Phenotypic, Functional, and Plasticity Features of Classical and Alternatively Activated Human Macrophages

Tarique, Abdullah A.; Logan, Jayden; Thomas, Emma; Holt, Patrick G.; Sly, Peter D.; Fantino, Emmanuelle

doi:10.1165/rcmb.2015-0012oc

Cited by 449 publications

(440 citation statements)

References 47 publications

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“…Macrophages (MΦ) form a large heterogeneous subpopulation with different tissue specific and multiple polarized subsets, depending on exposure to complex signalling events [108][109][110][111]. But, here we only focus on different MΦ subsets in atherosclerosis with a simplified view, because in humans polarized phenotypes are not well characterized so far.…”

Section: The Biology Of Monocytes and Macrophagesmentioning

confidence: 99%

Nanoparticle uptake by macrophages in vulnerable plaques for atherosclerosis diagnosis

Melzer

Ankri

Fixler

et al. 2015

Journal of Biophotonics

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The composition of atherosclerotic (AS) plaques is crucial concerning rupture, thrombosis and clinical events. Two plaque types are distinguished: stable and vulnerable plaques. Vulnerable plaques are rich in inflammatory cells, mostly only M1 macrophages, and are highly susceptible to rupture. These plaques represent a high risk particularly with the standard invasive diagnosis by coronary angiography. So far there are no non‐invasive low‐risk clinical approaches available to detect and distinguish AS plaque types in vivo. The perspective review introduces a whole work‐flow for a novel approach for non‐invasive detection and classification of AS plaques using the diffusion reflection method with gold nanoparticle loaded macrophages in combination with flow and image cytometric analysis for quality assurance. Classical biophotonic methods for AS diagnosis are summarized. Phenotyping of monocytes and macrophages are discussed for specific subset labelling by nanomaterials, as well as existing studies and first experimental proofs of concept for the novel approach are shown.

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Section: The Biology Of Monocytes and Macrophagesmentioning

confidence: 99%

Nanoparticle uptake by macrophages in vulnerable plaques for atherosclerosis diagnosis

Melzer

Ankri

Fixler

et al. 2015

Journal of Biophotonics

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“…Blood Services, Brisbane were used as controls (286). No demographic data apart from age were available for the controls.…”

Section: Study Participantsmentioning

confidence: 99%

“…Monocytes were isolated by CD14 + magnetic microbeads (Miltenyi, Germany) from blood samples of patients with CF, as previously described (Chapter 3) (286). Classical, intermediate and non-classical monocytes were analyzed by their surface expression of CD14 and CD16 as described in Chapter 2.…”

Section: Flow Cytometric Analysis Of Monocyte Subsets In Cfmentioning

confidence: 99%

“…M1/M2 surface markers were analyzed using antibodies to CD64, CD80, CD209 (286). Following M2 polarization by IL-13, CD209 + cells sorted by CD209 magnetic microbeads following manufacturer's instruction (Miltenyi, Germany).…”

Section: In Vitro Macrophage Differentiation and Polarizationmentioning

confidence: 99%

“…We have recently described a technique for differentiating and polarizing human monocytes into MDMs and characterizing their phenotypes and function (286), allowing us to examine M0, M1…”

Section: Introductionmentioning

confidence: 99%

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Macrophage Polarization and Function in Cystic Fibrosis

Tarique¹

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If "Diversity is the rule of nature", macrophages, one of the innate immune cells of our body, have proven to be a true apostle. At the early stage of infection, they protect the host by exhibiting the pro-inflammatory phenotype (M1). Upon clearance of microbial threats, macrophages engage themselves in the repair process of the damaged tissue by showing anti-inflammatory or wound healing (M2) attributes. While incomplete microbial clearance leads to recurrent infections, defects in macrophage-mediated tissue repair mechanism result in immunopathology. The classical (M1) and alternatively (M2) polarized macrophages are the two extreme ends of a spectrum of in vivo macrophages phenotypes that dictate the nature, duration and severity of inflammation. Murine models of chronic inflammatory and autoimmune diseases showed the necessity of an adequate balance between macrophage subsets to maintain homeostasis, while imbalance is likely to lead exaggerated inflammation. In humans, an association between defective macrophage function and disease severity has been reported in many diseases including asthma, cystic fibrosis (CF), COPD, and atherosclerosis. Unfortunately, human M1 and M2 macrophages have not been well characterized. Firstly, the lack of homologs for certain murine genes in humans makes murine markers of limited use in humans. Secondly, there was no consensus method for in vitro differentiation of human M1 and M2 macrophages. Therefore, the first part of this thesis aimed to develop a novel method to differentiate and characterize human M1 and M2 macrophages. Initial studies with THP-1 cell line derived macrophage-like cells demonstrated that they didn't fully represent human monocyte-derived macrophages (MDMs). MDMs were therefore chosen as starting materials for the rest of the study. MDMs were considered as uncommitted "M0" macrophages. A number of inducers were employed to polarize M0 macrophages into either M1s or M2s. LPS treated M1 macrophages showed CD64 + CD80 + phenotype, whereas, IFN- induced M1s exhibited CD64 ++ CD80 -phenotype. These M1s secreted pro-inflammatory cytokines including TNF-, IL-1, IL-8 and were highly phagocytic. On the contrary, IL-4/IL-13 induced M2 macrophages were identified as CD11b + CD209 + cell population and were endocytic. Once polarized, macrophages then were left in cytokine-deficient medium to assess the persistence of polarized phenotype over time. In cytokine-free condition, previously polarized macrophages reverted to M0 state by 12 days.Treatment with IL-13 on previously polarized M1 macrophages resulted in a switch to CD209 + M2sand vice versa indicating the plasticity nature of human macrophages.Excessive neutrophilic pulmonary inflammation is the hallmark of cystic fibrosis (CF).However, factors that trigger such dysregulated neutrophilic inflammation and why this is not

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Macrophage and Fibroblast Interactions in Biomaterial‐Mediated Fibrosis

Witherel

Abebayehu

Barker

et al. 2019

Adv Healthcare Materials

253

201

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Biomaterial‐mediated inflammation and fibrosis remain a prominent challenge in designing materials to support tissue repair and regeneration. Despite the many biomaterial technologies that have been designed to evade or suppress inflammation (i.e., delivery of anti‐inflammatory drugs, hydrophobic coatings, etc.), many materials are still subject to a foreign body response, resulting in encapsulation of dense, scar‐like extracellular matrix. The primary cells involved in biomaterial‐mediated fibrosis are macrophages, which modulate inflammation, and fibroblasts, which primarily lay down new extracellular matrix. While macrophages and fibroblasts are implicated in driving biomaterial‐mediated fibrosis, the signaling pathways and spatiotemporal crosstalk between these cell types remain loosely defined. In this review, the role of M1 and M2 macrophages (and soluble cues) involved in the fibrous encapsulation of biomaterials in vivo is investigated, with additional focus on fibroblast and macrophage crosstalk in vitro along with in vitro models to study the foreign body response. Lastly, several strategies that have been used to specifically modulate macrophage and fibroblast behavior in vitro and in vivo to control biomaterial‐mediated fibrosis are highlighted.

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Phenotypic, Functional, and Plasticity Features of Classical and Alternatively Activated Human Macrophages

Cited by 449 publications

References 47 publications

Nanoparticle uptake by macrophages in vulnerable plaques for atherosclerosis diagnosis

Nanoparticle uptake by macrophages in vulnerable plaques for atherosclerosis diagnosis

Macrophage Polarization and Function in Cystic Fibrosis

Macrophage and Fibroblast Interactions in Biomaterial‐Mediated Fibrosis

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