The Experts below are selected from a list of 30 Experts worldwide ranked by ideXlab platform
Yuguang Huang - One of the best experts on this subject based on the ideXlab platform.
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neuronal fc epsilon receptor i contributes to antigen evoked Pruritus in a murine model of Ocular allergy
Brain Behavior and Immunity, 2017Co-Authors: Fan Liu, Naze Chen, Mo Zhou, Qian Yang, Yikuan Xie, Yuguang HuangAbstract:Pruritus is the major symptom of Ocular allergy but currently available treatments are often ineffective. Previous studies demonstrated that subpopulations of primary sensory neurons express Fc receptors and may contribute to antigen-specific pain. We investigated the role of neuronal Fc-epsilon Receptor I (FceRI) in allergic Ocular Pruritus. Ovalbumin (OVA) was used as allergen together with alum adjuvant (OVA+alum) to produce a mouse model of Ocular allergy with a significant elevation in the serum levels of both antigen-specific IgE and IgG. Mice sensitized by OVA without alum only induced elevation of serum IgG but not IgE. Scratching behavior toward the eyes with the hindlimb was used as an indicator of Ocular itch. Topical OVA challenging to the eye dose-dependently induced scratching toward the eye in the OVA+alum sensitized mice, but not those sensitized by OVA only. The antigen-induced scratching was largely abolished by topical application of the blocking antibody to FceRIα, but was only partially alleviated by pretreatment of mast cell stabilizer or histamine I receptor antagonist. The expression of FceRI was detected in subpopulations of trigeminal ganglion (TG) neurons including those expressing pruriceptive markers and innervating the conjunctiva in the naive mice. Moreover, FceRI was found significantly upregulated in small-sized TG neurons in the OVA+alum sensitized mice. In acutely dissociated TG neurons, IgE-immune complex (IC), but not the antibody or antigen alone, induced intracellular calcium increase. The neuronal responses to IgE-IC could be specifically blocked by pre-application of a siRNA for FceRIα. Our results indicate that FceRI expressed on peripheral nociceptive neurons in the TG may be directly activated by IgE-IC and contribute to allergic Ocular Pruritus. This study may suggest a novel mechanism for the development of pathological itch in allergic diseases.
Fan Liu - One of the best experts on this subject based on the ideXlab platform.
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neuronal fc epsilon receptor i contributes to antigen evoked Pruritus in a murine model of Ocular allergy
Brain Behavior and Immunity, 2017Co-Authors: Fan Liu, Naze Chen, Mo Zhou, Qian Yang, Yikuan Xie, Yuguang HuangAbstract:Pruritus is the major symptom of Ocular allergy but currently available treatments are often ineffective. Previous studies demonstrated that subpopulations of primary sensory neurons express Fc receptors and may contribute to antigen-specific pain. We investigated the role of neuronal Fc-epsilon Receptor I (FceRI) in allergic Ocular Pruritus. Ovalbumin (OVA) was used as allergen together with alum adjuvant (OVA+alum) to produce a mouse model of Ocular allergy with a significant elevation in the serum levels of both antigen-specific IgE and IgG. Mice sensitized by OVA without alum only induced elevation of serum IgG but not IgE. Scratching behavior toward the eyes with the hindlimb was used as an indicator of Ocular itch. Topical OVA challenging to the eye dose-dependently induced scratching toward the eye in the OVA+alum sensitized mice, but not those sensitized by OVA only. The antigen-induced scratching was largely abolished by topical application of the blocking antibody to FceRIα, but was only partially alleviated by pretreatment of mast cell stabilizer or histamine I receptor antagonist. The expression of FceRI was detected in subpopulations of trigeminal ganglion (TG) neurons including those expressing pruriceptive markers and innervating the conjunctiva in the naive mice. Moreover, FceRI was found significantly upregulated in small-sized TG neurons in the OVA+alum sensitized mice. In acutely dissociated TG neurons, IgE-immune complex (IC), but not the antibody or antigen alone, induced intracellular calcium increase. The neuronal responses to IgE-IC could be specifically blocked by pre-application of a siRNA for FceRIα. Our results indicate that FceRI expressed on peripheral nociceptive neurons in the TG may be directly activated by IgE-IC and contribute to allergic Ocular Pruritus. This study may suggest a novel mechanism for the development of pathological itch in allergic diseases.
Mo Zhou - One of the best experts on this subject based on the ideXlab platform.
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neuronal fc epsilon receptor i contributes to antigen evoked Pruritus in a murine model of Ocular allergy
Brain Behavior and Immunity, 2017Co-Authors: Fan Liu, Naze Chen, Mo Zhou, Qian Yang, Yikuan Xie, Yuguang HuangAbstract:Pruritus is the major symptom of Ocular allergy but currently available treatments are often ineffective. Previous studies demonstrated that subpopulations of primary sensory neurons express Fc receptors and may contribute to antigen-specific pain. We investigated the role of neuronal Fc-epsilon Receptor I (FceRI) in allergic Ocular Pruritus. Ovalbumin (OVA) was used as allergen together with alum adjuvant (OVA+alum) to produce a mouse model of Ocular allergy with a significant elevation in the serum levels of both antigen-specific IgE and IgG. Mice sensitized by OVA without alum only induced elevation of serum IgG but not IgE. Scratching behavior toward the eyes with the hindlimb was used as an indicator of Ocular itch. Topical OVA challenging to the eye dose-dependently induced scratching toward the eye in the OVA+alum sensitized mice, but not those sensitized by OVA only. The antigen-induced scratching was largely abolished by topical application of the blocking antibody to FceRIα, but was only partially alleviated by pretreatment of mast cell stabilizer or histamine I receptor antagonist. The expression of FceRI was detected in subpopulations of trigeminal ganglion (TG) neurons including those expressing pruriceptive markers and innervating the conjunctiva in the naive mice. Moreover, FceRI was found significantly upregulated in small-sized TG neurons in the OVA+alum sensitized mice. In acutely dissociated TG neurons, IgE-immune complex (IC), but not the antibody or antigen alone, induced intracellular calcium increase. The neuronal responses to IgE-IC could be specifically blocked by pre-application of a siRNA for FceRIα. Our results indicate that FceRI expressed on peripheral nociceptive neurons in the TG may be directly activated by IgE-IC and contribute to allergic Ocular Pruritus. This study may suggest a novel mechanism for the development of pathological itch in allergic diseases.
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Neuronal Fc-epsilon receptor I contributes to antigen-evoked Pruritus in a murine model of Ocular allergy
The Authors. Published by Elsevier Inc., 2016Co-Authors: Liu Fan, Mo Zhou, Xu Lubin, Chen Naze, Li Chunyan, Yang Qian, Xie Yikuan, Huang Yuguang, Ma ChaoAbstract:AbstractPruritus is the major symptom of Ocular allergy but currently available treatments are often ineffective. Previous studies demonstrated that subpopulations of primary sensory neurons express Fc receptors and may contribute to antigen-specific pain. We investigated the role of neuronal Fc-epsilon Receptor I (FcεRI) in allergic Ocular Pruritus. Ovalbumin (OVA) was used as allergen together with alum adjuvant (OVA+alum) to produce a mouse model of Ocular allergy with a significant elevation in the serum levels of both antigen-specific IgE and IgG. Mice sensitized by OVA without alum only induced elevation of serum IgG but not IgE. Scratching behavior toward the eyes with the hindlimb was used as an indicator of Ocular itch. Topical OVA challenging to the eye dose-dependently induced scratching toward the eye in the OVA+alum sensitized mice, but not those sensitized by OVA only. The antigen-induced scratching was largely abolished by topical application of the blocking antibody to FcεRIα, but was only partially alleviated by pretreatment of mast cell stabilizer or histamine I receptor antagonist. The expression of FcεRI was detected in subpopulations of trigeminal ganglion (TG) neurons including those expressing pruriceptive markers and innervating the conjunctiva in the naïve mice. Moreover, FcεRI was found significantly upregulated in small-sized TG neurons in the OVA+alum sensitized mice. In acutely dissociated TG neurons, IgE-immune complex (IC), but not the antibody or antigen alone, induced intracellular calcium increase. The neuronal responses to IgE-IC could be specifically blocked by pre-application of a siRNA for FcεRIα. Our results indicate that FcεRI expressed on peripheral nociceptive neurons in the TG may be directly activated by IgE-IC and contribute to allergic Ocular Pruritus. This study may suggest a novel mechanism for the development of pathological itch in allergic diseases
Naze Chen - One of the best experts on this subject based on the ideXlab platform.
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neuronal fc epsilon receptor i contributes to antigen evoked Pruritus in a murine model of Ocular allergy
Brain Behavior and Immunity, 2017Co-Authors: Fan Liu, Naze Chen, Mo Zhou, Qian Yang, Yikuan Xie, Yuguang HuangAbstract:Pruritus is the major symptom of Ocular allergy but currently available treatments are often ineffective. Previous studies demonstrated that subpopulations of primary sensory neurons express Fc receptors and may contribute to antigen-specific pain. We investigated the role of neuronal Fc-epsilon Receptor I (FceRI) in allergic Ocular Pruritus. Ovalbumin (OVA) was used as allergen together with alum adjuvant (OVA+alum) to produce a mouse model of Ocular allergy with a significant elevation in the serum levels of both antigen-specific IgE and IgG. Mice sensitized by OVA without alum only induced elevation of serum IgG but not IgE. Scratching behavior toward the eyes with the hindlimb was used as an indicator of Ocular itch. Topical OVA challenging to the eye dose-dependently induced scratching toward the eye in the OVA+alum sensitized mice, but not those sensitized by OVA only. The antigen-induced scratching was largely abolished by topical application of the blocking antibody to FceRIα, but was only partially alleviated by pretreatment of mast cell stabilizer or histamine I receptor antagonist. The expression of FceRI was detected in subpopulations of trigeminal ganglion (TG) neurons including those expressing pruriceptive markers and innervating the conjunctiva in the naive mice. Moreover, FceRI was found significantly upregulated in small-sized TG neurons in the OVA+alum sensitized mice. In acutely dissociated TG neurons, IgE-immune complex (IC), but not the antibody or antigen alone, induced intracellular calcium increase. The neuronal responses to IgE-IC could be specifically blocked by pre-application of a siRNA for FceRIα. Our results indicate that FceRI expressed on peripheral nociceptive neurons in the TG may be directly activated by IgE-IC and contribute to allergic Ocular Pruritus. This study may suggest a novel mechanism for the development of pathological itch in allergic diseases.
Qian Yang - One of the best experts on this subject based on the ideXlab platform.
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neuronal fc epsilon receptor i contributes to antigen evoked Pruritus in a murine model of Ocular allergy
Brain Behavior and Immunity, 2017Co-Authors: Fan Liu, Naze Chen, Mo Zhou, Qian Yang, Yikuan Xie, Yuguang HuangAbstract:Pruritus is the major symptom of Ocular allergy but currently available treatments are often ineffective. Previous studies demonstrated that subpopulations of primary sensory neurons express Fc receptors and may contribute to antigen-specific pain. We investigated the role of neuronal Fc-epsilon Receptor I (FceRI) in allergic Ocular Pruritus. Ovalbumin (OVA) was used as allergen together with alum adjuvant (OVA+alum) to produce a mouse model of Ocular allergy with a significant elevation in the serum levels of both antigen-specific IgE and IgG. Mice sensitized by OVA without alum only induced elevation of serum IgG but not IgE. Scratching behavior toward the eyes with the hindlimb was used as an indicator of Ocular itch. Topical OVA challenging to the eye dose-dependently induced scratching toward the eye in the OVA+alum sensitized mice, but not those sensitized by OVA only. The antigen-induced scratching was largely abolished by topical application of the blocking antibody to FceRIα, but was only partially alleviated by pretreatment of mast cell stabilizer or histamine I receptor antagonist. The expression of FceRI was detected in subpopulations of trigeminal ganglion (TG) neurons including those expressing pruriceptive markers and innervating the conjunctiva in the naive mice. Moreover, FceRI was found significantly upregulated in small-sized TG neurons in the OVA+alum sensitized mice. In acutely dissociated TG neurons, IgE-immune complex (IC), but not the antibody or antigen alone, induced intracellular calcium increase. The neuronal responses to IgE-IC could be specifically blocked by pre-application of a siRNA for FceRIα. Our results indicate that FceRI expressed on peripheral nociceptive neurons in the TG may be directly activated by IgE-IC and contribute to allergic Ocular Pruritus. This study may suggest a novel mechanism for the development of pathological itch in allergic diseases.
