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Fachbereich Veterinärmedizin



    The expression of porins directs the intracellular multiplication of Mycobacterium fortuitum (2008)

    Sharbati-Tehrani, S.
    Schramm, K.
    Rempel, S.
    Wang, H.
    Tykiel, V.
    Kunisch, R.
    Lewin, A.
    60. Jahrestagung der DGHM
    Dresden, 21. – 24.09.2008
    International journal of medical microbiology : IJMM
    Seiten: 79
    ISSN: 1618-0607
    Institut für Veterinär-Biochemie

    Oertzenweg 19 b
    14163 Berlin
    +49 30 838 62225

    Abstract / Zusammenfassung

    Mycobacterium is a diverse genus comprising highly pathogenic
    slow-growing species like M. tuberculosis and M. leprae and also less
    pathogenic, opportunistic or saprophytic species belonging to the group
    of rapidly growing mycobacteria (RGM). Increasing RGM?associated
    diseases are an emerging health problem. Most infections occur from
    environmental sources, namely water and water-related equipment. The
    M. fortuitum group is involved in 60% of localised cutaneous infections
    caused by RGM [1]. Little is known about virulence mechanisms and
    persistence of M. fortuitum in host cells. In a previous study, we showed
    that the intracellular survival of the saprophytic M. smegmatis depends
    on the amount of porins in the mycobacterial outer membrane (OM) [2].
    Therefore, porins of M. fortuitum were characterised to address their
    impact on intracellular multiplication of the pathogenic fast growing M.
    fortuitum. Two novel porin encoding genes, porM1 and porM2,
    orthologous to the major porin of M. smegmatis MspA were cloned from
    M. fortuitum. Both porins were at least partially able to complement the
    mutations of a M. smegmatis mutant strain lacking the genes mspA and
    mspC with respect to the growth rate. PorM1 and porM2 mRNA and
    protein expression analysis revealed divergent expression among the M.
    fortuitum strains. Downregulation of porin expression by RNA antisense
    technique resulted in enhanced intracellular multiplication of M. fortuitum
    both in human and murine macrophage lines.
    These findings show that the porin density in the OM directs the
    intracellular multiplication of M. fortuitum. It can be suggested that
    increased impermeability of the mycobacterial OM caused by decreased
    porin expression or loss of efficient porins may be considered as a
    pathogenicity factor of mycobacteria.
    [1]. Howard, S.T.& Byrd,T.F. (2000) Microbes and Infection 2, 1845-1853
    [2]. Sharbati-Tehrani S, Stephan J, Holland G, Appel B, Niederweis M,
    Lewin A. (2005) Microbiology 2403-2410.