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Click on the blue word to follow us Listeria monocytogenes is a facultative anaerobic bacterium that is the causative agent of listeriosis, which can cause meningitis in severe cases
.
The virulence factor internalin proteins InlA and InlB are thought to play key roles in the cell-to-cell spread of Listeria across the gut and fetal barriers
.
The receptor for InlA is E-cadherin (Ecad), while the receptor for InlB is the tyrosine kinase Met
.
Monocytes can transfer Listeria from the peripheral blood to the brain, but the exact mechanism is unknown
.
On March 16, 2022, the research team of Marc Lecuit of the University of Paris established a Listeria infection model and found that Listeria can enter the brain parenchyma through intercellular diffusion through peripheral monocytes, which inhibits Fas apoptosis through InlB.
Decrease in signaling exerted by CD8+ T cell-mediated monocyte death
.
The researchers infected Listeria by humanized KIE16P mice (carrying a human-derived Ecad gene) and detected Listeria in the brain 5 days later
.
Intraperitoneal antibiotics cleared peripheral Listeria, but not the brain, which was mainly enriched in peripheral blood and monocytes in the spleen
.
After transplanting these Listeria-carrying monocytes into gentamicin-treated mice, Listeria monocytogenes was observed in the brain
.
These results suggest that monocytes are a key factor in promoting the entry of Listeria into the brain
.
Figure 1: Bacteria enter the brain by cell-to-cell diffusion.
Immunofluorescence found that monocytes adhered to endothelial cells of cerebral blood vessels and carried peripheral Listeria into the brain parenchyma by cell-to-cell diffusion
.
Transplantation of Listeria carrying a knockout of polymeric actin, which inhibits cell spreading, did not induce neuroinvasion
.
Knocking out InlA did not affect the entry of Listeria into the brain parenchyma, but knocking out InlB reduced the entry of Listeria into the brain parenchyma
.
On the other hand, knocking out InlB reduced the number of infected monocytes in the blood and spleen
.
Overexpression of InlB by genetic engineering technology can promote the invasion of Listeria
.
This suggests that InlB mediates the neuroinvasion process of Listeria
.
Studies have shown that suppressing T cells can promote Listeria infection of the brain parenchyma
.
After co-inoculation of wild-type and InlB-deficient Listeria, more wild-type Listeria entered the brain and had a more competitive advantage
.
But the aforementioned disadvantage of InlB-deficient L.
monocytogenes no longer persisted after treatment with the T-cell immunosuppressant cyclosporine: wild-type and InlB-deficient L.
monocytogenes were nearly equivalent in their ability to infect brain parenchyma
.
Furthermore, InlB-mediated neural invasion of Listeria was abolished in mice lacking functional T cells, but not in mice lacking functional B cells
.
This suggests that InlB-mediated neural invasion of Listeria may be related to T cells
.
CD8-positive T cells cause monocyte death in the spleen during Listeria infection
.
Interestingly, CD8-positive T cell-mediated monocyte death increased after InlB knockdown
.
This suggests that InlB may play a role in inhibiting monocyte death caused by CD8-positive T cells
.
The cytotoxicity of CD8-positive T cells is dependent on perforin and granzyme Fas ligand (FasL)–Fas signaling pathway
.
After inhibition of the Fas signaling downstream protein caspase-8, CD8-positive T cells induced monocytes similar to wild-type Listeria after InlB knockout
.
Furthermore, the inhibitory effect of InlB on cell death induced by CD8-positive T cells was abolished in Fas knockout mice
.
Collectively, we find that Listeria promotes infection of the brain parenchyma by inhibiting Fas-mediated T cell-dependent cell death, ultimately reducing monocyte death
.
[References] 1.
https://doi.
org/10.
1038/s41586-022-04505-7 The pictures in the text are from the references
.
The virulence factor internalin proteins InlA and InlB are thought to play key roles in the cell-to-cell spread of Listeria across the gut and fetal barriers
.
The receptor for InlA is E-cadherin (Ecad), while the receptor for InlB is the tyrosine kinase Met
.
Monocytes can transfer Listeria from the peripheral blood to the brain, but the exact mechanism is unknown
.
On March 16, 2022, the research team of Marc Lecuit of the University of Paris established a Listeria infection model and found that Listeria can enter the brain parenchyma through intercellular diffusion through peripheral monocytes, which inhibits Fas apoptosis through InlB.
Decrease in signaling exerted by CD8+ T cell-mediated monocyte death
.
The researchers infected Listeria by humanized KIE16P mice (carrying a human-derived Ecad gene) and detected Listeria in the brain 5 days later
.
Intraperitoneal antibiotics cleared peripheral Listeria, but not the brain, which was mainly enriched in peripheral blood and monocytes in the spleen
.
After transplanting these Listeria-carrying monocytes into gentamicin-treated mice, Listeria monocytogenes was observed in the brain
.
These results suggest that monocytes are a key factor in promoting the entry of Listeria into the brain
.
Figure 1: Bacteria enter the brain by cell-to-cell diffusion.
Immunofluorescence found that monocytes adhered to endothelial cells of cerebral blood vessels and carried peripheral Listeria into the brain parenchyma by cell-to-cell diffusion
.
Transplantation of Listeria carrying a knockout of polymeric actin, which inhibits cell spreading, did not induce neuroinvasion
.
Knocking out InlA did not affect the entry of Listeria into the brain parenchyma, but knocking out InlB reduced the entry of Listeria into the brain parenchyma
.
On the other hand, knocking out InlB reduced the number of infected monocytes in the blood and spleen
.
Overexpression of InlB by genetic engineering technology can promote the invasion of Listeria
.
This suggests that InlB mediates the neuroinvasion process of Listeria
.
Studies have shown that suppressing T cells can promote Listeria infection of the brain parenchyma
.
After co-inoculation of wild-type and InlB-deficient Listeria, more wild-type Listeria entered the brain and had a more competitive advantage
.
But the aforementioned disadvantage of InlB-deficient L.
monocytogenes no longer persisted after treatment with the T-cell immunosuppressant cyclosporine: wild-type and InlB-deficient L.
monocytogenes were nearly equivalent in their ability to infect brain parenchyma
.
Furthermore, InlB-mediated neural invasion of Listeria was abolished in mice lacking functional T cells, but not in mice lacking functional B cells
.
This suggests that InlB-mediated neural invasion of Listeria may be related to T cells
.
CD8-positive T cells cause monocyte death in the spleen during Listeria infection
.
Interestingly, CD8-positive T cell-mediated monocyte death increased after InlB knockdown
.
This suggests that InlB may play a role in inhibiting monocyte death caused by CD8-positive T cells
.
The cytotoxicity of CD8-positive T cells is dependent on perforin and granzyme Fas ligand (FasL)–Fas signaling pathway
.
After inhibition of the Fas signaling downstream protein caspase-8, CD8-positive T cells induced monocytes similar to wild-type Listeria after InlB knockout
.
Furthermore, the inhibitory effect of InlB on cell death induced by CD8-positive T cells was abolished in Fas knockout mice
.
Collectively, we find that Listeria promotes infection of the brain parenchyma by inhibiting Fas-mediated T cell-dependent cell death, ultimately reducing monocyte death
.
[References] 1.
https://doi.
org/10.
1038/s41586-022-04505-7 The pictures in the text are from the references
