Publication Database

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

Art

Poster

Autoren

Sharbati-Tehrani, S.

Schramm, K.

Rempel, S.

Wang, H.

Tykiel, V.

Kunisch, R.

Lewin, A.

Kongress

60. Jahrestagung der DGHM

Dresden, 21. – 24.09.2008

Quelle

International journal of medical microbiology : IJMM

Seiten: 79

ISSN: 1618-0607

Sprache

Englisch

Kontakt

Institut für Veterinär-Biochemie

Oertzenweg 19 b
14163 Berlin
+49 30 838 62225
biochemie@vetmed.fu-berlin.de

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.