A Liver Capsular Network of Monocyte-Derived Macrophages Restricts Hepatic Dissemination of Intraperitoneal Bacteria by Neutrophil Recruitment
Sierro, F
Evrard, M
Rizzetto, S
Melino, M
Mitchell, AJ
Florido, M
Beattie, L
Walters, SB
Tay, SS
Lu, B
Holz, LE
Roediger, B
Wong, YC
Warren, A
Ritchie, W
McGuffog, C
Weninger, W
Le Couteur, DG
Ginhoux, F
Britton, WJ
Heath, WR
Saunders, BM
McCaughan, GW
Luciani, F
MacDonald, KPA
Ng, LG
Bowen, DG
Bertolino, P
- Publication Type:
- Journal Article
- Citation:
- Immunity, 2017, 47 (2), pp. 374 - 388.e6
- Issue Date:
- 2017-08-15
Closed Access
Filename | Description | Size | |||
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Immunity 2017 Aug 15 47-374.pdf | Published Version | 7.42 MB | Adobe PDF |
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Full metadata record
Field | Value | Language |
---|---|---|
dc.contributor.author | Sierro, F | en_US |
dc.contributor.author | Evrard, M | en_US |
dc.contributor.author | Rizzetto, S | en_US |
dc.contributor.author | Melino, M | en_US |
dc.contributor.author | Mitchell, AJ | en_US |
dc.contributor.author | Florido, M | en_US |
dc.contributor.author | Beattie, L | en_US |
dc.contributor.author | Walters, SB | en_US |
dc.contributor.author | Tay, SS | en_US |
dc.contributor.author | Lu, B | en_US |
dc.contributor.author | Holz, LE | en_US |
dc.contributor.author | Roediger, B | en_US |
dc.contributor.author | Wong, YC | en_US |
dc.contributor.author | Warren, A | en_US |
dc.contributor.author | Ritchie, W | en_US |
dc.contributor.author | McGuffog, C | en_US |
dc.contributor.author | Weninger, W | en_US |
dc.contributor.author | Le Couteur, DG | en_US |
dc.contributor.author | Ginhoux, F | en_US |
dc.contributor.author | Britton, WJ | en_US |
dc.contributor.author | Heath, WR | en_US |
dc.contributor.author |
Saunders, BM |
en_US |
dc.contributor.author | McCaughan, GW | en_US |
dc.contributor.author | Luciani, F | en_US |
dc.contributor.author | MacDonald, KPA | en_US |
dc.contributor.author | Ng, LG | en_US |
dc.contributor.author | Bowen, DG | en_US |
dc.contributor.author | Bertolino, P | en_US |
dc.date.available | 2017-07-23 | en_US |
dc.date.issued | 2017-08-15 | en_US |
dc.identifier.citation | Immunity, 2017, 47 (2), pp. 374 - 388.e6 | en_US |
dc.identifier.issn | 1074-7613 | en_US |
dc.identifier.uri | http://hdl.handle.net/10453/119629 | |
dc.description.abstract | © 2017 Elsevier Inc. The liver is positioned at the interface between two routes traversed by pathogens in disseminating infection. Whereas blood-borne pathogens are efficiently cleared in hepatic sinusoids by Kupffer cells (KCs), it is unknown how the liver prevents dissemination of peritoneal pathogens accessing its outer membrane. We report here that the hepatic capsule harbors a contiguous cellular network of liver-resident macrophages phenotypically distinct from KCs. These liver capsular macrophages (LCMs) were replenished in the steady state from blood monocytes, unlike KCs that are embryonically derived and self-renewing. LCM numbers increased after weaning in a microbiota-dependent process. LCMs sensed peritoneal bacteria and promoted neutrophil recruitment to the capsule, and their specific ablation resulted in decreased neutrophil recruitment and increased intrahepatic bacterial burden. Thus, the liver contains two separate and non-overlapping niches occupied by distinct resident macrophage populations mediating immunosurveillance at these two pathogen entry points to the liver. | en_US |
dc.relation.ispartof | Immunity | en_US |
dc.relation.isbasedon | 10.1016/j.immuni.2017.07.018 | en_US |
dc.subject.classification | Immunology | en_US |
dc.subject.mesh | Peritoneum | en_US |
dc.subject.mesh | Liver | en_US |
dc.subject.mesh | Neutrophils | en_US |
dc.subject.mesh | Monocytes | en_US |
dc.subject.mesh | Macrophages | en_US |
dc.subject.mesh | Kupffer Cells | en_US |
dc.subject.mesh | Animals | en_US |
dc.subject.mesh | Mice, Inbred C57BL | en_US |
dc.subject.mesh | Mice, Knockout | en_US |
dc.subject.mesh | Humans | en_US |
dc.subject.mesh | Mice | en_US |
dc.subject.mesh | Listeria monocytogenes | en_US |
dc.subject.mesh | Cell Communication | en_US |
dc.subject.mesh | Neutrophil Infiltration | en_US |
dc.subject.mesh | Host-Pathogen Interactions | en_US |
dc.subject.mesh | Immunity, Innate | en_US |
dc.subject.mesh | Listeriosis | en_US |
dc.subject.mesh | Cell Self Renewal | en_US |
dc.title | A Liver Capsular Network of Monocyte-Derived Macrophages Restricts Hepatic Dissemination of Intraperitoneal Bacteria by Neutrophil Recruitment | en_US |
dc.type | Journal Article | |
utslib.citation.volume | 2 | en_US |
utslib.citation.volume | 47 | en_US |
utslib.for | 1107 Immunology | en_US |
pubs.embargo.period | Not known | en_US |
pubs.organisational-group | /University of Technology Sydney | |
pubs.organisational-group | /University of Technology Sydney/Faculty of Science | |
pubs.organisational-group | /University of Technology Sydney/Faculty of Science/School of Life Sciences | |
utslib.copyright.status | closed_access | |
pubs.issue | 2 | en_US |
pubs.publication-status | Published | en_US |
pubs.volume | 47 | en_US |
Abstract:
© 2017 Elsevier Inc. The liver is positioned at the interface between two routes traversed by pathogens in disseminating infection. Whereas blood-borne pathogens are efficiently cleared in hepatic sinusoids by Kupffer cells (KCs), it is unknown how the liver prevents dissemination of peritoneal pathogens accessing its outer membrane. We report here that the hepatic capsule harbors a contiguous cellular network of liver-resident macrophages phenotypically distinct from KCs. These liver capsular macrophages (LCMs) were replenished in the steady state from blood monocytes, unlike KCs that are embryonically derived and self-renewing. LCM numbers increased after weaning in a microbiota-dependent process. LCMs sensed peritoneal bacteria and promoted neutrophil recruitment to the capsule, and their specific ablation resulted in decreased neutrophil recruitment and increased intrahepatic bacterial burden. Thus, the liver contains two separate and non-overlapping niches occupied by distinct resident macrophage populations mediating immunosurveillance at these two pathogen entry points to the liver.
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