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  • 1
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    Adult Orbital Xanthogranuloma With Associated Adult-Onset Asthma
    Ovid Technologies (Wolters Kluwer Health) ; 2004
    In:  Ophthalmic Plastic & Reconstructive Surgery Vol. 20, No. 4 ( 2004-07), p. 329-332
    Details
    In: Ophthalmic Plastic & Reconstructive Surgery, Ovid Technologies (Wolters Kluwer Health), Vol. 20, No. 4 ( 2004-07), p. 329-332
    Type of Medium: Online Resource
    ISSN: 0740-9303
    URL: Article
    DOI: 10.1097/01.IOP.0000132177.20945.E9
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2004
    detail.hit.zdb_id: 2070654-6
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  • 2
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    α4 Integrin Is a Regulator of Leukocyte Recruitment After Experimental Intracerebral Hemorrhage
    Ovid Technologies (Wolters Kluwer Health) ; 2014
    In:  Stroke Vol. 45, No. 8 ( 2014-08), p. 2485-2487
    Details
    In: Stroke, Ovid Technologies (Wolters Kluwer Health), Vol. 45, No. 8 ( 2014-08), p. 2485-2487
    Abstract: Intracerebral hemorrhage (ICH) is swiftly followed by an inflammatory response. A key component of this response is the recruitment of leukocytes into the brain, which promotes neurological injury in rodent models. However, the mechanisms by which leukocytes transmigrate across the endothelium into the injured brain are unclear. The present study examines leukocyte adhesion molecules (α4 integrin, L-selectin, and αLβ2 integrin) on 4 leukocyte subtypes to determine which are important for leukocyte recruitment after ICH. Methods— We used the blood injection mouse model of ICH, whereby 25 μL of blood was injected into the striatum. Flow cytometry was used to quantify leukocyte populations and adhesion molecule expression in brain and blood. An α4 integrin–blocking antibody was administered to evaluate the contribution of α4 integrin in leukocyte migration and neurological injury. Results— α4 integrin was elevated on all leukocyte populations in brain after ICH, whereas L-selectin was unchanged and αLβ2 was increased only on T cells. Antagonism of α4 resulted in decreased leukocyte transmigration and lessened neurobehavioral disability. Conclusions— α4 integrin is an important cell adhesion molecule involved in neuroinflammation after ICH.
    Type of Medium: Online Resource
    ISSN: 0039-2499 , 1524-4628
    URL: Article
    DOI: 10.1161/STROKEAHA.114.005551
    RVK:
    XA 10000
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2014
    detail.hit.zdb_id: 1467823-8
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  • 3
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    Abstract 3867: Robust Infiltration of Inflammatory Monocytes 12 Hours After Experimental Intracerebral Hemorrhage
    Ovid Technologies (Wolters Kluwer Health) ; 2012
    In:  Stroke Vol. 43, No. suppl_1 ( 2012-02)
    Details
    In: Stroke, Ovid Technologies (Wolters Kluwer Health), Vol. 43, No. suppl_1 ( 2012-02)
    Abstract: Background and Purpose: Inflammation is a key component of injury in the initial hours following intracerebral hemorrhage (ICH). Neutrophils are thought to be the earliest cells infiltrating into brain, but traditional methods to identify leukocytes are unable to differentiate between infiltrating monocyte populations and resident microglia. We used flow cytometry on brains 12 hours after ICH to quantify the specific infiltrating leukocyte populations. This is an early timepoint when neurobehavioral deficit is maximal and treatment could realistically be initiated. Methods: ICH was modeled by injecting 15μ l of blood from a C57BL/6 mouse (carrying leukocyte marker CD45.2) into the right striatum of a B6Ly5.2 mouse (which expresses CD45.1). The different CD45 isoforms allowed infiltrating leukocytes from the recipient mouse to be distinguished from the blood that was injected to model the ICH. Brains were harvested 12 hours later, dissociated mechanically and enzymatically, and cells collected from the interphase of a 30%/70% percoll gradient. Cells were then stained for CD45.1, CD45.2, CD3, CD11b, CD11c, Ly6G, and GR-1 and analyzed on a BD LSRII flow cytometer. Blood-derived leukocytes were identified as CD45.1hi, neutrophils as CD45.1hiCD11b+Ly6G+, inflammatory monocytes as CD45.1hiCD11b+Ly6G-CD11c-Gr1+, monocytes as CD45.1hiCD11b+Ly6G-CD11c-Gr1-, and dendritic cells as CD45.1hiCD11b+Ly6G-CD11c+. Mean cell counts in the ipsilateral hemisphere were compared to the contralateral hemisphere by t-test. Results: At 12 hours after ICH, we observed a significant increase in blood-derived leukocytes within the ipsilateral hemisphere (p 〈 0.01, see figure ). Less than 4% of total leukocytes were CD45.2. Surprisingly, we noticed a robust inflammatory monocyte population in the ipsilateral hemisphere (p 〈 0.05, figure ). Significant changes were not observed in monocyte, dendritic, or T cell populations, although there was a trend towards an increase in neutrophils (p=.055, figure ). Conclusions: Using a CD45.1/CD45.2 blood transfer model, we determined that the cells injected into the striatum as part of the modeled hemorrhage are no longer detectable 12 hours later. Infiltrating inflammatory monocytes outnumbered neutrophils at 12 hours. This challenges conventional thought regarding the time course of invading immune cell populations following ICH, and suggests that future studies are needed to determine the contribution of inflammatory monocytes to early injury after ICH.
    Type of Medium: Online Resource
    ISSN: 0039-2499 , 1524-4628
    URL: Article
    DOI: 10.1161/str.43.suppl_1.A3867
    RVK:
    XA 10000
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2012
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  • 4
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    Abstract W MP49: Classifying M1/M2 Monocytes by JAK/STAT Activation After Murine Intracerebral Hemorrhage
    Ovid Technologies (Wolters Kluwer Health) ; 2015
    In:  Stroke Vol. 46, No. suppl_1 ( 2015-02)
    Details
    In: Stroke, Ovid Technologies (Wolters Kluwer Health), Vol. 46, No. suppl_1 ( 2015-02)
    Abstract: Background: The immune response following intracerebral hemorrhage (ICH) is an important component of secondary injury that requires further study. Flow cytometry is used to quantify and phenotype recruited leukocytes after murine ICH. Current methods using density gradients have long processing times that reduce the ability to detect phosphorylation states and often yield few neutrophils. Here, we demonstrate the utility of a new method for homogenizing brains and staining for intracellular signaling proteins. This technique results in improved cell recovery and allows us to more precisely classify monocyte polarization states as either M1 pro-inflammatory or M2 anti-inflammatory. Methods: Mouse brains were digested to single-cell suspensions 1-10 days after collagenase ICH. To compare methods, brains were centrifuged on a percoll density gradient or simply homogenized on ice with phosphatase inhibitors. The latter samples were stained extracellularly, fixed with paraformaldehyde, permeabilized in methanol, and then stained intracellularly for phosphorylated STAT molecules (pSTATs). Results: This new method resulted in better neutrophil recovery, yielding 12,190 ± 5,603 neutrophils vs. 1,576 ± 458 neutrophils with percoll at day 3 (p 〈 0.02; n=3-5). No differences were seen in the numbers of monocytes, T cells, or microglia collected between the two methods (p 〉 0.05; n=3-5). Intracellular staining for pSTATs allowed us to identify activated components of the JAK/STAT signaling pathway. All monocytes had high pSTAT1 at day 1, but it steadily declined to day 10. Ly6Clow and Ly6C– monocytes increased pSTAT6 over time, whereas Ly6Chi monocytes did not. Conclusions: This study demonstrates an improved method for recovering leukocytes from mouse brains and staining for pSTATs. Using this technique, we show that Ly6Chi monocytes, which are known to worsen ICH disability, lack pSTAT6 and display an early pro-inflammatory M1 phenotype. In contrast, the Ly6Clow and Ly6C– monocytes both elevate pSTAT6 over time, suggesting they become M2 polarized and may contribute to later repair. Decreasing M1 monocyte polarization and accelerating M2 polarization could be accomplished by targeting pSTATs and may represent a novel treatment strategy in ICH.
    Type of Medium: Online Resource
    ISSN: 0039-2499 , 1524-4628
    URL: Article
    DOI: 10.1161/str.46.suppl_1.wmp49
    RVK:
    XA 10000
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2015
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  • 5
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    Abstract 3940: Perihematomal Leukocytes Peak 3 Days After Intracerebral Hemorrhage
    Ovid Technologies (Wolters Kluwer Health) ; 2012
    In:  Stroke Vol. 43, No. suppl_1 ( 2012-02)
    Details
    In: Stroke, Ovid Technologies (Wolters Kluwer Health), Vol. 43, No. suppl_1 ( 2012-02)
    Abstract: Background: Intracerebral hemorrhage (ICH) is followed by a robust inflammatory response in the brain. Therapies inhibiting leukocyte migration to the brain have been developed, but their potential application to ICH relies on detailed understanding of the invading inflammatory cells after injury. Our objective was to quantify the various leukocyte populations between 1 and 7 days after ICH using a mouse model. Methods: Using the autologous blood injection model in WT (C3H/HeOuJ) mice, we injected 15μ l of blood into the basal ganglia 2.5mm right of bregma. At 24h, 72h, and 7 days following surgery, we isolated the brain and dissociated each hemisphere into a single cell suspension using collagenase, dispase, and mechanical digestions prior to staining with CD45, CD3, CD11b, Ly6G, CD11c, Gr-1, and NK1.1 antibodies. Immune cell populations were quantified by flow cytometry (see figure for gating) and the numbers of excess ipsilateral cells were calculated. Additionally, at 72 hours after ICH or sham surgery, we isolated the ipsilateral hemisphere for quantification of chemokine production by ELISA. Results: There was a significant increase in blood-derived leukocytes (CD45hi) between 24hr and 72hr, mostly accounted for by inflammatory monocytes and dendritic cells ( Figure ). We then saw a significant decrease between 72 hours and 7 days in the inflammatory monocyte population as well as a trend towards a decrease in the dendritic cell population. Natural killer cells accounted for less than 0.3% of all leukocytes detected. The monocyte-recruiting chemokine CCL2 (MCP-1) was increased in the brains at 72 hours after ICH (ICH 260.8 ± 31.1 pg/g brain vs sham 148.8 ± 12.4, p 〈 0.05) consistent with the peak of inflammatory monocyte recruitment. Conclusion: Leukocytes peak in the brain at 72 hours after ICH and are almost completely absent by 7 days. Inflammatory monocytes and dendritic cells account for the greatest numbers of leukocytes at 72 hours. CCL2 levels are elevated when inflammatory monocyte populations peak. Therapies inhibiting the CCL2-dependent migration of inflammatory monocytes across the blood-brain barrier should be investigated to determine if these cells contribute to injury.
    Type of Medium: Online Resource
    ISSN: 0039-2499 , 1524-4628
    URL: Article
    DOI: 10.1161/str.43.suppl_1.A3940
    RVK:
    XA 10000
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2012
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  • 6
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    Abstract W MP95: CCR2+ Monocytes Contribute to Hematoma Clearance After Experimental Intracerebral Hemorrhage
    Ovid Technologies (Wolters Kluwer Health) ; 2014
    In:  Stroke Vol. 45, No. suppl_1 ( 2014-02)
    Details
    In: Stroke, Ovid Technologies (Wolters Kluwer Health), Vol. 45, No. suppl_1 ( 2014-02)
    Abstract: Background: Inflammation is a key contributor to injury and recovery after intracerebral hemorrhage (ICH). CCR2+ monocytes were recently identified as mediators of early injury in a rodent ICH model, but their potential roles in ICH recovery have not been addressed. The purpose of this study was to determine how CCR2+ monocytes influence repair and recovery after ICH Methods: Ccr2-/- bone marrow was transplanted into wild type congenic mice to create chimeras with normal microglia, but few circulating monocytes. Control mice received wild type bone marrow. Mice were subjected to the blood injection ICH model, whereby 20 μl of blood were injected into the striatum. The resulting motor weakness was quantified using the cylinder and beam balance tests. Residual hemoglobin was quantified in brains at day 7 using Drabkin’s reagent. In wild type mice, 1-μm fluorescent beads were injected with the blood as a phagocytosis substrate. An imaging flow cytometer was used to visualize phagocytic cells. Results: Mice with Ccr2-/- bone marrow have less severe motor deficits up to day 3, but both genotypes were equally recovered at day 7. Despite normal behavior, mice with Ccr2-/- bone marrow had significantly more residual hemoglobin in their brains (8.92 ± 1.03 vs. 3.96 ± 2.80 μl, p 〈 0.05; Fig.), suggesting a role for monocytes in ICH clearance. To determine if monocytes have the capacity to phagocytose debris after ICH, we injected fluorescent beads with the ICH blood. CCR2+ monocytes engulfed more beads than resident microglia at day 1 (4.35 ± 2.23 vs. 0.23 ± 0.45 beads, p 〈 0.0001; Fig.), suggesting a more active role in phagocytosis. Conclusions: Hematoma clearance has been attributed mainly to microglia, but these results indicate that CCR2+ monocytes are also involved. Interestingly, the lack of a motor deficit at day 7 indicates that the presence of a hematoma does not inhibit functional recovery in the absence of CCR2+ inflammatory monocytes.
    Type of Medium: Online Resource
    ISSN: 0039-2499 , 1524-4628
    URL: Article
    DOI: 10.1161/str.45.suppl_1.wmp95
    RVK:
    XA 10000
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2014
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  • 7
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    Abstract 114: CX3CR1-null Microglia Fail to Transition to an M2 Phenotype after Intracerebral Hemorrhage
    Ovid Technologies (Wolters Kluwer Health) ; 2015
    In:  Stroke Vol. 46, No. suppl_1 ( 2015-02)
    Details
    In: Stroke, Ovid Technologies (Wolters Kluwer Health), Vol. 46, No. suppl_1 ( 2015-02)
    Abstract: Introduction: Intracerebral hemorrhage (ICH) results in the activation of microglia. Microglia can polarize into either a pro-inflammatory (M1), or a reparative (M2) phenotype; the effect of microglial polarization after ICH is unknown. Microglia express the chemokine receptor CX3CR1, which has been shown to regulate microglial neurotoxicity. CX3CR1 +/GFP mice have a functional CX3CR1 and are frequently used to identify microglia. We previously reported that mice with CX3CR1-null microglia do not show functional recovery 14 days after ICH. We hypothesize that 1) microglia transition from M1 to M2 phenotypes in the acute to subacute period after ICH and 2) CX3CR1-null microglia fail to make this transition, inhibiting recovery after ICH. Methods: ICH was modeled by injecting 20ul of WT blood into the right striatum. Microglia were sorted from male CX3CR1 +/GFP mice 0.5, 1, 3, 7, and 14 days after ICH in order to specifically study microglia phenotypes. RNA was extracted and qRT-PCR was performed to analyze changes in gene expression. To study microglial CX3CR1 function, C57BL/6 (WT) and CX3CR1 GFP/GFP (CX3CR1-null) mice were irradiated and reconstituted with WT bone marrow (CD45.1) to generate bone marrow chimeras (CD45.1- 〉 WT or CD45.1- 〉 CX3CR1-null). Brains were harvested for flow cytometry 14 days after ICH. Results: At 12 hours after ICH, microglia have high IL-6 gene expression (M1). However, M2 markers arginase-1, TGF-β and SOCS3 increase over time (Fig. 1), suggesting microglia transition from M1 to M2 over the first 2 weeks after ICH. By flow cytometry, CX3CR1-null microglia had significantly less SIRPα, a receptor involved in phagocytosis of erythrocytes, and CD206, an M2 marker, than WT microglia 14 days after ICH. Conclusions: Our data show WT microglia transition from an M1 to an M2 phenotype after ICH. Our results also suggest microglial CX3CR1 is necessary for transition toward an M2 phenotype after ICH and this transition is required for recovery after ICH.
    Type of Medium: Online Resource
    ISSN: 0039-2499 , 1524-4628
    URL: Article
    DOI: 10.1161/str.46.suppl_1.114
    RVK:
    XA 10000
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2015
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  • 8
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    Elevated Intracranial Pressure Associated With Idiopathic Retinal Vasculitis, Aneurysms, and Neuroretinitis Syndrome
    Ovid Technologies (Wolters Kluwer Health) ; 2004
    In:  Journal of Neuro-Ophthalmology Vol. 24, No. 3 ( 2004-09), p. 221-224
    Details
    In: Journal of Neuro-Ophthalmology, Ovid Technologies (Wolters Kluwer Health), Vol. 24, No. 3 ( 2004-09), p. 221-224
    Type of Medium: Online Resource
    ISSN: 1070-8022
    URL: Article
    DOI: 10.1097/00041327-200409000-00008
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2004
    detail.hit.zdb_id: 2062798-1
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  • 9
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    Divergent Functions of Tissue-Resident and Blood-Derived Macrophages in the Hemorrhagic Brain
    Ovid Technologies (Wolters Kluwer Health) ; 2021
    In:  Stroke Vol. 52, No. 5 ( 2021-05), p. 1798-1808
    Details
    In: Stroke, Ovid Technologies (Wolters Kluwer Health), Vol. 52, No. 5 ( 2021-05), p. 1798-1808
    Abstract: Brain tissue-resident microglia and monocyte-derived macrophages (MDMs) are innate immune cells that contribute to the inflammatory response, phagocytosis of debris, and tissue repair after injury. We have previously reported that both microglia and MDMs transition from proinflammatory to reparative phenotypes over days after an intracerebral hemorrhage (ICH). However, their individual functional properties in the brain remain largely unknown. Here we characterized the differences between microglia and MDMs and further elucidate their distinct activation states and functional contributions to the pathophysiology and recovery after ICH. Methods: Autologous blood injection was used to model ICH in mice. Longitudinal transcriptomic analyses on isolated microglia and MDMs from mice at days 1, 3, 7 and 10 after ICH and naive controls identified core transcriptional programs that distinguish these cells. Imaging flow cytometry and in vivo phagocytosis assays were used to study phagocytic ability of microglia and MDMs. Antigen presentation was evaluated by ovalbumin-OTII CD4 T-cell proliferation assays with bone marrow–derived macrophages and primary microglia cultures. Results: MDMs had higher phagocytic activity and higher erythrophagocytosis in the ICH brain. Differential gene expression revealed distinct transcriptional signatures in the MDMs and microglia after ICH. MDMs had higher expression of MHCII (major histocompatibility complex class II) genes than microglia at all time points and greater ability to induce antigen-specific T-cell proliferation. Conclusions: The different ontogeny of microglia and MDMs lead to divergent responses and functions in the inflamed brain as these 2 cell populations differ in phagocytic functions and antigen-presenting capabilities in the brain after ICH.
    Type of Medium: Online Resource
    ISSN: 0039-2499 , 1524-4628
    URL: Article
    DOI: 10.1161/STROKEAHA.120.032196
    RVK:
    XA 10000
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2021
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  • 10
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    Abstract T P238: Microglial CX3CR1 Required for M2 Polarization and Recovery After Intracerebral Hemorrhage
    Ovid Technologies (Wolters Kluwer Health) ; 2014
    In:  Stroke Vol. 45, No. suppl_1 ( 2014-02)
    Details
    In: Stroke, Ovid Technologies (Wolters Kluwer Health), Vol. 45, No. suppl_1 ( 2014-02)
    Abstract: Introduction: Intracerebral hemorrhage (ICH) results in the activation of microglia, the resident immune cells of the central nervous system. Microglia may polarize into an M1, pro-inflammatory phenotype, or an M2 phenotype associated with repair. CX3CR1 is a chemokine receptor on microglia and monocyte subsets. CX3CR1-null microglia have been shown to have dysregulated inflammation. We hypothesize that CX3CR1-null microglia have a prolonged M1 phenotype, contributing to worse functional outcome after ICH. Methods: ICH was modeled by injection of 20μl of blood into the right striatum. Neurological deficit was quantified using digital gait analysis, cylinder test, and beam walking. Mice were sacrificed 14 days after ICH; brains were harvested for flow cytometry and immunohistochemistry (IHC). C57BL/6 (WT) and CX3CR1 GFP/GFP (CX3CR1-null) mice were irradiated and reconstituted with bone marrow from WT mice carrying the congenic marker CD45.1 to generate bone marrow chimeras (CD45.1WT or CD45.1CX3CR1-null). M1 microglia were identified as expressing MHCII and M2 microglia with CD206. Results: The CD45.1CX3CR1-null mice show worse functional outcome 14 days after ICH by cylinder test (p=0.002), beam walking (p= 〈 0.001) and gait analysis (p=0.02). By flow cytometry, few peripheral leukocytes remain in the brain at 14 days, indicating that F4/80 + and CD11b + cells visualized by IHC are likely microglia, not peripheral macrophages. By IHC, CD45.1 CX3CR1-null mice have significantly more amoeboid F4/80 + MHCII + cells per field (M1 microglia) than CD45.1WT mice (p=0.02). CD45.1 CX3CR1-null mice have significantly fewer CD11b + CD206 + cells per field (M2 microglia) compared to CD45.1WT mice (p=0.04). Conclusions: Our results suggest microglial CX3CR1 signaling is necessary for microglia to transition from M1 to M2 and contribute to recovery after ICH.
    Type of Medium: Online Resource
    ISSN: 0039-2499 , 1524-4628
    URL: Article
    DOI: 10.1161/str.45.suppl_1.tp238
    RVK:
    XA 10000
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2014
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