610 Modern Food Microbiology
The most important subsets of T cells for resistance to listeriosis are helper or CD4 (L3T4
+ ) and
cytolytic (killer) or CD8 (Lyt2
+ ).
71 The CD4 T cells react with the foreign antigen, after which they
produce lymphokines (cytokines): IL-1, IL-2, IL-6, immune or γ -interferon, and others. γ -Interferon,
whose production is aided also by tumor necrosis factor,
22 induces the production of IL-2 receptor
expression on monocytes. Also, IL-2 may enhance the activation of lymphokine-activated killer cells
that can lyse infected macrophages. As little as 0.6 µg per mouse of exogenously administered IL-2 has
been shown to strengthen mouse resistance to L. monocytogenes.
54
γ -Interferon activates macrophages
and CD8 T cells, and the latter react with L. monocytogenes-infected host macrophages—and cause
their lysis. Both CD4 and CD8 T cells are stimulated by L. monocytogenes; they activate macrophages
via their production of γ -interferon and contribute to resistance to listeriosis.
70 CD8 also secretes
γ -interferon when exogenous IL-2 is provided, and both CD4 and CD8 can confer some passive
immunity to recipient mice.
70
Some of the events that occur in murine hosts following infection with L. monocytogenes are
presumed to be the same events that occur in humans. When macrophages engulf L. monocytogenes, a
factor-increasing monocytopoiesis (FIM) is secreted by the macrophages at the infection site. FIM is
transported to the bone marrow, where it stimulates the production of more macrophages. Only viable
L. monocytogenes cells can induce the T cell response and immunity to histeriosis. Because LLO is
the virulence factor of L. monocytogenes that elicits the T cell response, this heat-labile protein is
destroyed when cells are heat killed. The CD8 T cell subset appears to be the major T cell component
responsible for antilisterial immunity, for it acts by eliciting lymphokine production by macrophages;
passive immunity to L. monocytogenes can be achieved by transfer of the CD8 T cell subset.
4 The T cell
response does not occur even when mice are injected with both killed cells and recombinant IL-1a.
60
Neither avirulent nor killed cells induce IL-1 in vitro; viable L. monocytogenes cells do,
96 indicating
a critical role for IL-1 and γ -interferon in the initiation of the in vivo response, for it has been shown
that simultaneously administered IL-1a and γ -interferon increased resistance to L. monocytogenes
in mice better than either alone.
74 The combination was not synergistic, only additive. It appears that
the primary role of γ -interferon is to elicit lymphokine production rather than acting directly, and
it is known to increase the production of IL-1.
17
γ -Interferon is detectable in the blood stream and
spleen of mice only during the first 4 days after infection.
99 Infection of mice by L. monocytogenes
leads to an increase in IL-6, which is produced by nonlymphocyte cells.
80 Mice that are deficient in
IL-6 have increased susceptibility to listeriosis.
23 IL-6 appears to act by stimulating the production of
neutrophils.
23
This synopsis of murine resistance to L. monocytogenes reveals some of the multifunctional roles
of the lymphokines in T cell immunity (due to different E-cadherins needed for InlA receptors); and
the apparent critical importance of LLO as the primary virulence factor of this organism. What makes
immunocompromised hosts more susceptible to listeriosis is the dampening effect that immunosuppressive agents have on the T cell system. Possible therapy is suggested by the specific roles that some
of the lymphokines play, but whether the effects are similar in humans is unclear.
PERSISTENCE OF L. MONOCYTOGENES IN FOODS
Because it can grow over the temperature range of about 1–45
◦ C and the pH range of 4.1 to around
9.6, L. monocytogenes may be expected to survive in foods for long periods of time, and this has been
confirmed. Strains Scott A and V7, inoculated at levels of 10
4 –10
5 /g, survived in cottage cheese for
up to 28 days when held at 3
◦ C.
111 When these two strains, with two others, were inoculated into
a camembert cheese formulated with levels of 10
4 –10
5 , growth occurred during the first 18 days of
The most important subsets of T cells for resistance to listeriosis are helper or CD4 (L3T4
+ ) and
cytolytic (killer) or CD8 (Lyt2
+ ).
71 The CD4 T cells react with the foreign antigen, after which they
produce lymphokines (cytokines): IL-1, IL-2, IL-6, immune or γ -interferon, and others. γ -Interferon,
whose production is aided also by tumor necrosis factor,
22 induces the production of IL-2 receptor
expression on monocytes. Also, IL-2 may enhance the activation of lymphokine-activated killer cells
that can lyse infected macrophages. As little as 0.6 µg per mouse of exogenously administered IL-2 has
been shown to strengthen mouse resistance to L. monocytogenes.
54
γ -Interferon activates macrophages
and CD8 T cells, and the latter react with L. monocytogenes-infected host macrophages—and cause
their lysis. Both CD4 and CD8 T cells are stimulated by L. monocytogenes; they activate macrophages
via their production of γ -interferon and contribute to resistance to listeriosis.
70 CD8 also secretes
γ -interferon when exogenous IL-2 is provided, and both CD4 and CD8 can confer some passive
immunity to recipient mice.
70
Some of the events that occur in murine hosts following infection with L. monocytogenes are
presumed to be the same events that occur in humans. When macrophages engulf L. monocytogenes, a
factor-increasing monocytopoiesis (FIM) is secreted by the macrophages at the infection site. FIM is
transported to the bone marrow, where it stimulates the production of more macrophages. Only viable
L. monocytogenes cells can induce the T cell response and immunity to histeriosis. Because LLO is
the virulence factor of L. monocytogenes that elicits the T cell response, this heat-labile protein is
destroyed when cells are heat killed. The CD8 T cell subset appears to be the major T cell component
responsible for antilisterial immunity, for it acts by eliciting lymphokine production by macrophages;
passive immunity to L. monocytogenes can be achieved by transfer of the CD8 T cell subset.
4 The T cell
response does not occur even when mice are injected with both killed cells and recombinant IL-1a.
60
Neither avirulent nor killed cells induce IL-1 in vitro; viable L. monocytogenes cells do,
96 indicating
a critical role for IL-1 and γ -interferon in the initiation of the in vivo response, for it has been shown
that simultaneously administered IL-1a and γ -interferon increased resistance to L. monocytogenes
in mice better than either alone.
74 The combination was not synergistic, only additive. It appears that
the primary role of γ -interferon is to elicit lymphokine production rather than acting directly, and
it is known to increase the production of IL-1.
17
γ -Interferon is detectable in the blood stream and
spleen of mice only during the first 4 days after infection.
99 Infection of mice by L. monocytogenes
leads to an increase in IL-6, which is produced by nonlymphocyte cells.
80 Mice that are deficient in
IL-6 have increased susceptibility to listeriosis.
23 IL-6 appears to act by stimulating the production of
neutrophils.
23
This synopsis of murine resistance to L. monocytogenes reveals some of the multifunctional roles
of the lymphokines in T cell immunity (due to different E-cadherins needed for InlA receptors); and
the apparent critical importance of LLO as the primary virulence factor of this organism. What makes
immunocompromised hosts more susceptible to listeriosis is the dampening effect that immunosuppressive agents have on the T cell system. Possible therapy is suggested by the specific roles that some
of the lymphokines play, but whether the effects are similar in humans is unclear.
PERSISTENCE OF L. MONOCYTOGENES IN FOODS
Because it can grow over the temperature range of about 1–45
◦ C and the pH range of 4.1 to around
9.6, L. monocytogenes may be expected to survive in foods for long periods of time, and this has been
confirmed. Strains Scott A and V7, inoculated at levels of 10
4 –10
5 /g, survived in cottage cheese for
up to 28 days when held at 3
◦ C.
111 When these two strains, with two others, were inoculated into
a camembert cheese formulated with levels of 10
4 –10
5 , growth occurred during the first 18 days of