The chemokine system in diverse forms of macrophage activation and polarization

Mantovani, Alberto; Sica, Antonio; Sozzani, Silvano; Allavena, Paola; Vecchi, Annunciata; Locati, Massimo

doi:10.1016/j.it.2004.09.015

Cited by 5,486 publications

(5,522 citation statements)

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“…It has been established that monocytes, in response to different cytokine pattern and immunological microenvironment, can differentiate in two major subpopulations, referred to as M1 and M2 macrophages. M1 macrophages are considered to promote atherosclerosis development and plaque rupture, secreting cytokines and lytic enzymes involved in the thinning of fibrous cap, while M2 macrophages are expected to inhibit plaque growth and to promote reparative processes, mediating plaque stability [21,22]. Since in asymptomatic plaque ruptures we observed an intense M2 response, it could be hypothesized that in these lesions a reparative response rapidly occurs.…”

Section: Discussionmentioning

confidence: 75%

Asymptomatic carotid plaque rupture with unexpected thrombosis over a non-canonical vulnerable lesion

et al. 2011

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a b s t r a c tObjective: Several studies have demonstrated that carotid plaque rupture and thrombosis represent the most important factors correlated with the onset of acute cerebrovascular symptoms. Nevertheless, ruptured thrombotic plaques have been described also in asymptomatic patients. What still needs to be clarified is why a plaque rupture leads either to an acute ischemic syndrome or, in a minor group of patients, remains asymptomatic. The purpose of this study was to systematically compare the histologic features of thrombotic plaques both in asymptomatic and symptomatic patients in order to identify specific findings that could explain the peculiar clinical behavior that characterizes each of the clinical settings. Methods: A total of 157 thrombotic plaques from 60 asymptomatic patients and 97 with major stroke who consecutively underwent CEA were serially sectioned and studied by histology. Results: A minute cap disruption very frequently characterizes thrombotic plaques of asymptomatic patients and it was always smaller than large ulcers observed in thrombotic symptomatic plaques (651 ± 687 m vs. 4150 ± 3526, p = 0.001). In asymptomatics this typical feature was associated with fewer inflammatory cells (20.1 ± 8.8 vs. 33.9 ± 26.1 cells × hpf, p = 0.001), smaller lipidic-necrotic core (33.9% ± 2.9% vs. 42.0% ± 2.4%; p = 0.04) and larger calcification (16.2 ± 12.8% vs. 8.1 ± 12.2%, p = 0.02). Symptomatic patients with thrombotic plaques showed higher incidence of metabolic syndrome (p = 0.002) and moderate-high Framingham risk scores (p = 0.001) comparing to asymptomatic individuals. Conclusion: The transformation from a stable to a vulnerable plaque is a gradual process in the natural history of the disease and plaque rupture is an event not necessarily occurring at a late phase but also at earlier one. In this case, the rupture will be most likely smaller and clinically asymptomatic.

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Section: Discussionmentioning

confidence: 75%

Asymptomatic carotid plaque rupture with unexpected thrombosis over a non-canonical vulnerable lesion

et al. 2011

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“…Though CCL2 is the principal endogenous CCR2 agonist, alternative chemokines can also activate CCR2 and may contribute to our findings. For example, CCL7 (MCP-3), CCL8 (MCP-2), CCL13 (MCP-4), and CCL12 (MCP-5) can activate CCR2 in mice (Ma et al, 2002;Mantovani et al, 2004). We previously found that, in addition to CCL2, the release of CCL5 and CCL12 are markedly increased in opiate and/or Tat-exposed astrocytes , and concluded that CCL5, CCL12 or perhaps another chemokine contributed directly to opiate and HIV-1-induced reactive glial changes .…”

Section: Discussionmentioning

confidence: 99%

CCR2 mediates increases in glial activation caused by exposure to HIV-1 Tat and opiates

El‐Hage

Ambati

et al. 2006

Journal of Neuroimmunology

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To assess the role of CCL2/MCP-1 in opiate drug abuse and HIV-1 comorbidity, the effects of systemic morphine and intrastriatal HIV-1 Tat on macrophage/microglial and astroglial activation were assessed in wild type and CCR2 null mice. Tat and/or morphine additively increased the proportion of CCL2 immunoreactive astroglia. The effects of morphine were prevented by naltrexone. Glial activation was significantly reduced in CCR2(−/−) versus wild-type mice following Tat or morphine plus Tat exposure. Thus, CCR2 contributes to local glial activation caused by Tat alone or in the presence of opiates, implicating CCR2 signaling in HIV-1 neuropathogenesis in drug abusers and non-abusers.

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“…AAMΦs have been classified as a subset of M2 macrophages, which are activated macrophages distinguished by their low expression levels of IL-12 [15]. M2 macrophages can be divided into three groups distinguished by activation factors in vitro: IL-4 or IL-13 (M2a or AAMΦ), IL-10 or glucocorticoids (M2b), or immune complexes plus Toll-like receptor ligands (M2c).…”

Section: Alternative Activation Of Macrophagesmentioning

confidence: 99%