Technology in August 2021.

Techniques: In Vitro, Biomarker Discovery, Immunofluorescence, Staining, Marker, Negative Control, Expressing, Electron Microscopy, Binding Assay

a , Bacterial burden one day after UTI89 infection (200 CFUs intraperitoneal inoculation) in 3-day old pups administered sera from control mice without EcN colonization (n=8) compared with sera from EcN colonized WT (n=5) or EcN colonized μMT −/− (n=8) donors. b , Bacterial burden one day after UTI89 infection in 3-day old pup or 8-week old adult FcγR null , C3 −/−, C1q −/− or Cd22 −/− recipients administered sera from EcN colonized WT donor mice (n=6–8 mice/group, with each dot representing the data from an individual animal) compared with sera from control mice without E. coli colonization (n=6–8 mice/group, with each dot representing the data from an individual animal). c , EcN opsonization by sera from control mice without EcN colonization (n=7) compared with sera from WT (n=7), μMT −/− (n=7) or C3 −/− (n=7) EcN colonized donors in RAW264.7 murine macrophage cells. d , EcN opsonization by sera from control mice without E. coli colonization (n=6) compared with sera from EcN colonized donors (n=6) with anti-CD16/32 Fc blockade or rat IgG2b isotype control antibody in RAW264.7 murine macrophage cells. e, Opsonization of E. coli (pooled mix of neonatal clinical isolates RS218, SCB12, SCB29, SCB61, SCB34, SCB58, SCB37, SCB60) by cord blood sera from term pregnancy after heat-inactivation, supplementation with IgG-depleted human sera, or with anti-human Fc block compared with goat polyclonal IgG isotype control antibody in human THP1 activated macrophage cells (left) or HL60 differentiated neutrophil cells (right) (n=8 unique cord blood specimens/group [THP1 cells]; n=6 unique cord blood specimens/group [HL60 cells]). Data are presented as mean values (bar) ± one standard deviation. Differences between groups analyzed using one-way ANOVA (panels a, c-e) or unpaired Student’s t test (panel b). LOD, limits of detection.

Journal: Nature

Article Title: Natural maternal immunity protects neonates from Escherichia coli sepsis

doi: 10.1038/s41586-026-10225-z

Figure Lengend Snippet: a , Bacterial burden one day after UTI89 infection (200 CFUs intraperitoneal inoculation) in 3-day old pups administered sera from control mice without EcN colonization (n=8) compared with sera from EcN colonized WT (n=5) or EcN colonized μMT −/− (n=8) donors. b , Bacterial burden one day after UTI89 infection in 3-day old pup or 8-week old adult FcγR null , C3 −/−, C1q −/− or Cd22 −/− recipients administered sera from EcN colonized WT donor mice (n=6–8 mice/group, with each dot representing the data from an individual animal) compared with sera from control mice without E. coli colonization (n=6–8 mice/group, with each dot representing the data from an individual animal). c , EcN opsonization by sera from control mice without EcN colonization (n=7) compared with sera from WT (n=7), μMT −/− (n=7) or C3 −/− (n=7) EcN colonized donors in RAW264.7 murine macrophage cells. d , EcN opsonization by sera from control mice without E. coli colonization (n=6) compared with sera from EcN colonized donors (n=6) with anti-CD16/32 Fc blockade or rat IgG2b isotype control antibody in RAW264.7 murine macrophage cells. e, Opsonization of E. coli (pooled mix of neonatal clinical isolates RS218, SCB12, SCB29, SCB61, SCB34, SCB58, SCB37, SCB60) by cord blood sera from term pregnancy after heat-inactivation, supplementation with IgG-depleted human sera, or with anti-human Fc block compared with goat polyclonal IgG isotype control antibody in human THP1 activated macrophage cells (left) or HL60 differentiated neutrophil cells (right) (n=8 unique cord blood specimens/group [THP1 cells]; n=6 unique cord blood specimens/group [HL60 cells]). Data are presented as mean values (bar) ± one standard deviation. Differences between groups analyzed using one-way ANOVA (panels a, c-e) or unpaired Student’s t test (panel b). LOD, limits of detection.

Article Snippet: For neutrophil cells, human myeloid leukemia HL60 (ATCC CCL-240) cells (1 × 10 4 cells/well) were seeded into 384 well tissue culture treated plates (Corning, 3701) in RPMI 1640 media supplemented with L-glutamine, penicillin-streptomycin, HEPES, 10% FBS, and 1.3% DMSO for 5 days as described 85 .

Techniques: Infection, Control, Blocking Assay, Standard Deviation

a, Dried newborn blood spot specimens were obtained from cases of E. coli neonatal sepsis with 3 controls each matched for infant sex, gestational age and infection time. b , Birth gestational age and infection onset age distribution among 100 cases of neonatal E. coli sepsis. c , Anti- E. coli IgG titers in newborn blood spots from babies with E. coli sepsis (n=100) compared with the average in matched controls (n=100) titered to pooled eight neonatal infection clinical isolates (RS218, SCB12, SCB29, SCB61, SCB34, SCB58, SCB37, SCB60) evaluated by birth gestational age. d , IgG levels in newborn blood spots of babies described in panel c (n=100 [ E. coli sepsis]; n=100 [controls]). e-f, IgG titers against in newborn blood spots against five pooled OmpA loop peptides (e) or scramble control peptides (f) for babies described in panel c (n=100 [ E. coli sepsis]; n=100 [controls]). g-h, Anti- E. coli opsonization activity in newborn blood spot specimens against pooled eight neonatal infection clinical isolates in THP1 activated macrophage cells (g) or HL60 differentiated neutrophil cells (h) (n=100 [ E. coli sepsis]; n=100 [controls]). Each point represents the data from individual blood spot specimens of E. coli sepsis cases (blue) or the average from 3 matched controls for each case (red), with 95% confidence intervals highlighted. Data are presented as mean values (bar) ± one standard deviation. Differences between groups analyzed using unpaired Student’s t test (panel b, gestational weeks), Mann-Whitney U test (panel b, infection onset age), paired Student’s t test (panels e – h), or regression intercepts using Analysis of Covariance (panels e – h). Rights for use of pictures in panel a provided by March of Dimes (left) and Michigan Department of Health and Human Services (middle). Diagram in panel a (right) created using BioRender under Cincinnati Children’s Hospital Medical Center’s Academic Instutional License.

Journal: Nature

Article Title: Natural maternal immunity protects neonates from Escherichia coli sepsis

doi: 10.1038/s41586-026-10225-z

Figure Lengend Snippet: a, Dried newborn blood spot specimens were obtained from cases of E. coli neonatal sepsis with 3 controls each matched for infant sex, gestational age and infection time. b , Birth gestational age and infection onset age distribution among 100 cases of neonatal E. coli sepsis. c , Anti- E. coli IgG titers in newborn blood spots from babies with E. coli sepsis (n=100) compared with the average in matched controls (n=100) titered to pooled eight neonatal infection clinical isolates (RS218, SCB12, SCB29, SCB61, SCB34, SCB58, SCB37, SCB60) evaluated by birth gestational age. d , IgG levels in newborn blood spots of babies described in panel c (n=100 [ E. coli sepsis]; n=100 [controls]). e-f, IgG titers against in newborn blood spots against five pooled OmpA loop peptides (e) or scramble control peptides (f) for babies described in panel c (n=100 [ E. coli sepsis]; n=100 [controls]). g-h, Anti- E. coli opsonization activity in newborn blood spot specimens against pooled eight neonatal infection clinical isolates in THP1 activated macrophage cells (g) or HL60 differentiated neutrophil cells (h) (n=100 [ E. coli sepsis]; n=100 [controls]). Each point represents the data from individual blood spot specimens of E. coli sepsis cases (blue) or the average from 3 matched controls for each case (red), with 95% confidence intervals highlighted. Data are presented as mean values (bar) ± one standard deviation. Differences between groups analyzed using unpaired Student’s t test (panel b, gestational weeks), Mann-Whitney U test (panel b, infection onset age), paired Student’s t test (panels e – h), or regression intercepts using Analysis of Covariance (panels e – h). Rights for use of pictures in panel a provided by March of Dimes (left) and Michigan Department of Health and Human Services (middle). Diagram in panel a (right) created using BioRender under Cincinnati Children’s Hospital Medical Center’s Academic Instutional License.

Article Snippet: For neutrophil cells, human myeloid leukemia HL60 (ATCC CCL-240) cells (1 × 10 4 cells/well) were seeded into 384 well tissue culture treated plates (Corning, 3701) in RPMI 1640 media supplemented with L-glutamine, penicillin-streptomycin, HEPES, 10% FBS, and 1.3% DMSO for 5 days as described 85 .

Techniques: Activity Assay, Clinical Proteomics, Infection, Control, Standard Deviation, MANN-WHITNEY

a-d , Anti- E. coli IgG levels in blood spots from babies with E. coli sepsis (n=100) and matched controls (n=296) titered against pooled neonatal clinical isolates (RS218, SCB12, SCB29, SCB61, SCB34, SCB58, SCB37, SCB60) (a), titered to pooled OmpA outer loop peptides (b), opsonization activity against eight pooled E. coli clinical isolates in THP1 macrophage (c) or HL60 neutrophil cells (d) (left), and probability of E. coli sepsis for each parameter using conditional logistic regression accounting for 1:3 case-control matching (anti- E. coli IgG, anti-OmpA IgG, and anti- E. coli opsonization THP1 cells), or standard logistic regression for anti- E. coli opsonization HL60 cells where separation between matched cases and controls was sufficient to prevent convergence of conditional logistic regression, with shading indicating 95% confidence intervals (right). Data are presented as mean values (bar) ± one standard deviation. e, Anti- E. coli IgG titers in blood spots from babies with E. coli sepsis (n=100) compared with the average in matched controls (n=100) titered against pooled eight neonatal clinical isolates evaluated by infection onset timing. f , IgG levels in blood spots of babies described in panel e (n=100 [ E. coli sepsis]; n=100 [controls]). g-h, IgG titers against in blood spots against pooled OmpA loop peptides (g) or scramble control peptides (h) for babies described in panel e (n=100 [ E. coli sepsis]; n=100 [controls]). i-j, Anti- E. coli opsonization activity in blood spot specimens against eight pooled E. coli clinical isolates in THP1 macrophage (i) or HL60 neutrophil cells (j) for babies described in panel e (n=100 [ E. coli sepsis]; n=100 [controls]). Each point represents the data from individual blood spot specimens of E. coli sepsis cases (blue) or the average from 3 matched controls for each case (red) with 95% confidence intervals highlighted. k , Anti- E. coli or anti-OmpA IgG titers, or anti- E. coli opsonization activity in THP1 macrophage or HL60 neutrophil cells of blood spots of babies identified with E. coli sepsis within the first 2 days after birth (n=44) or later onset infection (n=56). Differences between groups analyzed using unparied (panel a-d) or paired Student’s t test (panel k), and between regression intercepts using Analysis of Covariance (e - j).

Journal: Nature

Article Title: Natural maternal immunity protects neonates from Escherichia coli sepsis

doi: 10.1038/s41586-026-10225-z

Figure Lengend Snippet: a-d , Anti- E. coli IgG levels in blood spots from babies with E. coli sepsis (n=100) and matched controls (n=296) titered against pooled neonatal clinical isolates (RS218, SCB12, SCB29, SCB61, SCB34, SCB58, SCB37, SCB60) (a), titered to pooled OmpA outer loop peptides (b), opsonization activity against eight pooled E. coli clinical isolates in THP1 macrophage (c) or HL60 neutrophil cells (d) (left), and probability of E. coli sepsis for each parameter using conditional logistic regression accounting for 1:3 case-control matching (anti- E. coli IgG, anti-OmpA IgG, and anti- E. coli opsonization THP1 cells), or standard logistic regression for anti- E. coli opsonization HL60 cells where separation between matched cases and controls was sufficient to prevent convergence of conditional logistic regression, with shading indicating 95% confidence intervals (right). Data are presented as mean values (bar) ± one standard deviation. e, Anti- E. coli IgG titers in blood spots from babies with E. coli sepsis (n=100) compared with the average in matched controls (n=100) titered against pooled eight neonatal clinical isolates evaluated by infection onset timing. f , IgG levels in blood spots of babies described in panel e (n=100 [ E. coli sepsis]; n=100 [controls]). g-h, IgG titers against in blood spots against pooled OmpA loop peptides (g) or scramble control peptides (h) for babies described in panel e (n=100 [ E. coli sepsis]; n=100 [controls]). i-j, Anti- E. coli opsonization activity in blood spot specimens against eight pooled E. coli clinical isolates in THP1 macrophage (i) or HL60 neutrophil cells (j) for babies described in panel e (n=100 [ E. coli sepsis]; n=100 [controls]). Each point represents the data from individual blood spot specimens of E. coli sepsis cases (blue) or the average from 3 matched controls for each case (red) with 95% confidence intervals highlighted. k , Anti- E. coli or anti-OmpA IgG titers, or anti- E. coli opsonization activity in THP1 macrophage or HL60 neutrophil cells of blood spots of babies identified with E. coli sepsis within the first 2 days after birth (n=44) or later onset infection (n=56). Differences between groups analyzed using unparied (panel a-d) or paired Student’s t test (panel k), and between regression intercepts using Analysis of Covariance (e - j).

Article Snippet: For neutrophil cells, human myeloid leukemia HL60 (ATCC CCL-240) cells (1 × 10 4 cells/well) were seeded into 384 well tissue culture treated plates (Corning, 3701) in RPMI 1640 media supplemented with L-glutamine, penicillin-streptomycin, HEPES, 10% FBS, and 1.3% DMSO for 5 days as described 85 .

Techniques: Activity Assay, Control, Standard Deviation, Infection, Clinical Proteomics