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keratinocyte growth kit components  (ATCC)


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    ATCC keratinocyte growth kit components
    Hematoxylin and eosin (H&E) staining of skin biopsy samples from mice (that allowed feeding of mock/ XM_002400035 -dsRNA-treated ticks) display that tick feeding causes inflammation at bite site in mock-dsRNA-treated group ( A ), but inflammation is reduced in XM_002400035 -dsRNA-treated group ( B ). Within the panniculus, there is downward projection of epidermis containing chitinous tick mouthparts (shown by black arrow). The panniculus contained moderate to large number of neutrophils, lymphocytes, plasma cells, and lower number of macrophages in mice that allowed feeding of mock-dsRNA-treated ticks ( A ). However, panniculus contained moderate number of inflammatory cells (shown by black arrow) with lymphocytes mixed with few macrophages and plasma cells in mice that allowed feeding of XM_002400035 -dsRNA-treated ticks. There is a mild crush artifact in this image. Magnification of both these images is 200×. Scale bar indicates 100 μm for each image. Enlarged images shown in Fig. 9A,B are repeated in Appendix Fig. for better visualization. ( C ) ELISA assay performed with skin lysates from mice that allowed feeding of ticks silenced for exosomal GRP or mock control ticks. Samples were probed with serum from immunized mice (1:1000 dilution). ( D ) Scratch assays performed on HaCaT cell monolayers incubated with 2 µg of GST/GST- GRP/GST-CXCL-12 protein (for 12 h), with/without 20 µl of tick exosomes from uninfected (UI), LGTV-infected (I), LGTV-infected and mock-dsRNA-treated or LGTV-infected and XM_002400035 -dsRNA-treated groups are shown. Phase contrast images (obtained using EVOS auto-fluorescence system, M7000) of HaCaT cell monolayers were taken for selected time-points (as before scratch, 0, 16, 20, and 24 h) and using 10× magnification. Untreated (UT) monolayers served as internal control. Scale bar indicates 275 μm for each image per group or timepoint. ( E ) Measurement of remaining wound size diameters (analyzed by ImageJ software) at different time-points (of 0, 16, 20, and 24 h) post-treatment of tick exosomes-derived from UI, I, mock/ XM_002400035 -dsRNA is shown. Wounds at 0 h were considered as 100% for all groups, including untreated (UT) control. Mouse CXCL-12 expression was analyzed in skin samples from mice immunized with GST/GST-GRP protein is shown ( F ). Exact number of sample numbers for each group representing multiple experiments is 5 mice for GST/6 mice for GST-GRP groups (in C , F ). Statistical differences were calculated using Mann–Whitney U test and p value is shown. p < 0.05 is considered as statistically significant. ( G ) Schematic model showing tick-borne flavivirus transmission to vertebrate host via tick saliva-derived exosomes. Ixodes scapularis tick attaches firmly and bites on host skin for longer feeding. Secreted saliva contains a plethora of substances including cement and perhaps cement-like GRPs to seal the feeding cone/cavity for directional blood flow and to defend from being groomed off by the vertebrate host. During blood meal ingestion, infected-ticks may continuously spit saliva containing infectious exosomes with viral full-length RNA genomes or polyproteins at host skin interface. We propose that incubation of tick exosomes containing exosomal GRP modulates the battle ground at skin interface by delaying cell migration/recruitment of immune cells (like neutrophils and dendritic cells from circulation) at the wound/bite site. Tick exosomes containing GRP inhibits residential <t>keratinocytes</t> and IL-8/CXCL-12 to delay injury, wound-healing, tissue damage, and repair process that will eventually enable ticks to acquire a successful blood meal at the host skin interface. .
    Keratinocyte Growth Kit Components, supplied by ATCC, used in various techniques. Bioz Stars score: 96/100, based on 218 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/keratinocyte+growth+kit+components/Keratinocyte+Growth+Kit/pmc12993085-592-40-46
    Average 96 stars, based on 218 article reviews
    keratinocyte growth kit components - by Bioz Stars, 2026-09
    96/100 stars

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    1) Product Images from "Arthropod exosomal glycine-rich protein as a potential vaccine candidate effectively reduces tick blood-feeding and pathogen transmission"

    Article Title: Arthropod exosomal glycine-rich protein as a potential vaccine candidate effectively reduces tick blood-feeding and pathogen transmission

    Journal: The EMBO Journal

    doi: 10.1038/s44318-026-00709-z

    Hematoxylin and eosin (H&E) staining of skin biopsy samples from mice (that allowed feeding of mock/ XM_002400035 -dsRNA-treated ticks) display that tick feeding causes inflammation at bite site in mock-dsRNA-treated group ( A ), but inflammation is reduced in XM_002400035 -dsRNA-treated group ( B ). Within the panniculus, there is downward projection of epidermis containing chitinous tick mouthparts (shown by black arrow). The panniculus contained moderate to large number of neutrophils, lymphocytes, plasma cells, and lower number of macrophages in mice that allowed feeding of mock-dsRNA-treated ticks ( A ). However, panniculus contained moderate number of inflammatory cells (shown by black arrow) with lymphocytes mixed with few macrophages and plasma cells in mice that allowed feeding of XM_002400035 -dsRNA-treated ticks. There is a mild crush artifact in this image. Magnification of both these images is 200×. Scale bar indicates 100 μm for each image. Enlarged images shown in Fig. 9A,B are repeated in Appendix Fig. for better visualization. ( C ) ELISA assay performed with skin lysates from mice that allowed feeding of ticks silenced for exosomal GRP or mock control ticks. Samples were probed with serum from immunized mice (1:1000 dilution). ( D ) Scratch assays performed on HaCaT cell monolayers incubated with 2 µg of GST/GST- GRP/GST-CXCL-12 protein (for 12 h), with/without 20 µl of tick exosomes from uninfected (UI), LGTV-infected (I), LGTV-infected and mock-dsRNA-treated or LGTV-infected and XM_002400035 -dsRNA-treated groups are shown. Phase contrast images (obtained using EVOS auto-fluorescence system, M7000) of HaCaT cell monolayers were taken for selected time-points (as before scratch, 0, 16, 20, and 24 h) and using 10× magnification. Untreated (UT) monolayers served as internal control. Scale bar indicates 275 μm for each image per group or timepoint. ( E ) Measurement of remaining wound size diameters (analyzed by ImageJ software) at different time-points (of 0, 16, 20, and 24 h) post-treatment of tick exosomes-derived from UI, I, mock/ XM_002400035 -dsRNA is shown. Wounds at 0 h were considered as 100% for all groups, including untreated (UT) control. Mouse CXCL-12 expression was analyzed in skin samples from mice immunized with GST/GST-GRP protein is shown ( F ). Exact number of sample numbers for each group representing multiple experiments is 5 mice for GST/6 mice for GST-GRP groups (in C , F ). Statistical differences were calculated using Mann–Whitney U test and p value is shown. p < 0.05 is considered as statistically significant. ( G ) Schematic model showing tick-borne flavivirus transmission to vertebrate host via tick saliva-derived exosomes. Ixodes scapularis tick attaches firmly and bites on host skin for longer feeding. Secreted saliva contains a plethora of substances including cement and perhaps cement-like GRPs to seal the feeding cone/cavity for directional blood flow and to defend from being groomed off by the vertebrate host. During blood meal ingestion, infected-ticks may continuously spit saliva containing infectious exosomes with viral full-length RNA genomes or polyproteins at host skin interface. We propose that incubation of tick exosomes containing exosomal GRP modulates the battle ground at skin interface by delaying cell migration/recruitment of immune cells (like neutrophils and dendritic cells from circulation) at the wound/bite site. Tick exosomes containing GRP inhibits residential keratinocytes and IL-8/CXCL-12 to delay injury, wound-healing, tissue damage, and repair process that will eventually enable ticks to acquire a successful blood meal at the host skin interface. .
    Figure Legend Snippet: Hematoxylin and eosin (H&E) staining of skin biopsy samples from mice (that allowed feeding of mock/ XM_002400035 -dsRNA-treated ticks) display that tick feeding causes inflammation at bite site in mock-dsRNA-treated group ( A ), but inflammation is reduced in XM_002400035 -dsRNA-treated group ( B ). Within the panniculus, there is downward projection of epidermis containing chitinous tick mouthparts (shown by black arrow). The panniculus contained moderate to large number of neutrophils, lymphocytes, plasma cells, and lower number of macrophages in mice that allowed feeding of mock-dsRNA-treated ticks ( A ). However, panniculus contained moderate number of inflammatory cells (shown by black arrow) with lymphocytes mixed with few macrophages and plasma cells in mice that allowed feeding of XM_002400035 -dsRNA-treated ticks. There is a mild crush artifact in this image. Magnification of both these images is 200×. Scale bar indicates 100 μm for each image. Enlarged images shown in Fig. 9A,B are repeated in Appendix Fig. for better visualization. ( C ) ELISA assay performed with skin lysates from mice that allowed feeding of ticks silenced for exosomal GRP or mock control ticks. Samples were probed with serum from immunized mice (1:1000 dilution). ( D ) Scratch assays performed on HaCaT cell monolayers incubated with 2 µg of GST/GST- GRP/GST-CXCL-12 protein (for 12 h), with/without 20 µl of tick exosomes from uninfected (UI), LGTV-infected (I), LGTV-infected and mock-dsRNA-treated or LGTV-infected and XM_002400035 -dsRNA-treated groups are shown. Phase contrast images (obtained using EVOS auto-fluorescence system, M7000) of HaCaT cell monolayers were taken for selected time-points (as before scratch, 0, 16, 20, and 24 h) and using 10× magnification. Untreated (UT) monolayers served as internal control. Scale bar indicates 275 μm for each image per group or timepoint. ( E ) Measurement of remaining wound size diameters (analyzed by ImageJ software) at different time-points (of 0, 16, 20, and 24 h) post-treatment of tick exosomes-derived from UI, I, mock/ XM_002400035 -dsRNA is shown. Wounds at 0 h were considered as 100% for all groups, including untreated (UT) control. Mouse CXCL-12 expression was analyzed in skin samples from mice immunized with GST/GST-GRP protein is shown ( F ). Exact number of sample numbers for each group representing multiple experiments is 5 mice for GST/6 mice for GST-GRP groups (in C , F ). Statistical differences were calculated using Mann–Whitney U test and p value is shown. p < 0.05 is considered as statistically significant. ( G ) Schematic model showing tick-borne flavivirus transmission to vertebrate host via tick saliva-derived exosomes. Ixodes scapularis tick attaches firmly and bites on host skin for longer feeding. Secreted saliva contains a plethora of substances including cement and perhaps cement-like GRPs to seal the feeding cone/cavity for directional blood flow and to defend from being groomed off by the vertebrate host. During blood meal ingestion, infected-ticks may continuously spit saliva containing infectious exosomes with viral full-length RNA genomes or polyproteins at host skin interface. We propose that incubation of tick exosomes containing exosomal GRP modulates the battle ground at skin interface by delaying cell migration/recruitment of immune cells (like neutrophils and dendritic cells from circulation) at the wound/bite site. Tick exosomes containing GRP inhibits residential keratinocytes and IL-8/CXCL-12 to delay injury, wound-healing, tissue damage, and repair process that will eventually enable ticks to acquire a successful blood meal at the host skin interface. .

    Techniques Used: Staining, Clinical Proteomics, Enzyme-linked Immunosorbent Assay, Control, Incubation, Infection, Fluorescence, Software, Derivative Assay, Expressing, MANN-WHITNEY, Transmission Assay, Migration

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    Cell Culture:

    Article Title: Perfusion Bioreactor Culture Incorporating Mechanical Confinement Enhances Mesenchymal Stem Cell Extracellular Vesicle Production and Wound Healing Potential
    Article Snippet: Human umbilical vein endothelial cells (HUVECs) and human dermal microvascular endothelial cells (HDMECs) were purchased from PromoCell (C-12203, C-12212) and cultured in endothelial growth media (PromoCell; C-2212) with 1% penicillin-streptomycin in 0.1% gelatin-coated tissue culture flasks. .. Human primary epidermal keratinocytes were purchased from ATCC (PCS-200-011) and cultured in dermal cell basal media (ATCC; PCS-200-030) supplemented with ATCC’s Keratinocyte Growth Kit components (ATCC; PCS-200-040) and 0.1% penicillin-streptomycin. .. Human dermal fibroblasts were purchased from ATCC (PCS-201-012) and cultured in Gibco DMEM/F-12 (ThermoFisher Scientific; 11320033 supplemented with 10% FBS and 1% penicillin-streptomycin.

    Article Title: The multicomponent Passerini reaction as a means of accessing diversity in structure, activity and properties: Soft and hard vanilloid/cannabinoid modulators.
    Article Snippet: Primary adult epidermal keratinocytes were purchased from American Type Culture Collection (ATCC, Manassas, VA, USA) (ATCC®, PCS 200-011TM) and maintained as reported in Serafini et al., 2018 [52]. .. Briefly, cells were cultured in Dermal Cell Basal Media (ATCC, PCS 200− 030) supplemented with Keratinocyte Growth kit components (Bovine Pituitary Extract (BPE), recombinant tumor growth factor alpha (rhTGFα), L-glutamine, hydrocortisone hemi-succinate, insulin, epinephrine, and apotransferrin, (ATCC PCS 200-040), 10 units/mL penicillin and 100 μg/mL streptomycin (Sigma-Aldrich, St. Louis, MO)). .. Primary adult dermal fibroblasts were purchased from American Type Culture Collection (ATCC, Manassas, VA, USA) (ATCC®, PCS 200-012TM) and maintained as reported in Serafini et al., 2018 [52].

    Article Title: Perfusion Bioreactor Culture Incorporating Mechanical Confinement Enhances Mesenchymal Stem Cell Extracellular Vesicle Production and Wound Healing Potential
    Article Snippet: Human umbilical vein endothelial cells (HUVECs) and human dermal microvascular endothelial cells (HDMECs) were purchased from PromoCell (C-12203, C-12212) and cultured in endothelial growth media (PromoCell; C-2212) with 1% penicillinstreptomycin in 0.1% gelatin-coated tissue culture flasks. .. Human primary epidermal keratinocytes were purchased from ATCC (PCS-200-011) and cultured in dermal cell basal media (ATCC; PCS-200-030) supplemented with ATCC’s Keratinocyte Growth Kit components (ATCC; PCS-200-040) and 0.1% penicillin-streptomycin. .. Human dermal fibroblasts were purchased from ATCC (PCS-201012) and cultured in Gibco DMEM/F-12 (ThermoFisher Scientific; 11320033 supplemented with 10% FBS and 1% penicillinstreptomycin.

    Recombinant:

    Article Title: The multicomponent Passerini reaction as a means of accessing diversity in structure, activity and properties: Soft and hard vanilloid/cannabinoid modulators.
    Article Snippet: Primary adult epidermal keratinocytes were purchased from American Type Culture Collection (ATCC, Manassas, VA, USA) (ATCC®, PCS 200-011TM) and maintained as reported in Serafini et al., 2018 [52]. .. Briefly, cells were cultured in Dermal Cell Basal Media (ATCC, PCS 200− 030) supplemented with Keratinocyte Growth kit components (Bovine Pituitary Extract (BPE), recombinant tumor growth factor alpha (rhTGFα), L-glutamine, hydrocortisone hemi-succinate, insulin, epinephrine, and apotransferrin, (ATCC PCS 200-040), 10 units/mL penicillin and 100 μg/mL streptomycin (Sigma-Aldrich, St. Louis, MO)). .. Primary adult dermal fibroblasts were purchased from American Type Culture Collection (ATCC, Manassas, VA, USA) (ATCC®, PCS 200-012TM) and maintained as reported in Serafini et al., 2018 [52].

    Wound Healing Assay:

    Article Title: Arthropod exosomal glycine-rich protein as a potential vaccine candidate effectively reduces tick blood-feeding and pathogen transmission
    Article Snippet: Note that CXCL-12 or SDF-1a (hBA-68) purified protein is produced from Escherichia coli bacterial lysates (>98%) and supplied as 35-kDa biologically active, GST-tagged fusion protein corresponding to 68 amino acids of the SDF-1a of human origin (Catalog number sc-4654, obtained from Santa Cruz Biotechnologies Inc., USA). .. For cell scratch assay, HaCaT cells (1–3 × 1e6) or human keratinocyte primary cultures (5 × 1e5) were seeded in six/twelve-well plates with Dulbecco’s modified Eagle’s medium (DMEM) containing 5% heat-inactivated FBS or with dermal cell basal medium supplemented with keratinocyte growth kit components (obtained from ATCC, USA). ..

    Article Title: Arthropod exosomal glycine-rich protein as a potential vaccine candidate effectively reduces tick blood-feeding and pathogen transmission.
    Article Snippet: Note that CXCL-12 or SDF-1a (hBA-68) purified protein is produced from Escherichia coli bacterial lysates (>98%) and supplied as 35-kDa biologically active, GST-tagged fusion protein corresponding to 68 amino acids of the SDF-1a of human origin (Catalog number sc-4654, obtained from Santa Cruz Biotechnologies Inc., USA). .. For cell scratch assay, HaCaT cells (1–3 × 1e6) or human keratinocyte primary cultures (5 × 1e5) were seeded in six/twelve-well plates with Dulbecco’s modified Eagle’s medium (DMEM) containing 5% heat-inactivated FBS or with dermal cell basal medium supplemented with keratinocyte growth kit components (obtained from ATCC, USA). ..

    Modification:

    Article Title: Arthropod exosomal glycine-rich protein as a potential vaccine candidate effectively reduces tick blood-feeding and pathogen transmission
    Article Snippet: Note that CXCL-12 or SDF-1a (hBA-68) purified protein is produced from Escherichia coli bacterial lysates (>98%) and supplied as 35-kDa biologically active, GST-tagged fusion protein corresponding to 68 amino acids of the SDF-1a of human origin (Catalog number sc-4654, obtained from Santa Cruz Biotechnologies Inc., USA). .. For cell scratch assay, HaCaT cells (1–3 × 1e6) or human keratinocyte primary cultures (5 × 1e5) were seeded in six/twelve-well plates with Dulbecco’s modified Eagle’s medium (DMEM) containing 5% heat-inactivated FBS or with dermal cell basal medium supplemented with keratinocyte growth kit components (obtained from ATCC, USA). ..

    Article Title: Arthropod exosomal glycine-rich protein as a potential vaccine candidate effectively reduces tick blood-feeding and pathogen transmission.
    Article Snippet: Note that CXCL-12 or SDF-1a (hBA-68) purified protein is produced from Escherichia coli bacterial lysates (>98%) and supplied as 35-kDa biologically active, GST-tagged fusion protein corresponding to 68 amino acids of the SDF-1a of human origin (Catalog number sc-4654, obtained from Santa Cruz Biotechnologies Inc., USA). .. For cell scratch assay, HaCaT cells (1–3 × 1e6) or human keratinocyte primary cultures (5 × 1e5) were seeded in six/twelve-well plates with Dulbecco’s modified Eagle’s medium (DMEM) containing 5% heat-inactivated FBS or with dermal cell basal medium supplemented with keratinocyte growth kit components (obtained from ATCC, USA). ..



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    keratinocyte growth kit components  (ATCC)
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    ATCC keratinocyte growth kit components
    Hematoxylin and eosin (H&E) staining of skin biopsy samples from mice (that allowed feeding of mock/ XM_002400035 -dsRNA-treated ticks) display that tick feeding causes inflammation at bite site in mock-dsRNA-treated group ( A ), but inflammation is reduced in XM_002400035 -dsRNA-treated group ( B ). Within the panniculus, there is downward projection of epidermis containing chitinous tick mouthparts (shown by black arrow). The panniculus contained moderate to large number of neutrophils, lymphocytes, plasma cells, and lower number of macrophages in mice that allowed feeding of mock-dsRNA-treated ticks ( A ). However, panniculus contained moderate number of inflammatory cells (shown by black arrow) with lymphocytes mixed with few macrophages and plasma cells in mice that allowed feeding of XM_002400035 -dsRNA-treated ticks. There is a mild crush artifact in this image. Magnification of both these images is 200×. Scale bar indicates 100 μm for each image. Enlarged images shown in Fig. 9A,B are repeated in Appendix Fig. for better visualization. ( C ) ELISA assay performed with skin lysates from mice that allowed feeding of ticks silenced for exosomal GRP or mock control ticks. Samples were probed with serum from immunized mice (1:1000 dilution). ( D ) Scratch assays performed on HaCaT cell monolayers incubated with 2 µg of GST/GST- GRP/GST-CXCL-12 protein (for 12 h), with/without 20 µl of tick exosomes from uninfected (UI), LGTV-infected (I), LGTV-infected and mock-dsRNA-treated or LGTV-infected and XM_002400035 -dsRNA-treated groups are shown. Phase contrast images (obtained using EVOS auto-fluorescence system, M7000) of HaCaT cell monolayers were taken for selected time-points (as before scratch, 0, 16, 20, and 24 h) and using 10× magnification. Untreated (UT) monolayers served as internal control. Scale bar indicates 275 μm for each image per group or timepoint. ( E ) Measurement of remaining wound size diameters (analyzed by ImageJ software) at different time-points (of 0, 16, 20, and 24 h) post-treatment of tick exosomes-derived from UI, I, mock/ XM_002400035 -dsRNA is shown. Wounds at 0 h were considered as 100% for all groups, including untreated (UT) control. Mouse CXCL-12 expression was analyzed in skin samples from mice immunized with GST/GST-GRP protein is shown ( F ). Exact number of sample numbers for each group representing multiple experiments is 5 mice for GST/6 mice for GST-GRP groups (in C , F ). Statistical differences were calculated using Mann–Whitney U test and p value is shown. p < 0.05 is considered as statistically significant. ( G ) Schematic model showing tick-borne flavivirus transmission to vertebrate host via tick saliva-derived exosomes. Ixodes scapularis tick attaches firmly and bites on host skin for longer feeding. Secreted saliva contains a plethora of substances including cement and perhaps cement-like GRPs to seal the feeding cone/cavity for directional blood flow and to defend from being groomed off by the vertebrate host. During blood meal ingestion, infected-ticks may continuously spit saliva containing infectious exosomes with viral full-length RNA genomes or polyproteins at host skin interface. We propose that incubation of tick exosomes containing exosomal GRP modulates the battle ground at skin interface by delaying cell migration/recruitment of immune cells (like neutrophils and dendritic cells from circulation) at the wound/bite site. Tick exosomes containing GRP inhibits residential <t>keratinocytes</t> and IL-8/CXCL-12 to delay injury, wound-healing, tissue damage, and repair process that will eventually enable ticks to acquire a successful blood meal at the host skin interface. .
    Keratinocyte Growth Kit Components, supplied by ATCC, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/keratinocyte+growth+kit+components/Keratinocyte+Growth+Kit/pmc12993085-592-40-46
    Average 96 stars, based on 1 article reviews
    keratinocyte growth kit components - by Bioz Stars, 2026-09
    96/100 stars
    		  Buy from Supplier

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    Hematoxylin and eosin (H&E) staining of skin biopsy samples from mice (that allowed feeding of mock/ XM_002400035 -dsRNA-treated ticks) display that tick feeding causes inflammation at bite site in mock-dsRNA-treated group ( A ), but inflammation is reduced in XM_002400035 -dsRNA-treated group ( B ). Within the panniculus, there is downward projection of epidermis containing chitinous tick mouthparts (shown by black arrow). The panniculus contained moderate to large number of neutrophils, lymphocytes, plasma cells, and lower number of macrophages in mice that allowed feeding of mock-dsRNA-treated ticks ( A ). However, panniculus contained moderate number of inflammatory cells (shown by black arrow) with lymphocytes mixed with few macrophages and plasma cells in mice that allowed feeding of XM_002400035 -dsRNA-treated ticks. There is a mild crush artifact in this image. Magnification of both these images is 200×. Scale bar indicates 100 μm for each image. Enlarged images shown in Fig. 9A,B are repeated in Appendix Fig. for better visualization. ( C ) ELISA assay performed with skin lysates from mice that allowed feeding of ticks silenced for exosomal GRP or mock control ticks. Samples were probed with serum from immunized mice (1:1000 dilution). ( D ) Scratch assays performed on HaCaT cell monolayers incubated with 2 µg of GST/GST- GRP/GST-CXCL-12 protein (for 12 h), with/without 20 µl of tick exosomes from uninfected (UI), LGTV-infected (I), LGTV-infected and mock-dsRNA-treated or LGTV-infected and XM_002400035 -dsRNA-treated groups are shown. Phase contrast images (obtained using EVOS auto-fluorescence system, M7000) of HaCaT cell monolayers were taken for selected time-points (as before scratch, 0, 16, 20, and 24 h) and using 10× magnification. Untreated (UT) monolayers served as internal control. Scale bar indicates 275 μm for each image per group or timepoint. ( E ) Measurement of remaining wound size diameters (analyzed by ImageJ software) at different time-points (of 0, 16, 20, and 24 h) post-treatment of tick exosomes-derived from UI, I, mock/ XM_002400035 -dsRNA is shown. Wounds at 0 h were considered as 100% for all groups, including untreated (UT) control. Mouse CXCL-12 expression was analyzed in skin samples from mice immunized with GST/GST-GRP protein is shown ( F ). Exact number of sample numbers for each group representing multiple experiments is 5 mice for GST/6 mice for GST-GRP groups (in C , F ). Statistical differences were calculated using Mann–Whitney U test and p value is shown. p < 0.05 is considered as statistically significant. ( G ) Schematic model showing tick-borne flavivirus transmission to vertebrate host via tick saliva-derived exosomes. Ixodes scapularis tick attaches firmly and bites on host skin for longer feeding. Secreted saliva contains a plethora of substances including cement and perhaps cement-like GRPs to seal the feeding cone/cavity for directional blood flow and to defend from being groomed off by the vertebrate host. During blood meal ingestion, infected-ticks may continuously spit saliva containing infectious exosomes with viral full-length RNA genomes or polyproteins at host skin interface. We propose that incubation of tick exosomes containing exosomal GRP modulates the battle ground at skin interface by delaying cell migration/recruitment of immune cells (like neutrophils and dendritic cells from circulation) at the wound/bite site. Tick exosomes containing GRP inhibits residential keratinocytes and IL-8/CXCL-12 to delay injury, wound-healing, tissue damage, and repair process that will eventually enable ticks to acquire a successful blood meal at the host skin interface. .

    Journal: The EMBO Journal

    Article Title: Arthropod exosomal glycine-rich protein as a potential vaccine candidate effectively reduces tick blood-feeding and pathogen transmission

    doi: 10.1038/s44318-026-00709-z

    Figure Lengend Snippet: Hematoxylin and eosin (H&E) staining of skin biopsy samples from mice (that allowed feeding of mock/ XM_002400035 -dsRNA-treated ticks) display that tick feeding causes inflammation at bite site in mock-dsRNA-treated group ( A ), but inflammation is reduced in XM_002400035 -dsRNA-treated group ( B ). Within the panniculus, there is downward projection of epidermis containing chitinous tick mouthparts (shown by black arrow). The panniculus contained moderate to large number of neutrophils, lymphocytes, plasma cells, and lower number of macrophages in mice that allowed feeding of mock-dsRNA-treated ticks ( A ). However, panniculus contained moderate number of inflammatory cells (shown by black arrow) with lymphocytes mixed with few macrophages and plasma cells in mice that allowed feeding of XM_002400035 -dsRNA-treated ticks. There is a mild crush artifact in this image. Magnification of both these images is 200×. Scale bar indicates 100 μm for each image. Enlarged images shown in Fig. 9A,B are repeated in Appendix Fig. for better visualization. ( C ) ELISA assay performed with skin lysates from mice that allowed feeding of ticks silenced for exosomal GRP or mock control ticks. Samples were probed with serum from immunized mice (1:1000 dilution). ( D ) Scratch assays performed on HaCaT cell monolayers incubated with 2 µg of GST/GST- GRP/GST-CXCL-12 protein (for 12 h), with/without 20 µl of tick exosomes from uninfected (UI), LGTV-infected (I), LGTV-infected and mock-dsRNA-treated or LGTV-infected and XM_002400035 -dsRNA-treated groups are shown. Phase contrast images (obtained using EVOS auto-fluorescence system, M7000) of HaCaT cell monolayers were taken for selected time-points (as before scratch, 0, 16, 20, and 24 h) and using 10× magnification. Untreated (UT) monolayers served as internal control. Scale bar indicates 275 μm for each image per group or timepoint. ( E ) Measurement of remaining wound size diameters (analyzed by ImageJ software) at different time-points (of 0, 16, 20, and 24 h) post-treatment of tick exosomes-derived from UI, I, mock/ XM_002400035 -dsRNA is shown. Wounds at 0 h were considered as 100% for all groups, including untreated (UT) control. Mouse CXCL-12 expression was analyzed in skin samples from mice immunized with GST/GST-GRP protein is shown ( F ). Exact number of sample numbers for each group representing multiple experiments is 5 mice for GST/6 mice for GST-GRP groups (in C , F ). Statistical differences were calculated using Mann–Whitney U test and p value is shown. p < 0.05 is considered as statistically significant. ( G ) Schematic model showing tick-borne flavivirus transmission to vertebrate host via tick saliva-derived exosomes. Ixodes scapularis tick attaches firmly and bites on host skin for longer feeding. Secreted saliva contains a plethora of substances including cement and perhaps cement-like GRPs to seal the feeding cone/cavity for directional blood flow and to defend from being groomed off by the vertebrate host. During blood meal ingestion, infected-ticks may continuously spit saliva containing infectious exosomes with viral full-length RNA genomes or polyproteins at host skin interface. We propose that incubation of tick exosomes containing exosomal GRP modulates the battle ground at skin interface by delaying cell migration/recruitment of immune cells (like neutrophils and dendritic cells from circulation) at the wound/bite site. Tick exosomes containing GRP inhibits residential keratinocytes and IL-8/CXCL-12 to delay injury, wound-healing, tissue damage, and repair process that will eventually enable ticks to acquire a successful blood meal at the host skin interface. .

    Article Snippet: For cell scratch assay, HaCaT cells (1–3 × 1e6) or human keratinocyte primary cultures (5 × 1e5) were seeded in six/twelve-well plates with Dulbecco’s modified Eagle’s medium (DMEM) containing 5% heat-inactivated FBS or with dermal cell basal medium supplemented with keratinocyte growth kit components (obtained from ATCC, USA).

    Techniques: Staining, Clinical Proteomics, Enzyme-linked Immunosorbent Assay, Control, Incubation, Infection, Fluorescence, Software, Derivative Assay, Expressing, MANN-WHITNEY, Transmission Assay, Migration