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Start Over Author "Nie H" Journal arthritis & rheumatism
6 results on '"Nie H"'

4. Spinal interleukin-1β in a mouse model of arthritis and joint pain

Author

Jen-nie H. Miller, Ross H. Tallents, Paolo M. Fiorentino, Stephanos Kyrkanides, Sabine M. Brouxhon, J. Edward Puzas, and M. Kerry O'Banion

Subjects
medicine.medical_specialty, Pathology, Feline immunodeficiency virus, Interleukin-1beta, Immunology, Pain, Arthritis, Mice, Transgenic, Inflammation, Cisterna magna, Mice, Rheumatology, Internal medicine, Osteoarthritis, medicine, Animals, Immunology and Allergy, Pharmacology (medical), Sensitization, Neuroinflammation, Temporomandibular Joint, biology, business.industry, Receptors, Interleukin-1, biology.organism_classification, medicine.disease, Arthritis, Experimental, Up-Regulation, Posterior Horn Cells, medicine.anatomical_structure, Joint pain, medicine.symptom, business
Abstract

Objective Pain from arthritis has been associated with peripheral sensitization of primary sensory afferents and the development of inflammation at the dorsal horns. This study was undertaken to determine whether the role of spinal interleukin-1β (IL-1β) in central processing of pain is important in the development of arthritis. Methods Col1-IL-1βXAT mice and GFAP-IL-1βXAT mice were injected with the feline immunodeficiency virus (FIV) (Cre) vector in the right and left temporomandibular joints (TMJs), or in the cisterna magna, respectively, to induce IL-1β expression in the dorsal horns of the spinal horn. To inhibit intrathecal IL-1 receptor type I (IL-1RI) signaling, FIV(IL-1Ra) vector was injected into the cisterna magna of Col1-IL-1βXAT mice. The effects of IL-1RI receptor inhibition in GFAP-IL-1βXAT mice were studied in the GFAP-IL-1βXAT–IL-1RI−/− compound mouse model. Neuroinflammatory, sensory, and behavioral changes were evaluated in conjunction with arthritic changes in the TMJ, assessed by histopathologic and immunohistochemical analyses. Results Induction of an osteoarthritis-like condition in the TMJ in the Col1-IL-1βXAT mouse model resulted in up-regulation of murine IL-1β at the dorsal horns. Moreover, intrathecal inhibition of IL-1RI in Col1-IL-1βXAT mice with arthritis led to amelioration of joint pathology and attenuation of the attendant joint pain. Overexpression of spinal IL-1β in the recently developed GFAP-IL-1βXAT somatic mosaic model of neuroinflammation led to development of arthritis-like pathology accompanied by increased pain-like behavior. Conclusion Our results indicate that joint pathology and pain are dependent on spinal IL-1β, and suggest the presence of a bidirectional central nervous system–peripheral joints crosstalk that may contribute to the development, expansion, and exacerbation of arthritis.

Published
2008

5. Amelioration of Pain and Histopathologic Joint Abnormalities in the Col1-IL-1βXAT Mouse Model of Arthritis by Intraarticular Induction of ·-Opioid Receptor Into the Temporomandibular Joint.

Author

Kyrkanides, Stephanos, Fiorentino, Paolo M., Miller, Jen-nie H., Gan, Yanjun, Yu-Ching Lai, Shaftel, Solomon S., Puzas, J. Edward, Piancino, Maria G., O'Banion, M. Kerry, and Tallents, Ross H.

Subjects
OPIOID receptors, DRUG receptors, TREATMENT of arthritis, FELINE immunodeficiency virus, LENTIVIRUSES, GENE expression
Abstract

The article focuses on a study which evaluated opioid receptor function as a basis for novel antinociceptive therapy in arthritis. Using the feline immunodeficiency virus (FIV) vector, the human µ-opioid receptor (HuMOR) expression in arthritic joints of mice was induced. The results of the study indicated that prophylactic therapy with MOR overexpression in joints can successfully prevent the development of pain, dysfunction and histopathologic abnormalities in the joints in arthritis.

Published
2007
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6. Intraarticular induction of interleukin‐1β expression in the adult mouse, with resultant temporomandibular joint pathologic changes, dysfunction, and pain.

Author

Yu‐Ching Lai, Solomon S. Shaftel, Jen‐nie H. Miller, Ross H. Tallents, Yoon Chang, Carl A. Pinkert, John A. Olschowka, Ian M. Dickerson, J. Edward Puzas, M. Kerry O'Banion, and Stephanos Kyrkanides

Subjects
INTERLEUKIN-1, ARTHRITIS, INFLAMMATION, CALCITONIN, PROTEINS
Abstract

To examine the effects of intraarticular induction of interleukin‐1β (IL‐1β) expression in adult mice.We used somatic mosaic analysis in a novel transgenic mouse with an inducible IL‐1β transcription unit. Transgene activation was induced by Cre recombinase in the temporomandibular joints (TMJs) of adult transgenic mice (conditional knockin model). The effects of intraarticular IL‐1β induction were subsequently evaluated at the cellular, histopathologic, and behavioral levels.We developed transgenic mice capable of germline transmission of a dormant transcription unit consisting of the mature form of human IL‐1β as well as the reporter gene β‐galactosidase driven by the rat procollagen 1A1 promoter. Transgene activation by a feline immunodeficiency virus Cre vector resulted in histopathologic changes, including articular surface fibrillations, cartilage remodeling, and chondrocyte cloning. We also demonstrated up‐regulation of genes implicated in arthritis (cyclooxygenase 2, IL‐6, matrix metalloproteinase 9). There was a lack of inflammatory cells in these joints. Behavioral changes, including increased orofacial grooming and decreased resistance to mouth opening, were used as measures of nociception and joint dysfunction, respectively. The significant increase in expression of the pain‐related neurotransmitter calcitonin gene‐related peptide (CGRP) in the sensory ganglia as well as the auxiliary protein CGRP receptor component protein of the calcitonin‐like receptor in the brainstem further substantiated the induction of pain.Induction of IL‐1β expression in the TMJs of adult mice led to pathologic development, dysfunction, and related pain in the joints. The somatic mosaic model presented herein may prove useful in the preclinical evaluation of existing and new treatments for the management of joint pathologic changes and pain, such as in osteoarthritis. [ABSTRACT FROM AUTHOR]

Published
2006
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