TNF-alpha modulates adipose macrophage polarization to M1 phenotype in response to scorpion venom

Aït-Lounis, Aouatef; Laraba-Djebari, Fatima

doi:10.1007/s00011-015-0876-z

Cited by 17 publications

(9 citation statements)

References 31 publications

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“…IL10RA is a key inflammatory receptor, and its overexpression is associated with kidney graft atrophy and fibrosis [33]. IL1B is a key cytokine involved in the inflammatory response to injury in adipose tissue [34], and TNF encourages the activation of M1 macrophages in adipose tissue [35].…”

Section: Discussionmentioning

confidence: 99%

The angiogenic potential of CD271+ human adipose tissue-derived mesenchymal stem cells

et al. 2021

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Background Autologous fat grafting is often a crucial aspect of reconstructive and aesthetic surgeries, yet poor graft retention is a major issue with this technique. Enriching fat grafts with adipose tissue-derived mesenchymal stem cells (AD-MSCs) improves graft survival—however, AD-MSCs represent a heterogeneous population. Selection of subpopulations of AD-MSCs would allow the targeting of specific AD-MSCs that may benefit fat graft survival more than the general AD-MSC population. Methods Human AD-MSCs were selected for the surface marker CD271 using magnetic-activated cell sorting and compared to the CD271 negative phenotype. These subpopulations were analysed for gene expression using Real-Time qPCR and RNA sequencing; surface marker characteristics using immunostaining; ability to form tubules when cultured with endothelial cells; and gene and protein expression of key angiogenic mediators when cultured with ex-vivo adipose tissue. Results Human AD-MSCs with the surface marker CD271 express angiogenic genes at higher levels, and inflammatory genes at lower levels, than the CD271− AD-MSC population. A greater proportion of CD271+ AD-MSCs also possess the typical complement of stem cell surface markers and are more likely to promote effective neoangiogenesis, compared to CD271− AD-MSCs. Conclusion Enriching grafts with the CD271+ AD-MSC subpopulation holds potential for the improvement of reconstructive and aesthetic surgeries involving adipose tissue.

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Section: Discussionmentioning

confidence: 99%

The angiogenic potential of CD271+ human adipose tissue-derived mesenchymal stem cells

et al. 2021

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“…Increasing secretion of IFN-γ and IL-12 could promote CD4 + T-cells to differentiate into Th1 cells and suppress Th2 formation [25, 26]. On the other hand, TNF-α and IL-6 also activate some other immune cell types, such as macrophages and DCs, in addition to T cells [27, 28]. Therefore, significant decrease in secretion of these cytokines could lead to the inhibition of DC activation by soluble CTLA-4-Fc.…”

Section: Discussionmentioning

confidence: 99%

CTLA-4 positive breast cancer cells suppress dendritic cells maturation and function

et al. 2017

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Cytotoxic T lymphocyte-associated antigen 4 (CTLA-4), a potent immunoregulatory molecule, can down-regulate T-cell activation and inhibit anti-tumor immune response. This study showed that LPS-stimulated human dendritic cells (DCs) decreased the expression of HLA-DR, CD83 and costimulatory molecules (CD40, CD80 and CD86) following coculturing with CTLA-4+ breast cancer cells. Moreover, the suppressed DCs further inhibited proliferation of allogeneic CD4+/CD8+ T-cells, differentiation of Th1 and function of cytotoxic lymphocytes (CTLs). However, CTLA-4 blockade in breast cancer cells could recover DC maturation and cytokine production, elevate antigen-presenting function of DCs, reverse Th1/CTLs response and cytokine secretion. Subsequent study demonstrated that the activation of extracellular-signal regulated kinase and signal transducer and activator of transcription 3 of DCs caused by CTLA-4+ breast cancer cells were the predominant mechanism of DC suppression. In addition, CTLA-4 blockade treatment also directly inhibited proliferation and induced apoptosis of CTLA-4+ breast cancer cells. Collectively, CTLA-4 was expressed and functional on human breast cancer cells through influencing maturation and function of DCs in vitro, and CTLA-4 blockage not only recovered the antigen-presenting function of DCs and T-cells activation but also suppressed the biological activity of breast cancer cells themselves. This study highlights the clinical application of CTLA-4 blockade therapy in breast cancer.

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“…This is of importance from the perspective of impaired efferocytosis, as macrophages polarised in such a manner display inhibited phagocytosis compared to their M2 polarised counterparts [ 230 ]. Increased polarisation of M1 polarisation is also driven by increased levels of TNF-alpha [ 231 , 232 ] and IL-6 [ 233 , 234 ].…”

Section: The Recruitment Of Activated Neutrophils Into Alveolae and Imentioning

confidence: 99%

The pathophysiology of SARS-CoV-2: A suggested model and therapeutic approach

Morris

Bortolasci

Puri³

et al. 2020

Life Sciences

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In this paper, a model is proposed of the pathophysiological processes of COVID-19 starting from the infection of human type II alveolar epithelial cells (pneumocytes) by SARS-CoV-2 and culminating in the development of ARDS. The innate immune response to infection of type II alveolar epithelial cells leads both to their death by apoptosis and pyroptosis and to alveolar macrophage activation. Activated macrophages secrete proinflammatory cytokines and chemokines and tend to polarise into the inflammatory M1 phenotype. These changes are associated with activation of vascular endothelial cells and thence the recruitment of highly toxic neutrophils and inflammatory activated platelets into the alveolar space. Activated vascular endothelial cells become a source of proinflammatory cytokines and reactive oxygen species (ROS) and contribute to the development of coagulopathy, systemic sepsis, a cytokine storm and ARDS. Pulmonary activated platelets are also an important source of proinflammatory cytokines and ROS, as well as exacerbating pulmonary neutrophil-mediated inflammatory responses and contributing to systemic sepsis by binding to neutrophils to form platelet-neutrophil complexes (PNCs). PNC formation increases neutrophil recruitment, activation priming and extraversion of these immune cells into inflamed pulmonary tissue, thereby contributing to ARDS. Sequestered PNCs cause the development of a procoagulant and proinflammatory environment. The contribution to ARDS of increased extracellular histone levels, circulating mitochondrial DNA, the chromatin protein HMGB1, decreased neutrophil apoptosis, impaired macrophage efferocytosis, the cytokine storm, the toll-like receptor radical cycle, pyroptosis, necroinflammation, lymphopenia and a high Th17 to regulatory T lymphocyte ratio are detailed.

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TNF-alpha modulates adipose macrophage polarization to M1 phenotype in response to scorpion venom

Abstract: These results indicate that TNF-α is a physiological regulator of inflammation and macrophage activation induced by scorpion venom.

Cited by 17 publications

References 31 publications

The angiogenic potential of CD271+ human adipose tissue-derived mesenchymal stem cells

The angiogenic potential of CD271+ human adipose tissue-derived mesenchymal stem cells

CTLA-4 positive breast cancer cells suppress dendritic cells maturation and function

The pathophysiology of SARS-CoV-2: A suggested model and therapeutic approach

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