Topical Application of Nano-Sized Graphene Oxide Cream Ameliorates Acute Skin Inflammation in Mice.

We have previously shown that nano-sized graphene oxide (NGO) displays anti-inflammatory activities against NKT cell-mediated sepsis. To address whether NGO could be applied to treat acute skin inflammation, we developed a conventional skin Cetaphil cream containing NGO (denoted as NGO cream) for topical application to skin lesions and investigated its therapeutic efficacy by employing the tape-stripping-induced acute skin inflammation model. Topical application of NGO cream to the wounded area significantly reduced skin lesions compared with application of the control cream.

Overexpression of Chromatin Remodeling Factor SRG3 Down-Regulates IL1β-Expressing M1 Macrophages and IL17-Producing T Cells in Adipose Tissues.

The SWItch3-related gene (SRG3) is a core component of ATP-dependent SWI/SNF complexes, which are crucial for regulating immune cell development and function (e.g., macrophages and CD4 T cells), embryonic development, and non-immune cell differentiation.

The iNKT cell ligand α-GalCer prevents murine septic shock by inducing IL10-producing iNKT and B cells.

Introduction: α-galactosylceramide (α-GalCer), a prototypical agonist of invariant natural killer T (iNKT) cells, stimulates iNKT cells to produce various cytokines such as IFNγ and IL4. Moreover, repeated α-GalCer treatment can cause protective or pathogenic outcomes in various immune-mediated diseases. However, the precise role of α-GalCer-activated iNKT cells in sepsis development remains unclear.

Alpha-galactosylceramide pre-treatment attenuates clinical symptoms of LPS-induced acute neuroinflammation by converting pathogenic iNKT cells to anti-inflammatory iNKT10 cells in the brain.

Background: Invariant natural killer T (iNKT) cells play protective or pathogenic roles in a variety of immune and inflammatory diseases. However, whether iNKT cells contribute to the progression of acute neuroinflammation remains unclear. Thus, we addressed this question with a mouse model of lipopolysaccharide (LPS)-induced acute neuroinflammation.

In Vivo Zymosan Treatment Induces IL15-Secreting Macrophages and KLRG1-Expressing NK Cells in Mice.

Beta-glucan (β-glucan) is a natural polysaccharide produced by fungi, bacteria, and plants. Although it has been reported that β-glucan enhances innate immune memory responses, it is unclear whether different types of β-glucans display similar immune effects. To address this issue, we employed zymosan (β-1,3-glycosidic linkage) and pustulan (β-1,6-glycosidic linkage) to investigate their in vivo effects on innate memory immune responses.

Phosphorothioate-linked guanine/cytosine-based stem-loop oligonucleotides induce the extracellular release of mitochondrial DNA from peritoneal B1a cells.

It has been previously demonstrated that phosphorothioate-linked GpC-based stem-loop oligonucleotides (GC-SL ODN) induce the release of mitochondrial DNA (mtDNA) from chronic lymphocytic leukemia (CLL) B cells. Although CLL B cells are believed to originate from CD5 B cells because of their phenotypic similarities, it remains unclear whether GC-SL ODN can stimulate CD5 B1 cells to secrete mtDNA. To explore this possibility, we compared the frequency of the mtDNA-producing population among peritoneal cells after GC-SL ODN treatment.

CD1d-independent NK1.1 Treg cells are IL2-inducible Foxp3 T cells co-expressing immunosuppressive and cytotoxic molecules.

Regulatory T cells (Treg) play pivotal roles in maintaining self-tolerance and preventing immunological diseases such as allergy and autoimmunity through their immunosuppressive properties. Although Treg cells are heterogeneous populations with distinct suppressive functions, expression of natural killer (NK) cell receptors (NKR) by these cells remains incompletely explored. Here we identified that a small population of Foxp3CD4 Treg cells in mice expresses the NK1.

Repeated α-GalCer Administration Induces a Type 2 Cytokine-Biased iNKT Cell Response and Exacerbates Atopic Skin Inflammation in Vα14 NC/Nga Mice.

We have previously shown that Vα14 TCR Tg (Vα14) NC/Nga (NC) mice contain increased numbers of double-negative (DN) invariant natural killer T (iNKT) cells that protect against spontaneous development of atopic dermatitis (AD). iNKT cells can regulate immune responses by producing various cytokines such as IFNγ and IL4 rapidly upon stimulation with α-galactosylceramide (α-GalCer), a prototypical iNKT cell agonist. However, the precise role of α-GalCer-activated iNKT cells in AD development remains unclear.

Chromatin Regulator SRG3 Overexpression Protects against LPS/D-GalN-Induced Sepsis by Increasing IL10-Producing Macrophages and Decreasing IFNγ-Producing NK Cells in the Liver.

We previously showed that ubiquitous overexpression of the chromatin remodeling factor SWItch3-related gene (SRG3) promotes M2 macrophage differentiation, resulting in anti-inflammatory responses in the experimental autoimmune encephalomyelitis model of multiple sclerosis. Since hepatic macrophages are responsible for sepsis-induced liver injury, we investigated herein the capacity of transgenic SRG3 overexpression (SRG3 mice) to modulate sepsis in mice exposed to lipopolysaccharide (LPS) plus d-galactosamine (d-GalN). Our results demonstrated that ubiquitous SRG3 overexpression significantly protects mice from LPS/d-GalN-induced lethality mediated by hepatic M1 macrophages.

Ubiquitous Overexpression of Chromatin Remodeling Factor SRG3 Exacerbates Atopic Dermatitis in NC/Nga Mice by Enhancing Th2 Immune Responses.

The SWItch (SWI)3-related gene (SRG3) product, a SWI/Sucrose Non-Fermenting (SNF) chromatin remodeling subunit, plays a critical role in regulating immune responses. We have previously shown that ubiquitous SRG3 overexpression attenuates the progression of Th1/Th17-mediated experimental autoimmune encephalomyelitis. However, it is unclear whether SRG3 overexpression can affect the pathogenesis of inflammatory skin diseases such as atopic dermatitis (AD), a Th2-type immune disorder.

Integration of sputter-deposited multiferroic CoFeO-BiFeO nanocomposites on conductive LaSrMnO electrodes.

The structure, magnetic and ferroelectric properties of sputtered epitaxial CoFeO-BiFeO (CFO-BFO) nanocomposite thin films grown on LaSrMnO (LSMO) layers on (001) oriented SrTiO (STO) substrates and on STO-buffered Si are described. The as-grown LSMO thin films were smooth and poorly conductive but the resistivity was reduced and the surfaces roughened after annealing. Cosputtered CFO and BFO on STO formed vertically aligned nanostructures consisting of epitaxial spinel CFO pillars within a perovskite BFO matrix, but the rough surface of the annealed LSMO film promoted additional CFO pillar orientations.

Magnetic Phase Formation in Self-Assembled Epitaxial BiFeO3-MgO and BiFeO3-MgAl2O4 Nanocomposite Films Grown by Combinatorial Pulsed Laser Deposition.

Self-assembled epitaxial BiFeO3-MgO and BiFeO3-MgAl2O4 nanocomposite thin films were grown on SrTiO3 substrates by pulsed laser deposition. A two-phase columnar structure was observed for BiFeO3-MgO codeposition within a small window of growth parameters, in which the pillars consisted of a magnetic spinel phase (Mg,Fe)3O4 within a BiFeO3 matrix, similar to the growth of BiFeO3-MgFe2O4 nanocomposites reported elsewhere. Further, growth of a nanocomposite with BiFeO3-(CoFe2O4/MgO/MgFe2O4), in which the minority phase was grown from three different targets, gave spinel pillars with a uniform (Mg,Fe,Co)3O4 composition due to interdiffusion during growth, with a bifurcated shape from the merger of neighboring pillars.