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  1. Article ; Online: Persistence of Contact Lens-Induced Corneal Parainflammation Following Lens Removal.

    Datta, Ananya / Lee, Ji Hyun / Truong, Tiffany / Flandrin, Orneika / Yang, Yujia / Evans, David J / Fleiszig, Suzanne M J

    Investigative ophthalmology & visual science

    2024  Volume 65, Issue 3, Page(s) 8

    Abstract: Purpose: Contact lens wear induces corneal parainflammation involving increased immune cell numbers after 24 hours' (CD11c+, Lyz2+, γδ-T cells) and six days' (Ly6G+ cells) wear. We investigated the time course of onset and resolution of these responses.! ...

    Abstract Purpose: Contact lens wear induces corneal parainflammation involving increased immune cell numbers after 24 hours' (CD11c+, Lyz2+, γδ-T cells) and six days' (Ly6G+ cells) wear. We investigated the time course of onset and resolution of these responses.
    Methods: LysMcre or C57BL/6J mice were fitted with a contact lens (four to 48 hours). Contralateral eyes did not wear lenses. After lens removal, Lyz2+, MHC-II+ or Ly6G+ cells were examined by quantitative imaging. RT-qPCR determined cytokine gene expression.
    Results: Lens wear for 24 hours increased corneal Lyz2+ cells versus contralateral eyes approximately two-fold. Corneas remained free of visible pathology. The Lyz2+ response was not observed after four or 12 hours' wear, nor after 12 hours' wear plus 12 hours' no wear. Lens removal after 24 hours' wear further increased Lyz2+ cells (∼48% after one day), which persisted for four days, returning to baseline by seven days. Lyz2+ cells in contralateral eyes remained at baseline. MHC-II+ cells showed a similar response but without increasing after lens removal. Lens wear for 48 hours showed reduced Lyz2+ cells versus 24 hours' wear with one day discontinuation, correlating with reduced IL-1β and IL-18 gene expression. Lens wear for 24 hours did not induce Ly6G+ responses six days after removal.
    Conclusions: Lens-induced corneal parainflammation involving Lyz2+ cells requires 24 hours' wear but persists after lens discontinuation, requiring seven days for reversal. Lens wear for 48 hours may suppress initial Lyz2+ cell and cytokine responses. The significance of parainflammation during and after lens wear remains to be determined.
    MeSH term(s) Mice ; Animals ; Mice, Inbred C57BL ; Lens, Crystalline ; Contact Lenses/adverse effects ; Cornea ; Cytokines/genetics
    Chemical Substances Cytokines
    Language English
    Publishing date 2024-03-11
    Publishing country United States
    Document type Journal Article
    ZDB-ID 391794-0
    ISSN 1552-5783 ; 0146-0404
    ISSN (online) 1552-5783
    ISSN 0146-0404
    DOI 10.1167/iovs.65.3.8
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 45: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (1.OG)
    ab Jg. 2022: Lesesaal (EG)

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  2. Article ; Online: Contact lens-induced corneal parainflammation involving Ly6G+ cell infiltration requires IL-17A and γδ T cells.

    Datta, Ananya / Truong, Tiffany / Lee, Ji Hyun / Horneman, Hart / Flandrin, Orneika / Lee, Justin / Kumar, Naren G / Caspi, Rachel R / Evans, David J / Fleiszig, Suzanne M J

    The ocular surface

    2023  Volume 28, Page(s) 79–89

    Abstract: Purpose: Previously, using a murine model, we reported that contact lens (CL) wear induced corneal parainflammation involving CD11c+ cells after 24 h and Ly6G+ cells (neutrophils) after 5-6 days. Here, we investigated the role of IL-17 and γδ T cells in ...

    Abstract Purpose: Previously, using a murine model, we reported that contact lens (CL) wear induced corneal parainflammation involving CD11c+ cells after 24 h and Ly6G+ cells (neutrophils) after 5-6 days. Here, we investigated the role of IL-17 and γδ T cells in the CL-induced neutrophil response.
    Methods: CL-wearing C57BL/6 wild-type (WT) mice were compared to lens-wearing IL-17A/F single or double gene knock-out mice, or mice treated with UC7-13D5 monoclonal antibody to functionally deplete γδ T cells. Contralateral eyes served as no lens wear controls. Corneal Ly6G+ and γδ T cell responses were quantified as was expression of genes encoding pro-inflammatory cytokines IL-17A/F, IL-β, IL-18 and expression of IL-17A/F protein.
    Results: After 6 days lens wear, WT corneas showed Ly6G+ cell infiltration while remaining free of visible pathology. In contrast, lens-wearing corneas of IL-17AF (-/-), IL-17A (-/-) mice and γδ T cell-depleted mice showed little or no Ly6G+ cell infiltration. No Ly6G+ cell infiltration was detected in contralateral eye controls. Lens-wearing WT corneas also showed a significant increase in γδ T cells after 24 h that was maintained after 6 days of wear, and significantly increased cytokine gene expression after 6 days versus contralateral controls: IL-18 & IL-17A (∼3.9 fold) and IL-23 (∼6.5-fold). Increased IL-17A protein (∼4-fold) was detected after 6 days lens wear. γδ T cell-depletion abrogated these lens-induced changes in cytokine gene and protein expression.
    Conclusion: Together, these data show that IL-17A and γδ T cells are required for Ly6G+ cell (neutrophil) infiltration of the cornea during contact lens-induced parainflammation.
    MeSH term(s) Mice ; Animals ; Interleukin-17/genetics ; Interleukin-17/metabolism ; Interleukin-18/metabolism ; Mice, Inbred C57BL ; T-Lymphocytes/metabolism ; Cornea/metabolism ; Cytokines/metabolism ; Contact Lenses ; Mice, Knockout
    Chemical Substances Interleukin-17 ; Interleukin-18 ; Cytokines
    Language English
    Publishing date 2023-02-08
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 2208578-6
    ISSN 1937-5913 ; 1542-0124
    ISSN (online) 1937-5913
    ISSN 1542-0124
    DOI 10.1016/j.jtos.2023.02.004
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 6458: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular
    ab Jg. 2022: Lesesaal (EG)

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  3. Article ; Online: TRPA1 and TPRV1 Ion Channels Are Required for Contact Lens-Induced Corneal Parainflammation and Can Modulate Levels of Resident Corneal Immune Cells.

    Datta, Ananya / Lee, Ji Hyun / Flandrin, Orneika / Horneman, Hart / Lee, Justin / Metruccio, Matteo M E / Bautista, Diana / Evans, David J / Fleiszig, Suzanne M J

    Investigative ophthalmology & visual science

    2023  Volume 64, Issue 11, Page(s) 21

    Abstract: Purpose: Contact lens wear can induce corneal parainflammation involving CD11c+ cell responses (24 hours), γδ T cell responses (24 hours and 6 days), and IL-17-dependent Ly6G+ cell responses (6 days). Topical antibiotics blocked these CD11c+ responses. ... ...

    Abstract Purpose: Contact lens wear can induce corneal parainflammation involving CD11c+ cell responses (24 hours), γδ T cell responses (24 hours and 6 days), and IL-17-dependent Ly6G+ cell responses (6 days). Topical antibiotics blocked these CD11c+ responses. Because corneal CD11c+ responses to bacteria require transient receptor potential (TRP) ion-channels (TRPA1/TRPV1), we determined if these channels mediate lens-induced corneal parainflammation.
    Methods: Wild-type mice were fitted with contact lenses for 24 hours or 6 days and compared to lens wearing TRPA1 (-/-) or TRPV1 (-/-) mice or resiniferatoxin (RTX)-treated mice. Contralateral eyes were not fitted with lenses. Corneas were examined for major histocompatibility complex (MHC) class II+, CD45+, γδ T, or TNF-α+ cell responses (24 hours) or Ly6G+ responses (6 days) by quantitative imaging. The quantitative PCR (qPCR) determined cytokine gene expression.
    Results: Lens-induced increases in MHC class II+ cells after 24 hours were abrogated in TRPV1 (-/-) but not TRPA1 (-/-) mice. Increases in CD45+ cells were unaffected. Increases in γδ T cells after 24 hours of wear were abrogated in TRPA1 (-/-) and TRPV1 (-/-) mice, as were 6 day Ly6G+ cell responses. Contralateral corneas of TRPA1 (-/-) and TRPV1 (-/-) mice showed reduced MHC class II+ and γδ T cells at 24 hours. RTX inhibited lens-induced parainflammatory phenotypes (24 hours and 6 days), blocked lens-induced TNF-α and IL-18 gene expression, TNF-α+ cell infiltration (24 hours), and reduced baseline MHC class II+ cells.
    Conclusions: TRPA1 and TRPV1 mediate contact lens-induced corneal parainflammation after 24 hours and 6 days of wear and can modulate baseline levels of resident corneal immune cells.
    MeSH term(s) Animals ; Mice ; Contact Lenses ; Cornea/metabolism ; Histocompatibility Antigens Class II/metabolism ; Ion Channels ; TRPA1 Cation Channel/genetics ; TRPV Cation Channels/genetics ; TRPV Cation Channels/metabolism ; Tumor Necrosis Factor-alpha/metabolism
    Chemical Substances Histocompatibility Antigens Class II ; Ion Channels ; TRPA1 Cation Channel ; TRPV Cation Channels ; Tumor Necrosis Factor-alpha ; Trpa1 protein, mouse ; TRPV1 protein, mouse
    Language English
    Publishing date 2023-08-16
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 391794-0
    ISSN 1552-5783 ; 0146-0404
    ISSN (online) 1552-5783
    ISSN 0146-0404
    DOI 10.1167/iovs.64.11.21
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 45: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
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    Jg. 1995 - 2021: Lesesall (1.OG)
    ab Jg. 2022: Lesesaal (EG)

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  4. Article ; Online: Autonomous regulation of retinal insulin biosynthesis in diabetes.

    Jones, Malita A / Jadeja, Ravirajsinh N / Flandrin, Orneika / Abdelrahman, Ammar A / Thounojam, Menaka C / Thomas, Shakera / Dai, Caihong / Xiao, Haiyan / Chen, Jian-Kang / Smith, Sylvia B / Bartoli, Manuela / Martin, Pamela M / Powell, Folami L

    Neuropeptides

    2022  Volume 94, Page(s) 102258

    Abstract: Diabetic retinopathy (DR) is a neurodegenerative disease that results as a complication of dysregulated glucose metabolism, or diabetes. The signaling of insulin is lost or dampened in diabetes, but this hormone has also been shown to be an important ... ...

    Abstract Diabetic retinopathy (DR) is a neurodegenerative disease that results as a complication of dysregulated glucose metabolism, or diabetes. The signaling of insulin is lost or dampened in diabetes, but this hormone has also been shown to be an important neurotrophic factor which supports neurons of the brain. The role of local insulin synthesis and secretion in the retina, however, is unclear. We have investigated whether changes in local insulin synthesis occur in the diabetic retina and in response to stressors known to initiate retinal neurodegenerative processes. The expression of insulin and its cleavage product, c-peptide, were examined in retinas of a Type I diabetes animal model and human postmortem donors with DR. We detected mRNAs for insulin I (Ins1), insulin II (Ins2) and human insulin (Ins) by quantitative real-time polymerase chain reaction (qRT-PCR) and in situ hybridization. Using an ex-vivo system, isolated neuroretinas and retinal pigmented epithelium (RPE) layers were exposed to glycemic, oxidative and inflammatory environments to measure insulin gene transcripts produced de novo in the retina under disease-relevant conditions. The expression of insulin in the retina was altered with the progression of diabetes in STZ mice and donors with DR. Transcription factors for insulin, were simultaneously expressed in a pattern matching insulin genes. Furthermore, de novo insulin mRNA in isolated retinas was induced by acute stress. RPE explants displayed the most pronounced changes in Ins1 and Ins2. This data reveals that the retina, like the brain, is an organ capable of producing local insulin and this synthesis is altered in diabetes.
    MeSH term(s) Animals ; Diabetes Mellitus, Experimental/metabolism ; Diabetic Retinopathy/metabolism ; Insulin/pharmacology ; Mice ; Neurodegenerative Diseases ; RNA, Messenger/metabolism ; Retina/metabolism
    Chemical Substances Insulin ; RNA, Messenger
    Language English
    Publishing date 2022-05-20
    Publishing country Netherlands
    Document type Journal Article
    ZDB-ID 9048-7
    ISSN 1532-2785 ; 0143-4179
    ISSN (online) 1532-2785
    ISSN 0143-4179
    DOI 10.1016/j.npep.2022.102258
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 1592: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
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    ab Jg. 2022: Lesesaal (EG)

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  5. Article ; Online: Nerve-associated transient receptor potential ion channels can contribute to intrinsic resistance to bacterial adhesion in vivo.

    Wan, Stephanie J / Datta, Ananya / Flandrin, Orneika / Metruccio, Matteo M E / Ma, Sophia / Nieto, Vincent / Kroken, Abby R / Hill, Rose Z / Bautista, Diana M / Evans, David J / Fleiszig, Suzanne M J

    FASEB journal : official publication of the Federation of American Societies for Experimental Biology

    2021  Volume 35, Issue 10, Page(s) e21899

    Abstract: The cornea of the eye differs from other mucosal surfaces in that it lacks a viable bacterial microbiome and by its unusually high density of sensory nerve endings. Here, we explored the role of corneal nerves in preventing bacterial adhesion. ... ...

    Abstract The cornea of the eye differs from other mucosal surfaces in that it lacks a viable bacterial microbiome and by its unusually high density of sensory nerve endings. Here, we explored the role of corneal nerves in preventing bacterial adhesion. Pharmacological and genetic methods were used to inhibit the function of corneal sensory nerves or their associated transient receptor potential cation channels TRPA1 and TRPV1. Impacts on bacterial adhesion, resident immune cells, and epithelial integrity were examined using fluorescent labeling and quantitative confocal imaging. TRPA1/TRPV1 double gene-knockout mice were more susceptible to adhesion of environmental bacteria and to that of deliberately-inoculated Pseudomonas aeruginosa. Supporting the involvement of TRPA1/TRPV1-expressing corneal nerves, P. aeruginosa adhesion was also promoted by treatment with bupivacaine, or ablation of TRPA1/TRPV1-expressing nerves using RTX. Moreover, TRPA1/TRPV1-dependent defense was abolished by enucleation which severs corneal nerves. High-resolution imaging showed normal corneal ultrastructure and surface-labeling by wheat-germ agglutinin for TRPA1/TRPV1 knockout murine corneas, and intact barrier function by absence of fluorescein staining. P. aeruginosa adhering to corneas after perturbation of nerve or TRPA1/TRPV1 function failed to penetrate the surface. Single gene-knockout mice showed roles for both TRPA1 and TRPV1, with TRPA1
    MeSH term(s) Animals ; Bacterial Adhesion ; Cornea/innervation ; Cornea/metabolism ; Cornea/microbiology ; Female ; Male ; Mice ; Mice, Knockout ; Pseudomonas aeruginosa/metabolism ; TRPA1 Cation Channel/genetics ; TRPA1 Cation Channel/metabolism ; TRPV Cation Channels/genetics ; TRPV Cation Channels/metabolism
    Chemical Substances TRPA1 Cation Channel ; TRPV Cation Channels ; TRPV1 protein, mouse ; Trpa1 protein, mouse
    Language English
    Publishing date 2021-09-06
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 639186-2
    ISSN 1530-6860 ; 0892-6638
    ISSN (online) 1530-6860
    ISSN 0892-6638
    DOI 10.1096/fj.202100874R
    Database MEDical Literature Analysis and Retrieval System OnLINE

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