Proinflammatory Clearance of Apoptotic Neutrophils Induces an IL-12lowIL-10high Regulatory Phenotype in Macrophages

Filardy, Alessandra A.; Pires, Dayana R.; Nunes, Marise P.; Takiya, Christina Maeda; Freire-de-Lima, Célio Geraldo; Ribeiro-Gomes, Flávia L.; DosReis, George A.

doi:10.4049/jimmunol.1000017

Cited by 198 publications

(158 citation statements)

References 46 publications

Supporting

Mentioning

152

Contrasting

Unclassified

Order By: Relevance

“…Possible mechanisms underlying the induction of IL-10 production by tissue-resident macrophages may be associated, for example, with their function to phagocyte apoptotic cells and to uptake immune complexes. These processes have been shown to induce IL-10 production by macrophages (49,(55)(56)(57). Taken together, we suggest ubiquitous interdependence between homeostatic functions of resident macrophages and IL-10 production.…”

Section: Discussionsupporting

confidence: 52%

Novel Highly Sensitive IL-10–β-Lactamase Reporter Mouse Reveals Cells of the Innate Immune System as a Substantial Source of IL-10 In Vivo

Bouabe

Liu

Moser

et al. 2011

The Journal of Immunology

View full text Add to dashboard Cite

In this study, we report on a novel, highly sensitive IL-10 reporter mouse based on the reporter enzyme β-lactamase and the fluorescence resonance energy transfer substrate coumarin-cephalosporin-fluorescein (4). In contrast to an IL-10 reporter mouse model that we generated by using enhanced GFP as reporter and allowed tracking IL-10 expression only in T cells, the IL-10–β-lactamase reporter (ITIB) mouse enables us to easily analyze and quantify IL-10 production at the single-cell level in all myeloid and lymphoid cell types. Furthermore, the ITIB mouse allows studying of the kinetics of IL-10 expression on a single-cell basis and provides a valuable tool for in vivo screening of cell type-specific IL-10–modulating drugs. Remarkably, the ITIB mouse revealed that, although a significant portion of each myeloid and lymphoid cell type produces IL-10, macrophages represent the major IL-10 producer population in several organs of naive mice. Moreover, using the examples of bacterial infection and transplantable skin melanoma models, we demonstrate the exceptional applicability of the ITIB mouse for the identification of IL-10–producing cells during immune responses in vivo. In this study, we identified tumor-infiltrating F4/80+ macrophages as the major source for IL-10 in B16-F10 melanoma in vivo. During systemic infection with Yersinia enterocolitica, although the proportion of IL-10+ cells increased in each myeloid and lymphoid cell type population, infiltrating CD11b+Ly6G+ neutrophils represent a majority among IL-10–producing cells at the site of infection. We conclude that cells of the innate immune system that are involved in immune homeostasis or immune responses are substantial sources of IL-10.

show abstract

Section: Discussionsupporting

confidence: 52%

Novel Highly Sensitive IL-10–β-Lactamase Reporter Mouse Reveals Cells of the Innate Immune System as a Substantial Source of IL-10 In Vivo

Bouabe

Liu

Moser

et al. 2011

The Journal of Immunology

View full text Add to dashboard Cite

show abstract

“…Mast cells can secrete mouse mast cell protease 4 (mMCP4), a chymase that is able to degrade inflammatory-associated cytokines and to reduce astrogliosis (Nelissen et al, 2014), while eosinophils might amplify complement-dependent cell-mediated cytotoxicity (CDCC) on astrocytes (Boulanger, 2009;Zhang and Verkman, 2013). Apoptotic neutrophils within the lesion border can affect nearby reactive microglia/macrophages by promoting a switch towards the alternative anti-inflammatory phenotype (M2) (Filardy et al, 2010). Once polarized, M2-like macrophages start producing anti-inflammatory IL-10 and increase the expression of MMP-13, which allows the remodelling of the scar matrix into a more permissive environment for axonal re-growth (Shechter et al, 2011).…”

Section: Bbb Damage and Reactive Gliosismentioning

confidence: 99%

The role of the immune system in central nervous system plasticity after acute injury

Peruzzotti-Jametti¹,

Donegá²,

Giusto³

et al. 2014

Neuroscience

View full text Add to dashboard Cite

Acute brain injuries cause rapid cell death that activates bidirectional crosstalks between the injured brain and the immune system.In the acute phase, the damaged central nervous system (CNS) activates resident and circulating immune cells via the local and systemic release of soluble mediators. This early immune activation is necessary to confine the injured tissue and foster the clearance of cellular debris, which would ultimately bring the inflammatory reaction to a close. In the chronic phase, a sustained immune activation is described in many CNS disorders, and the degree of this prolonged response has variable effects on the spontaneous brain regenerative processes. The challenge for treating acute CNS damages is to understand how to optimally engage and modify these immune responses, thus providing new strategies that will compensate for tissue lost to injury.Here we have reviewed the available information about the role and function of the innate and adaptive immune responses in influencing CNS plasticity during the acute and chronic phases of recovery after injury. We have examined how CNS damage evolves along the activation of main Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. Europe PMC Funders Group

show abstract

“…Neu were sorted with a FACSAria (BD Biosciences) based on the expression of Ly6G + . Apoptotic Neu (APO-PMNs) were obtained by overnight incubation in serumfree DMEM as described previously (22). Aged cells contained .…”

Section: Differentiation Of Macrophages Cocultured With Apoptotic Neumentioning

confidence: 99%

Pristane-Induced Granulocyte Recruitment Promotes Phenotypic Conversion of Macrophages and Protects against Diffuse Pulmonary Hemorrhage in Mac-1 Deficiency

Shi

Tsuboi

Furuhashi

et al. 2014

The Journal of Immunology

View full text Add to dashboard Cite

Diffuse pulmonary hemorrhage (DPH) is an uncommon but critical complication of systemic lupus erythematosus. Peritoneal administration of 2,6,10,14-tetramethylpentadecane (pristane) can recapitulate a lupus-like syndrome in mice, which can develop into DPH within a few weeks, especially in C57BL/6 mice. Mac-1 (CD11b/CD18), a leukocyte adhesion molecule, is known to play a role in inflammation by regulating migration of leukocytes into injured tissue. In this study, we aimed to clarify the role of Mac-1 in pristane-induced DPH, using Mac-1−/− and wild-type (WT) mice on a C57BL/6 background. After pristane injection, Mac-1−/− mice showed reduced prevalence of DPH and attenuated peritonitis compared with WT mice. Analysis of the peritoneal lavage on days 5 and 10 after pristane treatment revealed increased numbers of eosinophils and alternatively activated macrophages, but decreased numbers of neutrophils and classically activated macrophages in Mac-1−/− mice compared with WT. Enhanced production of IL-4 and IL-13, both key mediators of macrophage polarization toward the mannose receptor+ (MMR+) phenotype, was observed in the peritoneal cavity of Mac-1−/− mice. Depletion of neutrophils and eosinophils or adoptive transfer of classically activated macrophages resulted in the exacerbation of pristane-mediated DPH in both WT and Mac-1−/− mice. Moreover, peritoneal transfer of F4/80highMMR+ alternatively activated macrophages successfully reduced the prevalence of DPH in WT mice. Collectively, Mac-1 promoted acute inflammatory responses in the peritoneal cavity and the lungs by downregulating granulocyte migration and subsequent phenotypic conversion of macrophages in a pristane-induced systemic lupus erythematosus model.

show abstract

Proinflammatory Clearance of Apoptotic Neutrophils Induces an IL-12lowIL-10high Regulatory Phenotype in Macrophages

Cited by 198 publications

References 46 publications

Novel Highly Sensitive IL-10–β-Lactamase Reporter Mouse Reveals Cells of the Innate Immune System as a Substantial Source of IL-10 In Vivo

Novel Highly Sensitive IL-10–β-Lactamase Reporter Mouse Reveals Cells of the Innate Immune System as a Substantial Source of IL-10 In Vivo

The role of the immune system in central nervous system plasticity after acute injury

Pristane-Induced Granulocyte Recruitment Promotes Phenotypic Conversion of Macrophages and Protects against Diffuse Pulmonary Hemorrhage in Mac-1 Deficiency

Contact Info

Product

Resources

About