Literature DB >> 8231110

Exocrinopathy resembling Sjögren's syndrome induced by a murine retrovirus.

K Suzuki1, M Makino, Y Okada, J Kinoshita, R Yui, H Kanazawa, H Asakura, M Fujiwara, T Mizuochi, K Komuro.   

Abstract

BACKGROUND: Sjögren's syndrome (SS) is characterized by lymphocytic infiltration into, and destruction of exocrine glands, resulting in dryness of the mouth and eyes. The disease is considered to have an autoimmune etiology, however, its etiopathogenesis remains largely unknown. Recently, retrovirus is suggested to participate in the pathogenesis of SS, because SS-like lesions are reported in HIV infection or in human T cell leukemia virus type I infection. Moreover, human intracisternal A-type retroviral particles are reported to be detected in SS patients. During the course of our study on the histopathology of mice infected with a murine retrovirus, we happened to find SS-like exocrinopathy in those mice. EXPERIMENTAL
DESIGN: Four-week-old C57BL/6 (B6) mice were injected intraperitoneally with LP-BM5 murine leukemia virus. This virus is known to induce splenomegaly, lymphadenopathy followed by lymphoid malignancy, and profound immunodeficiency in sensitive strains of mice. From 4 to 16 weeks after the virus inoculation, the infected mice were sacrificed and their submandibular and lacrimal glands were analyzed light and electron microscopically and immunohistochemically. The existence of the virus in the lesion in situ was also analyzed by the same method, and additionally by a polymerase chain reaction method.
RESULTS: Periductal lymphocytic infiltration into the submandibular and lacrimal glands was observed in all the virus-infected mice at 4 weeks after the infection and progressed with time. Extraglandular lymphocytic infiltration was also observed in liver, kidney, lung, and pancreas. Immunohistochemical examination revealed that most infiltrating cells into the glands were composed of CD3+ T cells (CD4-dominant), Mac-1+ cells, and B220+ cells. The virus genome was detected in submandibular glands by immunohistochemistry or by polymerase chain reaction. In addition, retroviral particles were secreted into the lumen of exocrine ducts of submandibular glands.
CONCLUSIONS: This might be an SS animal model that is induced by a certain defined retrovirus. This experimental system might provide us with valuable information for analyzing the mechanisms of how a retrovirus could induce SS.

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Year:  1993        PMID: 8231110

Source DB:  PubMed          Journal:  Lab Invest        ISSN: 0023-6837            Impact factor:   5.662


  9 in total

1.  LP-BM5 virus-infected mice produce activating autoantibodies to the AMPA receptor.

Authors:  E Koustova; Y Sei; L Fossom; M L Wei; P N Usherwood; N B Keele; M A Rogawski; A S Basile
Journal:  J Clin Invest       Date:  2001-03       Impact factor: 14.808

2.  Induction of intestinal lesions in nu/nu mice induced by transfer of lymphocytes from syngeneic mice infected with murine retrovirus.

Authors:  K Suzuki; T Narita; R Yui; K Ohtsuka; S Inada; T Kimura; Y Okada; M Makino; T Mizuochi; H Asakura; M Fujiwara
Journal:  Gut       Date:  1997-08       Impact factor: 23.059

Review 3.  Is Sjögren's syndrome a retroviral disease?

Authors:  Nikolaos V Sipsas; Maria N Gamaletsou; Haralampos M Moutsopoulos
Journal:  Arthritis Res Ther       Date:  2011-04-13       Impact factor: 5.156

4.  CD28-B7 costimulatory blockade by CTLA4Ig delays the development of retrovirus-induced murine AIDS.

Authors:  L de Leval; S Colombi; S Debrus; M A Demoitié; R Greimers; P Linsley; M Moutschen; J Boniver
Journal:  J Virol       Date:  1998-06       Impact factor: 5.103

Review 5.  The Epstein-Barr virus in autoimmunity.

Authors:  J H Vaughan
Journal:  Springer Semin Immunopathol       Date:  1995

6.  Sialadenitis histologically resembling Sjogren syndrome in mice transgenic for hepatitis C virus envelope genes.

Authors:  K Koike; K Moriya; K Ishibashi; H Yotsuyanagi; Y Shintani; H Fujie; K Kurokawa; Y Matsuura; T Miyamura
Journal:  Proc Natl Acad Sci U S A       Date:  1997-01-07       Impact factor: 11.205

7.  Possible involvement of Toll-like receptor 7 in the development of type 1 autoimmune pancreatitis.

Authors:  Yuri Fukui; Kazushige Uchida; Yutaku Sakaguchi; Toshiro Fukui; Akiyoshi Nishio; Nobuaki Shikata; Noriko Sakaida; Yoshiko Uemura; Sohei Satoi; Kazuichi Okazaki
Journal:  J Gastroenterol       Date:  2014-07-09       Impact factor: 7.527

8.  Are dysregulated inflammatory responses to commensal bacteria involved in the pathogenesis of hepatobiliary-pancreatic autoimmune disease? An analysis using mice models of primary biliary cirrhosis and autoimmune pancreatitis.

Authors:  Naoko Yanagisawa; Ikuko Haruta; Ken Kikuchi; Noriyuki Shibata; Junji Yagi
Journal:  ISRN Gastroenterol       Date:  2011-06-15

9.  Commensal Flora, is it an Unwelcomed Companion as a Triggering Factor of Autoimmune Pancreatitis?

Authors:  Ikuko Haruta; Kyoko Shimizu; Naoko Yanagisawa; Keiko Shiratori; Junji Yagi
Journal:  Front Physiol       Date:  2012-04-02       Impact factor: 4.566

  9 in total

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