Macrophage-Derived Chemokine MDC/CCL22: An Ambiguous Finding in COVID-19

Korobova, Zoia R.; Arsentieva, Natalia A.; Totolian, Areg A.

doi:10.3390/ijms241713083

Cited by 3 publications

(3 citation statements)

References 68 publications

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“…This was supported by the transwell migration assay, which showed a notable increase in TD cell count in the OGD media. This is consistent with previous studies reporting the importance of the CCL22-CCR4 interaction in Treg cell migration 29,39,41 , suggesting the therapeutic potential of Treg cells to reduce ischemic damage and promote recovery in the brain post-stroke. Taken together, the importance of the CCL22-CCR4 interaction in reducing stroke severity via Treg cell recruitment may be a potent candidate for cell therapy.…”

Section: Discussionsupporting

confidence: 93%

“…CCL22 is an effective chemoattractant for Treg cells and is secreted by monocytes 39 , which is in agreement with the chemokine profiling array results shown in this study. Notably, a few studies have shown a significant reduction in CCL22 levels during the acute phase of ischemic stroke in the circulation and infarct core, resulting in a higher National Institute of Health Stroke Scale (NIHSS) 40 .…”

Section: Discussionsupporting

confidence: 92%

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Ischemic stroke outcome after promoting CD4+CD25+ Treg cell migration through CCR4 overexpression in a tMCAO animal model

Lee,

Kim,

You

et al. 2024

Sci Rep

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The importance of neuroinflammation during the ischemic stroke has been extensively studied. The role of CD4+CD25+ regulatory T (Treg) cells during the recovery phase have shown infarct size reduction and functional improvement, possibly through the mitigation of inflammatory immune responses. We aimed to investigate the molecular factors involved in microglia-Treg cell communication that result in Treg trafficking. First, we observed the migration patterns of CD8+ (cytotoxic) T cells and Treg cells and then searched for chemokines released by activated microglia in an oxygen–glucose deprivation (OGD) model. The transwell migration assay showed increased migration into OGD media for both cell types, in agreement with the increase in chemokines involved in immune cell trafficking from the mouse chemokine profiling array. MSCV retrovirus was transduced to overexpress CCR4 in Treg cells. CCR4-overexpressed Treg cells were injected into the mouse transient middle cerebral artery occlusion (tMCAO) model to evaluate the therapeutic potential via the tetrazolium chloride (TTC) assay and behavioral tests. A general improvement in the prognosis of animals after tMCAO was observed. Our results suggest the increased mobility of CCR4-overexpressed Treg cells in response to microglia-derived chemokines in vitro and the therapeutic potential of Treg cells with increased mobility in cellular therapy.

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Section: Discussionsupporting

confidence: 93%

Section: Discussionsupporting

confidence: 92%

Ischemic stroke outcome after promoting CD4+CD25+ Treg cell migration through CCR4 overexpression in a tMCAO animal model

Lee,

Kim,

You

et al. 2024

Sci Rep

View full text Add to dashboard Cite

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“… 325 , 326 In addition to intracellular killing mechanisms, M1 macrophages employ extracellular strategies to combat pathogens, such as neutrophil extracellular trap formation, antimicrobial peptide and enzyme secretion, and cytokine and chemokine production to recruit and activate additional immune cells. 327 , 328 , 329 , 330 …”

Section: Macrophages: Orchestrators Of Tissue Repair and Regenerationmentioning

confidence: 99%

Macrophage plasticity: signaling pathways, tissue repair, and regeneration

Yan,

Wang,

Cai

et al. 2024

MedComm

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Macrophages are versatile immune cells with remarkable plasticity, enabling them to adapt to diverse tissue microenvironments and perform various functions. Traditionally categorized into classically activated (M1) and alternatively activated (M2) phenotypes, recent advances have revealed a spectrum of macrophage activation states that extend beyond this dichotomy. The complex interplay of signaling pathways, transcriptional regulators, and epigenetic modifications orchestrates macrophage polarization, allowing them to respond to various stimuli dynamically. Here, we provide a comprehensive overview of the signaling cascades governing macrophage plasticity, focusing on the roles of Toll‐like receptors, signal transducer and activator of transcription proteins, nuclear receptors, and microRNAs. We also discuss the emerging concepts of macrophage metabolic reprogramming and trained immunity, contributing to their functional adaptability. Macrophage plasticity plays a pivotal role in tissue repair and regeneration, with macrophages coordinating inflammation, angiogenesis, and matrix remodeling to restore tissue homeostasis. By harnessing the potential of macrophage plasticity, novel therapeutic strategies targeting macrophage polarization could be developed for various diseases, including chronic wounds, fibrotic disorders, and inflammatory conditions. Ultimately, a deeper understanding of the molecular mechanisms underpinning macrophage plasticity will pave the way for innovative regenerative medicine and tissue engineering approaches.

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Laboratory blood markers in COVID-19 and their connection to Viral variant

Korobova,

Liubimova,

Arsentieva

et al. 2024

Russian Journal of Infection and Immunity

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Morality rates in COVID-19 are dependent on timely diagnosis. Therefore, studying the relationship between laboratory markers and the severity of disease is important. The first wave of COVID-19 associated with the spread of the original strain of SARS-CoV-2, showed higher mortality rates caused by cytokine storm. As the viral variant changed, a change in the disease course towards a less pronounced inflammatory reaction was observed. These changes affected major players of inflammation, cytokines. However, cytokines are not the only markers in the inflammatory response. The purpose of this work was to determine the significance of laboratory markers in inflammation: WBC, C-reactive protein, ferritin, fibrinogen, and D-dimer. The study included 227 patients with acute COVID-19 in the first 5–7 days from the onset of the disease from January 2021 to March 2022. When compared with reference, all groups were characterized by reduced absolute values of lymphocytes. Correlation analysis between the absolute value of lymphocytes and plasma cytokine concentrations also revealed statistically significant strong relationships with the level of the chemokine CCL22/MDC. Given that CCL22/MDC is an important component of lymphopoiesis, its low concentrations may indicate dysregulation of this process in COVID-19. In addition, we noted a positive correlation between the level of C-reactive protein and IL-6 in peripheral blood. IL-6 is a proinflammatory cytokine, and its elevated levels have been associated with the development of severe COVID-19. One of its functions is the induction of C-reactive protein, and this trend persists regardless of which variant causes COVID-19. We also noted positive correlations between the concentrations of fibrinogen and IL-18, ferritin and IL-6, IL-18. Both of these proteins are involved in inflammation along with cytokines. The literature provides data on the significance of these markers for determining the severity of COVID-19. There is evidence of a synergistic effect of ferritin and IL-18 against viral pathogens. Of interest was the negative correlation between plasma D-dimer levels and IFNα. At the same time, data on the role of the latter in thrombus formation processes are increasingly appearing in the literature.

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Macrophage-Derived Chemokine MDC/CCL22: An Ambiguous Finding in COVID-19

Cited by 3 publications

References 68 publications

Ischemic stroke outcome after promoting CD4+CD25+ Treg cell migration through CCR4 overexpression in a tMCAO animal model

Ischemic stroke outcome after promoting CD4+CD25+ Treg cell migration through CCR4 overexpression in a tMCAO animal model

Macrophage plasticity: signaling pathways, tissue repair, and regeneration

Laboratory blood markers in COVID-19 and their connection to Viral variant

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