Chocolate Cysts Associated With Porous Polyethylene Orbital Implants.

Late-onset orbital hemorrhage is a rare complication of alloplastic implant use in orbital wall reconstruction following trauma. The authors report 3 patients with chocolate cysts presenting 3 to 9 years after orbital fracture repair with porous polyethylene implants. All patients were managed by implant removal and evacuation of cyst contents. Complete excision of the cyst was performed in 1 patient, while partial excision of the capsule was performed in 2 patients. Improvement of symptoms associated with the mass effects of the cyst was noted after surgical intervention. The authors also report the first case of orbital volume expansion from a chocolate cyst associated with a nonbarriered porous polyethylene implant. Delayed hemorrhage with capsule formation, although extremely rare, is a possible complication following orbital fracture repair with porous polyethylene implants.

Porphyromonas gingivalis influences actin degradation within epithelial cells during invasion and apoptosis.

Porphyromonas gingivalis, a Gram-negative oral pathogen, has been shown to induce apoptosis in human gingival epithelial cells, yet the underlining cellular mechanisms controlling this process are poorly understood. We have previously shown that the P. gingivalis proteases arginine and lysine gingipains, are necessary and sufficient to induce host cell apoptosis. In the present study, we demonstrate that 'P. gingivalis-induced apoptosis' is mediated through degradation of actin leading to cytoskeleton collapse. Stimulation of human gingival epithelial cells with P. gingivalis strains 33277 and W50 at moi:100 induced ß-actin cleavage as early as 1 h and human serum inhibited this effect. By using gingipain-deficient mutants of P. gingivalis and purified gingipains, we demonstrate that lysine gingipain is involved in actin hydrolysis in a dose and time-dependent manner. Use of Jasplakinolide and cytochalasin D revealed that P. gingivalis internalization is necessary for actin cleavage. Further, we also show that lysine gingipain from P. gingivalis can cleave active caspase 3. Taken together, we have identified actin as a substrate for lysine gingipain and demonstrated a novel mechanism involved in microbial host cell invasion and apoptosis.

Polydopamine functionalized graphene oxide membrane with the sandwich structure for osmotic energy conversion.

Ion-selective membrane is the key component for osmotic energy conversion. Nanofluid channels based on two-dimensional materials have advantages of facile preparation, tunable channel size, and easy upscaling, which is promising for efficient osmotic energy harvesting. However, further improvement of the output power is hindered by the low ion sensitivity for the limited charge density. Herein, we demonstrate the preparation of a cation-selective polydopamine-coated graphene oxide composite membrane with the sandwich structure by a simple interfacial polymerization technique, which greatly improves the surface charge density and further generates a power density of 3.4 W/m2 under river water and seawater. The GO membrane is firstly fabricated to function as the supporting layer and provide the reaction sites. And the ultrathin selective layer of the polydopamine membrane is chemically bonded with the GO layer by the in-situ polymerization on both sides of the GO membrane. The sandwiched nanofluidic membrane with ultrahigh charge density exhibits both high cation selectivity and ionic conductivity, benefiting the performance of osmotic energy conversion. The economic, easy-prepared method of the sandwiched nanofluidic membrane provides a promising strategy for high-performance osmotic energy conversion.

Modulation of TLR2 protein expression by miR-105 in human oral keratinocytes.

Mammalian biological processes such as inflammation, involve regulation of hundreds of genes controlling onset and termination. MicroRNAs (miRNAs) can translationally repress target mRNAs and regulate innate immune responses. Our model system comprised primary human keratinocytes, which exhibited robust differences in inflammatory cytokine production (interleukin-6 and tumor necrosis factor-alpha) following specific Toll-like receptor 2 and 4 (TLR-2/TLR-4) agonist challenge. We challenged these primary cells with Porphyromonas gingivalis (a Gram-negative bacterium that triggers TLR-2 and TLR-4) and performed miRNA expression profiling. We identified miRNA (miR)-105 as a modulator of TLR-2 protein translation in human gingival keratinocytes. There was a strong inverse correlation between cells that had high cytokine responses following TLR-2 agonist challenge and miR-105 levels. Knock-in and knock-down of miR-105 confirmed this inverse relationship. In silico analysis predicted that miR-105 had complementarity for TLR-2 mRNA, and the luciferase reporter assay verified this. Further understanding of the role of miRNA in host responses may elucidate disease susceptibility and suggest new anti-inflammatory therapeutics.

IFN-ß secretion is through TLR3 but not TLR4 in human gingival epithelial cells.

The oral cavity is home for a plethora of bacteria and viruses. Epithelial barriers encounter these micro-organisms and recognize them via pathogen recognition receptors (PRRs) that instigate antibacterial and antiviral responses. We and others have shown that human gingival epithelial cells (HGECs) express PRRs to defend invading pathogens. Among these PRRs, TLR2, TLR3 and TLR4 are highly expressed in HGECs and appear to be important based on our previous findings. IFN-ß is one of the major type 1 interferons induced to defend viral attack. In this report, we sought to dissect TLR3 and TLR4 mediated secretion of IFN-ß in HGECs. We stimulated HGECs with ultrapure LPS (TLR4 ligand) and Poly I:C (TLR3 ligand) for 24 h and supernatant was used to determine IFN-ß secretion. We show that cells treated with Poly I:C induced IFN-ß secretion but not cells treated with LPS. In addition, silencing of TLR3 prior to Poly I:C stimulation significantly downregulated IFN-ß secretion. On the contrary, overexpression of MD2 and TLR4 in HGECs restored IFN-ß secretion. Upon further evaluation, we found that TLR3 stimulation but not TLR4 induced the phosphorylation of interferon regulatory factor 3 (IRF3), which is critical for IFN-ß secretion. We conclude that IFN-ß secretion is through TLR3 and not via TLR4 in HGECs.

Interleukin-1beta modulates proinflammatory cytokine production in human epithelial cells.

Periodontitis is a chronic human inflammatory disease initiated and sustained by dental plaque microorganisms. A major contributing pathogen is Porphyromonas gingivalis, a gram-negative bacterium recognized by Toll-like receptor 2 (TLR2) and TLR4, which are expressed by human gingival epithelial cells (HGECs). However, it is still unclear how these cells respond to P. gingivalis and initiate inflammatory and immune responses. We have reported previously that HGECs produce a wide range of proinflammatory cytokines, including interleukin-6 (IL-6), IL-8, granulocyte-macrophage colony-stimulating factor, tumor necrosis factor alpha (TNF-alpha), and IL-1beta. In this study, we show that IL-1beta has a special role in the modulation of other inflammatory cytokines in HGECs challenged with P. gingivalis. Our results show that the increased production of IL-1beta correlates with the cell surface expression of TLR4, and more specifically, TLR4-normal HGECs produce fourfold more IL-1beta than do TLR4-deficient HGECs after challenge. Moreover, blocking the IL-1beta receptor greatly reduces the production of "secondary" proinflammatory cytokines such as IL-8 or IL-6. Our data indicate that the induction of IL-1beta plays an important role in mediating the release of other proinflammatory cytokines from primary human epithelial cells following challenge with P. gingivalis, and this process may be an inflammatory enhancement mechanism adopted by epithelial cells.