Molecular Biology of the Cell by Bruce Alberts, Alexander Johnson, Julian Lewis, David Morgan, Martin Raff, Keith Roberts, Peter Walter by by Bruce Alberts, Alexander Johnson, Julian Lewis, David Morg

CELL BIOLOGY OF INFECTION
1285
early
endosome
Mycobacterium
tuberculosis
late
endosome
lysosome
recycling
Salmonella
enterica
TGN
ER
vesicles
Golgi
Legionella
pneumophila
Figure 23–24 Modifications of
membrane traffic in host cells by
bacterial pathogens. Intracellular bacterial
pathogens, including Mycobacterium
tuberculosis, Salmonella enterica, and
Legionella pneumophila, all replicate in
membrane-enclosed compartments, but
the compartments differ. M. tuberculosis
remains in a compartment that has early
endosomal markers and continues to
communicate with the plasma membrane
via transport vesicles. S. enterica replicates
in a compartment that has late endosomal
markers and does not communicate with
the plasma membrane. L. pneumophila
replicates in an unusual compartment that
is wrapped in rough endoplasmic reticulum
(ER) membrane and communicates with
the ER via transport vesicles. TGN, trans
Golgi network.
normal endocytic
pathway
ER
resist the lysosome’s antimicrobial armaments. Intracellular pathogens must also
provide a pathway for importing nutrients from the host cytosol into their compartment
of choice.
Different pathogens have distinct MBoC6 m24.32/23.24
strategies for altering membrane traffic in
the host cell (Figure 23–24). M. tuberculosis prevents the early endosome that
contains the bacteria from maturing, so the endosome never acidifies or acquires
the other characteristics of a late endosome or lysosome. This strategy requires
the activity of its type VII secretion system, as well as mycobacterial lipid products
that mimic host lipids and influence vesicular traffic. Phagosomes containing Salmonella
enterica, in contrast, acidify and acquire markers of late endosomes and
lysosomes, but the bacteria slow the process of phagosomal maturation. They do
so by injecting effector proteins through a second type III secretion system. These
effectors activate host kinesin motor proteins to pull membrane tubules outward
from the phagosome along cytoplasmic microtubules, forming a specialized compartment
called the Salmonella-containing vacuole (Figure 23–25).
Other bacteria seem to find shelter in intracellular compartments that are distinct
from those of the usual endocytic system. One example is Legionella pneumophila,
which was first recognized as a human pathogen in 1976, when it was
found to be the cause of a type of pneumonia known as Legionnaire’s disease.
L. pneumophila is normally a parasite of freshwater amoebae, but it is commonly
(A)
SPI1
Salmonella
nucleus
SPI2
Salmonellacontaining
vacuole
Golgi
Salmonellainduced
filament
microtubules
kinesin
(B)
10 µm
Figure 23–25 Salmonella enterica
residing in a modified phagosomal
compartment called the Salmonellacontaining
vacuole. These bacteria invade
the host cell using an SPI1 type III secretion
system to inject effector proteins that
induce the trigger mechanism of microbe
entry illustrated in Figure 23–19B.
(A) Following its engulfment into a
phagosome, the bacterium inactivates its
SPI1 type III secretion system and activates
its SPI2 type III secretion system to inject
different effector proteins, which remodel
the phagosome into the specialized
Salmonella-containing vacuole. One of the
injected effector proteins activates host
kinesin motor proteins to pull membrane
tubules outward toward the plus ends
of the microtubules (see Figure 16–42).
(B) Fluorescence micrograph showing
S. enterica in a Salmonella-containing
vacuole. The bacteria are stained green,
the microtubules red, and the nucleus blue.
(B, courtesy of Stephane Meresse.)