M-CSF Inhibits Anti–HIV-1 Activity of IL-32, but They Enhance M2-like Phenotypes of Macrophages

Osman, Abu; Bhuyan, Farzana; Hashimoto, Michihiro; Nasser, Hesham; Maekawa, Taira; Suzu, Shinya

doi:10.4049/jimmunol.1302732

Cited by 23 publications

(32 citation statements)

References 45 publications

(71 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Human peripheral blood monocyte-derived macrophages (MDMs) were prepared as described previously (25,26). Approval for this study was obtained from the Kumamoto University medical ethics committee.…”

Section: Human Peripheral Blood Monocyte-derived Macrophagesmentioning

confidence: 99%

“…HIV-1 infection was performed essentially as described previously (26). The MDMs cultured on 24-well tissue culture plates were incubated with 200 ml of the supernatants of 293 cells containing HIV-1 (Gag concentration: 100 ng/ml unless otherwise stated) for 2 h at 37˚C.…”

Section: Hiv-1 Replication and Tnt Countsmentioning

confidence: 99%

“…Western blotting was performed as described previously (26). The Abs used were as follows: M-Sec (F-6; Santa Cruz Biotechnology), Gag (#65; BioAcademia, Osaka, Japan), and actin (C-2; Santa Cruz Biotechnology, as a loading control).…”

Section: Western Blottingmentioning

confidence: 99%

See 2 more Smart Citations

Potential Role of the Formation of Tunneling Nanotubes in HIV-1 Spread in Macrophages

Hashimoto

Bhuyan

Hiyoshi

et al. 2016

The Journal of Immunology

Self Cite

104

146

View full text Add to dashboard Cite

Tunneling nanotubes (TNTs), the long membrane extensions connecting distant cells, have emerged as a novel form of cell-to-cell communication. However, it is not fully understood how and to what extent TNTs contribute to intercellular spread of pathogens including HIV-1. In this study, we show that HIV-1 promotes TNT formation per se via its protein Nef and a cellular protein M-Sec, which appears to mediate approximately half of viral spread among monocyte-derived macrophages (MDMs). A small compound that inhibits M-Sec–induced TNT formation reduced HIV-1 production by almost half in MDMs. Such inhibition was not observed with Nef-deficient mutant HIV-1 that fails to promote TNT formation and replicates less efficiently than the wild-type HIV-1 in MDMs. The TNT inhibitor–sensitive/Nef-promoting viral production was also observed in a T cell line ectopically expressing M-Sec, but not in another M-Sec− T cell line. Our results suggest the importance of TNTs in HIV-1 spread among MDMs and might answer the long-standing question how Nef promotes HIV-1 production in a cell type–specific manner.

show abstract

Section: Human Peripheral Blood Monocyte-derived Macrophagesmentioning

confidence: 99%

Section: Hiv-1 Replication and Tnt Countsmentioning

confidence: 99%

See 1 more Smart Citation

Potential Role of the Formation of Tunneling Nanotubes in HIV-1 Spread in Macrophages

Hashimoto

Bhuyan

Hiyoshi

et al. 2016

The Journal of Immunology

Self Cite

104

146

View full text Add to dashboard Cite

show abstract

“…These results indicate that, while M1 and M2 activation states can be induced irrespective of a rigid segregation of differentiation signals, it is the balance of these signals (growth factors) which defines the ultimate macrophage activation phenotype [53]. CSF-1R is also able to interfere with IL-32-induced macrophage polarization [54]. IL-32 promotes the differentiation of monocytes into macrophage-like cells and induces the production of various cytokines including TNFα and IL-8, so that it is considered an inducer of M1-like macrophages [55,56].…”

mentioning

confidence: 90%

“…These results suggest that IL-32γ induces macrophages with both M1 and M2 phenotypes, and that CSF-1 preferentially accelerates the M2 polarization induced by IL-32γ. Thus, CSF-1 seems to have either additive or inhibitory effects on IL-32γ action as far as the M1 and M2 phenotypes are concerned [54]. [58] where an autocrine mechanism may also be involved [60].…”

mentioning

confidence: 99%

Colony-Stimulating Factor-1 Receptor in the Polarization of Macrophages: A Target for Turning Bad to Good Ones?

Rovida¹,

Sbarba²

2015

J Clin Cell Immunol

View full text Add to dashboard Cite

Macrophages, which are found in all tissues, are an essential component of the innate immune system, and they play important roles in host defense, inflammation, autoimmune diseases as well as cancer. Functionally, macrophages are classified into two types: classically-activated M1 macrophages and alternatively-activated M2 macrophages. The M1 macrophages typically produce high levels of proinflammatory cytokines and chemokines, whereas M2 macrophages show an efficient phagocytic and scavenging activity. Because the phenotypes of polarized M1 and M2 macrophages can be induced, and reversed to some extent, by various signals, different phases of many diseases are associated with dynamic changes in the balance between M1 and M2 macrophages. The colony-stimulating factor 1 receptor (CSF-1R), a class III receptor tyrosine kinase, sustains the survival, proliferation and differentiation of monocytes and macrophages. Drugging CSF-1R may be the only way to target macrophages within a pathological context. However, CSF-1R-dependent signals may be either positive or detrimental depending on the disease and even on the phase of disease. The role of CSF-1R and its ligands, the colony-stimulating factor-1 and interleukin-34, in macrophages with respect to the pathogenesis of several inflammatory or neoplastic diseases has been reviewed previously. This review will focus specifically on evidences obtained about the role of CSF-1R in macrophage polarization in the context of physiological as well as pathological conditions including inflammation and cancer. The possibility to target CSF-1R, using the several inhibitors already available, for the treatment of inflammatory diseases as well as cancer will be also discussed.

show abstract

Silk Fibroin and Sericin Differentially Potentiate the Paracrine and Regenerative Functions of Stem Cells Through Multiomics Analysis

et al. 2023

View full text Add to dashboard Cite

emerging as a potential alternative to these problems. The tissue engineering triad involves the effective integration of cells, scaffolds, and signals for the development of biological substitutes to restore, maintain, and replace injured tissues and organs. [2] The scaffold plays a substantial role in the field of tissue engineering, primarily by providing physical support (structures and substrates) for cells to attach and grow, subsequently resulting in tissue formation. [3] A variety of natural and synthetic biomaterials have been explored to develop tissue-engineered scaffolds. By incorporating exogenous growthstimulating signals, such as growth factors or small molecules, scaffolds can provide specific bioactivities, that is, biochemical signals required for cellular behaviors and tissue regeneration. [4] As biomaterials are essentially comprised of chemical molecules, they are capable of supplying inherent biochemical signals to guide and influence cells. For example, cells residing in tissue-engineered scaffolds can establish cell-biomaterial communication networks partially through biochemical signaling. The degradation products of various biodegradable biomaterials after implantation in vivo also provide specific biochemical signals to the cells in and around the Silk fibroin (SF) and sericin (SS), the two major proteins of silk, are attractive biomaterials with great potential in tissue engineering and regenerative medicine. However, their biochemical interactions with stem cells remain unclear. In this study, multiomics are employed to obtain a global view of the cellular processes and pathways of mesenchymal stem cells (MSCs) triggered by SF and SS to discern cell-biomaterial interactions at an in-depth, high-throughput molecular level. Integrated RNA sequencing and proteomic analysis confirm that SF and SS initiate widespread but distinct cellular responses and potentiate the paracrine functions of MSCs that regulate extracellular matrix deposition, angiogenesis, and immunomodulation through differentially activating the integrin/PI3K/Akt and glycolysis signaling pathways. These paracrine signals of MSCs stimulated by SF and SS effectively improve skin regeneration by regulating the behavior of multiple resident cells (fibroblasts, endothelial cells, and macrophages) in the skin wound microenvironment. Compared to SS, SF exhibits better immunomodulatory effects in vitro and in vivo, indicating its greater potential as a carrier material of MSCs for skin regeneration. This study provides comprehensive and reliable insights into the cellular interactions with SF and SS, enabling the future development of silk-based therapeutics for tissue engineering and stem cell therapy.

show abstract

M-CSF Inhibits Anti–HIV-1 Activity of IL-32, but They Enhance M2-like Phenotypes of Macrophages

Cited by 23 publications

References 45 publications

Potential Role of the Formation of Tunneling Nanotubes in HIV-1 Spread in Macrophages

Potential Role of the Formation of Tunneling Nanotubes in HIV-1 Spread in Macrophages

Colony-Stimulating Factor-1 Receptor in the Polarization of Macrophages: A Target for Turning Bad to Good Ones?

Silk Fibroin and Sericin Differentially Potentiate the Paracrine and Regenerative Functions of Stem Cells Through Multiomics Analysis

Contact Info

Product

Resources

About