Mesenchymal stem cells in allergic diseases: Current status.

Allergic diseases, which include asthma, allergic skin diseases, allergic rhinitis and allergic conjunctivitis, have already garnered worldwide public health attention over recent decades. Mesenchymal stem cells (MSCs) have gradually emerged as a potential method for treating allergic diseases due to their immunosuppressive characteristics, tissue repair ability and secretion of various biological factors. This potential of MSC-based therapy has been confirmed in clinical and preclinical studies, which report the therapeutic benefits of MSCs for various allergic diseases and explore the antiallergic mechanisms. In this review, we focus on the discoveries and biological mechanisms of MSCs as a therapeutic tool in allergic diseases. We discuss the challenges of conducting MSC studies as well as future directions.

Promoting Water Activation by Photogenerated Holes in Monolayer C2N.

In photocatalytic reactions, the activation of H2O is very important for achieving high energy conversion efficiency. However, its activation mechanism under photoirradiation is still not fully understood. Here, on the basis of first-principles calculations, the role of photogenerated holes on the activation of H2O is investigated in a typical photocatalytic material C2N. The H2O molecule adsorbs at the six-membered N pore of C2N with a dual H-bonding configuration. Due to the electrostatic repulsion between the O atom of H2O and six N atoms of C2N, the energy level of the H2O molecule's highest occupied molecular orbital is raised significantly to exceed the valence band maximum of C2N, so that the photogenerated holes in C2N can be quickly captured by the H2O molecule. The captured photogenerated holes boost the activation of H2O and reduce the dissociation energy barrier from 1.61 to 0.69 eV. Besides, p-type defects of C2N have similar effects as photogenerated holes.

Determining structural and chemical heterogeneities of surface species at the single-bond limit.

The structure determination of surface species has long been a challenge because of their rich chemical heterogeneities. Modern tip-based microscopic techniques can resolve heterogeneities from their distinct electronic, geometric, and vibrational properties at the single-molecule level but with limited interpretation from each. Here, we combined scanning tunneling microscopy (STM), noncontact atomic force microscopy (AFM), and tip-enhanced Raman scattering (TERS) to characterize an assumed inactive system, pentacene on the Ag(110) surface. This enabled us to unambiguously correlate the structural and chemical heterogeneities of three pentacene-derivative species through specific carbon-hydrogen bond breaking. The joint STM-AFM-TERS strategy provides a comprehensive solution for determining chemical structures that are widely present in surface catalysis, on-surface synthesis, and two-dimensional materials.

Tensile Strain-Controlled Photogenerated Carrier Dynamics at the van der Waals Heterostructure Interface.

Customizing the photogenerated carrier dynamics would make the two-dimensional (2D) materials highly adaptable to various application scenarios. On the basis of time-domain ab initio nonadiabatic molecular dynamics simulation, we find that 4% tensile strain can suppress the electron transfer at the van der Waals heterostructure MoS2/WS2 interface. Our analysis shows that after the electron-hole pair is excited in the K valley in WS2 direct electron transfer from WS2@K to MoS2@K is very difficult because of the weak interlayer coupling in the K valley, and thus, it happens through the T valley as WS2@K-MoS2@T-MoS2@K. When the tensile strain is applied, the energy of WS2@K is decreased, resulting in the suppression of electron transfer. Our study suggests that tuning of the interlayer charge-transfer dynamics by external strain is possible, which provides valuable insights into the functional design of photonic devices based on 2D materials.

Pharmacological Inhibition of Caspase-8 Suppresses Inflammation-Induced Angiogenesis in the Cornea.

Inflammation-induced angiogenesis is closely related to many diseases and has been regarded as a therapeutic target. Caspase-8 has attracted increasing attention for its immune properties and therapeutic potential in inflammatory disorders. The aim of our study is to investigate the clinical application of pharmacological inhibition of caspase-8 and the underlying molecular mechanisms in inflammation-induced angiogenesis in the cornea. A model of alkali burn (AB)-induced corneal neovascularization (CNV) in C57BL/6 wild-type (WT) mice and toll-like receptor 4 knockout (Tlr4-/-) mice was used. We found that AB increased caspase-8 activity and the pharmacological inhibition of caspase-8 exerted substantial inhibitory effects on CNV, with consistent decreases in caspase-8 activity, inflammatory cell infiltration, macrophage recruitment and activation, VEGF-A, TNF-α, IL-1ß, MIP-1, and MCP-1 expression in the cornea. In vitro, caspase-8 mediated TLR4-dependent chemokines and VEGF-A production by macrophages. The TLR4 knockout significantly alleviated CNV, suppressed caspase-8 activity and downregulated expression of inflammatory cytokines and chemokines after AB. Taken together, these findings provide the first demonstration that the pharmacological inhibition of caspase-8 suppresses inflammation-induced angiogenesis and support the use of a pharmacological caspase-8 inhibitor as a novel clinical treatment for CNV and other angiogenic disorders.

Teriflunomide suppresses T helper cells and dendritic cells to alleviate experimental autoimmune uveitis.

Autoimmune uveitis (AU), a sight-threatening intraocular disorder, is still a challenge for ophthalmologists in clinic. Teriflunomide has been approved for multiple sclerosis (MS) in 2012 for its immunoregulatory function. However, the effect and mechanisms of teriflunomide in uveitis are still unknown. In this investigation, we used a murine model of non-infectious uveitis, experimental autoimmune uveitis (EAU), to explore the anti-inflammatory features of teriflunomide. Treatment with teriflunomide resulted in reduced clinical and pathological scores of retinal inflammations, accompanied by decreased intraocular infiltration of Th17 and Th1 cells in EAU mice. Meanwhile, teriflunomide treatment inhibited the proliferation and polarization of CD4+ T cells to Th17 and Th1 cells. Moreover, adoptive transfer of teriflunomide primed IRBP1-20-T cells failed to induce EAU. Interestingly, we found that teriflunomide suppressed the maturation and function of dendritic cells (DCs) both in vivo and in vitro. In conclusion, our findings suggest that teriflunomide alleviates inflammation in EAU mice by down-regulating Th17 and Th1 cells and suppresses the maturation and function of DCs for the first time.

The Effect of Interleukin 38 on Angiogenesis in a Model of Oxygen-induced Retinopathy.

Interleukin 38 (IL-38) is a novel identified cytokine of IL-1 family in which some members are important in inflammation and angiogenesis. However, the role of IL-38 in regulating angiogenesis is unknown. The aim of the present study is to explore the effect of IL-38 on angiogenesis. Oxygen-induced retinopathy (OIR) of C57BL/6 J mice was induced by exposure of hyperoxia (75% oxygen) from postnatal day 7 (P7) to P12 and then returned to room air. The mice were injected with IL-38. At P17, neovascular region (tufts) and avascular area of the retinas were analyzed. The data showed that administration of IL-38 in vivo inhibited retinal angiogenesis significantly. Furthermore, the addition of IL-38 to the cell cultures attenuated the proliferation, scratch wound healing and tube formation of vascular endothelial cells induced by VEGF significantly. Our findings suggest that IL-38 is an antiangiogenic cytokine in pathophysiological settings and may have therapeutic potential for angiogenesis related diseases.