Distinct bone marrow-derived and tissue-resident macrophage lineages proliferate at key stages during inflammation

Davies, Luke C.; Rosas, Marcela; Jenkins, Stephen J.; Liao, Chia‐Te; Scurr, Martin; Brombacher, Frank; Fraser, Donald; Allen, Judith E.; Jones, Simon A.; Taylor, Philip Russel

doi:10.1038/ncomms2877

Cited by 274 publications

(280 citation statements)

References 39 publications

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“…However, unlike in other murine peritonitis models (17)(18)(19)(20) and also, for example, unlike in atherosclerotic lesions (62), local proliferation of AIP macrophages does not appear to be contributing to their increased numbers at least over the short 3-d period, but rather monocyte recruitment is the principal mechanism for the macrophage accumulation; their reduced numbers upon CSF-1 neutralization cannot therefore be due to suppressed proliferation in this model.…”

Section: Discussionmentioning

confidence: 89%

“…There has been more interest recently in the contribution of local proliferation of inflammatory macrophage/DC populations to their increased numbers (17,19,20,62). To explore whether reduced cell cycling in the inflamed cavity itself might be contributing to the lower numbers of AIP MPS populations observed earlier upon CSF neutralization, we pulse-labeled mAb-treated AIP mice with BrdU 2 h before termination at day 3.…”

Section: Csfs and Mps Cycling And Gene Expression In Aipmentioning

confidence: 99%

“…A unified nomenclature has recently been proposed to attempt to circumvent this fundamental problem in which MPS cells can be classified primarily by their ontogeny and secondarily by their location, function, and phenotype in the steady-state and in inflammatory conditions (13). Even though a number of articles using sophisticated in vivo technology in mice have recently appeared addressing the origins of tissue macrophages during development, there is still debate around the fundamental question of the contribution, if any, of blood monocytes, including their subpopulations, to tissue macrophages in the adult at steady-state, and also to what extent local macrophage proliferation contributes to their homeostatic control or to that during inflammatory reactions (3,(15)(16)(17)(18)(19)(20)(21)(22)(23)(24).…”

mentioning

confidence: 99%

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Specific Contributions of CSF-1 and GM-CSF to the Dynamics of the Mononuclear Phagocyte System

Louis

Cook

Lacey

et al. 2015

The Journal of Immunology

109

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M-CSF (or CSF-1) and GM-CSF can regulate the development and function of the mononuclear phagocyte system (MPS). To address some of the outstanding and sometimes conflicting issues surrounding this biology, we undertook a comparative analysis of the effects of neutralizing mAbs to these CSFs on murine MPS populations in the steady-state and during acute inflammatory reactions. CSF-1 neutralization, but not of GM-CSF, in normal mice rapidly reduced the numbers of more mature Ly6C− monocytes in blood and bone marrow, without any effect on proliferating precursors, and also the numbers of the resident peritoneal macrophages, observations consistent with CSF-1 signaling being essential only at a relatively late state in steady-state MPS development; in contrast, GM-CSF neutralization had no effect on the numbers of these particular populations. In Ag-induced peritonitis (AIP), thioglycolate-induced peritonitis, and LPS-induced lung inflammation, CSF-1 neutralization lowered inflammatory macrophage number; in the AIP model, this reduced number was not due to suppressed proliferation. More detailed studies with the convenient AIP model indicated that CSF-1 neutralization led to a relatively uniform reduction in all inflammatory cell populations; GM-CSF neutralization, in contrast, was more selective, resulting in the preferential loss among the MPS populations of a cycling, monocyte-derived inflammatory dendritic cell population. Some mechanistic options for the specific CSF-dependent biologies enumerated are discussed.

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Section: Discussionmentioning

confidence: 89%

Section: Csfs and Mps Cycling And Gene Expression In Aipmentioning

confidence: 99%

mentioning

confidence: 99%

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Specific Contributions of CSF-1 and GM-CSF to the Dynamics of the Mononuclear Phagocyte System

Louis

Cook

Lacey

et al. 2015

The Journal of Immunology

109

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“…40 This is due to not only inflammatory macrophage recruitment but also to local macrophage proliferation that is M-CSF dependent. 41 We injected zymosan into the peritoneal cavity of both WT and Nbs1 ΔB/ΔB mice, and after 48 hours, we euthanized the mice and performed peritoneal lavages. The cells obtained were stained for CD11b, F4/80, and the intracellular proliferation marker Ki-67.…”

Section: Nbs1 Is Required For M-csf-dependent Proliferation In Macropmentioning

confidence: 99%

NBS1 is required for macrophage homeostasis and functional activity in mice

Pereira-Lopes

Tur

Calatayud-Subias

et al. 2015

Blood

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• Nbs1 is a component of the MRE11 complex, which is a sensor of DNA double-strand breaks and plays a crucial role in the DNA damage response.• In mice with a hypomorphic allele of Nbs1, macrophages exhibit increased senescence and abnormal proliferation and inflammatory responses. , macrophage activation-induced ROS caused increased levels of DNA damage that were associated with defects in proliferation, delayed differentiation, and increased senescence. Furthermore, upon stimulation, Nbs1 ΔB/ΔB macrophages exhibited increased expression of proinflammatory cytokines. In the in vivo 2,4-dinitrofluorobenezene model of inflammation, Nbs1 ΔB/ΔB animals showed increased weight and ear thickness. By using the sterile inflammation by zymosan injection, we found that macrophage proliferation was drastically decreased in the peritoneal cavity of Nbs1 ΔB/ΔB mice. Our findings show that NBS1 is crucial for macrophage function during normal aging. These results have implications for understanding the immune defects observed in patients with NBS and related disorders. (Blood. 2015;126(22):2502-2510

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“…Certain tissue MF types (e.g., Kupffer cells, peritoneal, lung, splenic red pulp MFs, and microglia), are long-lived, reside in their specific tissue in a steady-state, and are not replenished by infiltrating monocytes (16). These MFs originate from different sources (e.g., the fetal liver and yolk sac) (17,18).…”

mentioning

confidence: 99%

Streptococci Engage TLR13 on Myeloid Cells in a Site-Specific Fashion

Kolter

Feuerstein

Spoeri

et al. 2016

The Journal of Immunology

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International audienceStreptococci are common human colonizers with a species-specific mucocutaneous distribution. At the same time, they are among the most important and most virulent invasive bacterial pathogens. Thus, site-specific cellular innate immunity, which is predominantly executed by resident and invading myeloid cells, has to be adapted with respect to streptococcal sensing, handling, and response. In this article, we show that TLR13 is the critical mouse macrophage (MΦ) receptor in the response to group B Streptococcus, both in bone marrow-derived MΦs and in mature tissue MΦs, such as those residing in the lamina propria of the colon and the dermis, as well as in microglia. In contrast, TLR13 and its chaperone UNC-93B are dispensable for a potent cytokine response of blood monocytes to group B Streptococcus, although monocytes serve as the key progenitors of intestinal and dermal MΦs. Furthermore, a specific role for TLR13 with respect to MΦ function is supported by the response to staphylococci, where TLR13 and UNC-93B limit the cytokine response in bone marrow-derived MΦs and microglia, but not in dermal MΦs. In summary, TLR13 is a critical and site-specific receptor in the single MΦ response to β-hemolytic streptococci

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Distinct bone marrow-derived and tissue-resident macrophage lineages proliferate at key stages during inflammation

Cited by 274 publications

References 39 publications

Specific Contributions of CSF-1 and GM-CSF to the Dynamics of the Mononuclear Phagocyte System

Specific Contributions of CSF-1 and GM-CSF to the Dynamics of the Mononuclear Phagocyte System

NBS1 is required for macrophage homeostasis and functional activity in mice

Streptococci Engage TLR13 on Myeloid Cells in a Site-Specific Fashion

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