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Neutrophil Responses to Sterile Implant Materials.

ABSTRACT: In vivo implantation of sterile materials and devices results in a foreign body immune response leading to fibrosis of implanted material. Neutrophils, one of the first immune cells to be recruited to implantation sites, have been suggested to contribute to the establishment of the inflammatory microenvironment that initiates the fibrotic response. However, the precise numbers and roles of neutrophils in response to implanted devices remains unclear. Using a mouse model of peritoneal microcapsule implantation, we show 30-500 fold increased neutrophil presence in the peritoneal exudates in response to implants. We demonstrate that these neutrophils secrete increased amounts of a variety of inflammatory cytokines and chemokines. Further, we observe that they participate in the foreign body response through the formation of neutrophil extracellular traps (NETs) on implant surfaces. Our results provide new insight into neutrophil function during a foreign body response to peritoneal implants which has implications for the development of biologically compatible medical devices.

SUBMITTER: Jhunjhunwala S

PROVIDER: S-EPMC4565661 | biostudies-literature | 2015

REPOSITORIES: biostudies-literature

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Neutrophil Responses to Sterile Implant Materials.

Jhunjhunwala Siddharth S Aresta-DaSilva Stephanie S Tang Katherine K Alvarez David D Webber Matthew J MJ Tang Benjamin C BC Lavin Danya M DM Veiseh Omid O Doloff Joshua C JC Bose Suman S Vegas Arturo A Ma Minglin M Sahay Gaurav G Chiu Alan A Bader Andrew A Langan Erin E Siebert Sean S Li Jie J Greiner Dale L DL Newburger Peter E PE von Andrian Ulrich H UH Langer Robert R Anderson Daniel G DG

PloS one 20150910 9

In vivo implantation of sterile materials and devices results in a foreign body immune response leading to fibrosis of implanted material. Neutrophils, one of the first immune cells to be recruited to implantation sites, have been suggested to contribute to the establishment of the inflammatory microenvironment that initiates the fibrotic response. However, the precise numbers and roles of neutrophils in response to implanted devices remains unclear. Using a mouse model of peritoneal microcapsul ...[more]

PMID: 26355958

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Project description:BACKGROUND & AIMS:Neutrophils and liver sinusoidal endothelial cells (LSECs) both contribute to sterile inflammatory injury during ischemia/reperfusion (I/R), a well-known liver surgical stress. Interleukin-33 (IL-33) has been shown to drive neutrophil infiltration during inflammatory responses through its receptor ST2. We recently reported that infiltrating neutrophils form neutrophil extracellular traps (NETs), which exacerbate sterile inflammatory injury in liver I/R. Here, we sought to determine the role of IL-33 in NET formation during liver sterile inflammation. METHODS:Evaluation of IL-33 forming NETs was investigated using a partial liver I/R model to generate sterile injury in healthy WT, IL-33 and ST2 knockouts. Serum levels of IL-33 and myeloperoxidase (MPO)-DNA complex were measured in both humans and mice after the first surgery. Liver damage was assessed. Mouse neutrophil depletion was performed by intraperitoneal injection of anti-Ly6G antibody before I/R. RESULTS:Patients undergoing liver resection showed a significant increase in serum IL-33 compared to healthy volunteers. This coincided with higher serum MPO-DNA complexes. NET formation was decreased in IL-33 and ST2 knockout mice compared with control mice, after liver I/R. IL-33 or ST2 deficiency protected livers from I/R injury, whereas rIL-33 administration during I/R exacerbated hepatotoxicity and systemic inflammation. In vitro, IL-33 is released from LSECs to promote NET formation. IL-33 deficient LSECs failed to induce NETs. ST2 deficient neutrophils limited their capacity to form NETs in vitro and adoptive transfer of ST2 knockout neutrophils to neutrophil-depleted WT mice significantly decreased NET formation. CONCLUSIONS:Data establish that IL-33, mainly released from LSECs, causes excessive sterile inflammation after hepatic I/R by inducing NET formation. Therapeutic targeting of IL-33/ST2 might extend novel strategies to minimize organ damage in various clinical settings associated with sterile inflammation. LAY SUMMARY:Liver ischemia and reperfusion injury results in the formation of neutrophil extracellular traps, which contribute to organ damage in liver surgeries. Herein, we show that IL-33 is released from liver sinusoidal endothelial cells to promote NET formation during liver I/R, which exacerbates inflammatory cascades and sterile inflammation.

Project description:BackgroundLong-term success of implant restoration depends on many factors one of them is the sufficient implant stability which is lowered in compromised bone density sites such as the maxilla as it is categorized as type III & IV bone, so searching for a new innovation and updates in implant material and features is very mandatory. So, the aim of this study was to compare between two implant materials (roxolid and traditional titanium) on the primary and secondary stability of implant retained maxillary overdenture.MethodsEighteen completely edentulous patients were selected. All patients received maxillary implant-retained overdentures and lower complete dentures; patients were divided equally into two groups according to the type of implant materials. Group A received a total number of 36 implants made of roxolid material and Group B received a total number of 36 implants made of traditional titanium alloys. Implant stability was assessed using ostell device, the primary implant stability was measured at the day of implant installation however, secondary implant stability was measured after six weeks of implant placement. Paired t-test was used to compare between primary and secondary stability in the same group and an independent t-test was used to compare between the two groups with a significant level < 0.05.ResultsIndependent t-test revealed a significant difference between the two groups with p -value = 0.0141 regarding primary stability and p-value < 0.001 regarding secondary stability, as roxolid implant group was statistically higher stability than titanium group in both. Paired t- test showed a statistically significant difference in roxolid implant group with p-value = 0.0122 however, there was non-statistically significant difference in titanium group with p-value = 0.636. Mann Whitney test showed a significant difference between the two groups regarding amount of change in stability with p value = 0.191. roxolid implant group showed a higher amount of change in stability than the titanium implant group.ConclusionWithin the limitation of this study, it could be concluded that: Roxolid implants showed promising results regarding primary and secondary stability compared to conventional Titanium implants and can be a better alternative in implant retained maxillary overdentures.Trial registrationRetrospectively NCT06334770 at 26-3-2024.

Project description:UnlabelledInnate immunity plays a crucial role in the response to sterile inflammation such as liver ischemia/reperfusion (I/R) injury. The initiation of liver I/R injury results in the release of damage-associated molecular patterns, which trigger an innate immune and inflammatory cascade through pattern recognition receptors. Neutrophils are recruited to the liver after I/R and contribute to organ damage and innate immune and inflammatory responses. Formation of neutrophil extracellular traps (NETs) has been recently found in response to various stimuli. However, the role of NETs during liver I/R injury remains unknown. We show that NETs form in the sinusoids of ischemic liver lobes in vivo. This was associated with increased NET markers, serum level of myeloperoxidase-DNA complexes, and tissue level of citrullinated-histone H3 compared to control mice. Treatment with peptidyl-arginine-deiminase 4 inhibitor or DNase I significantly protected hepatocytes and reduced inflammation after liver I/R as evidenced by inhibition of NET formation, indicating the pathophysiological role of NETs in liver I/R injury. In vitro, NETs increase hepatocyte death and induce Kupffer cells to release proinflammatory cytokines. Damage-associated molecular patterns, such as High Mobility Group Box 1 and histones, released by injured hepatocytes stimulate NET formation through Toll-like receptor (TLR4)- and TLR9-MyD88 signaling pathways. After neutrophil depletion in mice, the adoptive transfer of TLR4 knockout or TLR9 knockout neutrophils confers significant protection from liver I/R injury with a significant decrease in NET formation. In addition, we found inhibition of NET formation by the peptidyl-arginine-deiminase 4 inhibitor and that DNase I reduces High Mobility Group Box 1 and histone-mediated liver I/R injury.ConclusionDamage-associated molecular patterns released during liver I/R promote NET formation through the TLR signaling pathway. Development of NETs subsequently exacerbates organ damage and initiates inflammatory responses during liver I/R.

Project description:Implant-retained custom-milled framework enhances the stability of palatal obturator prostheses. Therefore, to evaluate the mechanical response of implant-retained obturator prostheses with bar-clip attachment and milled bars, in three different materials under two load incidences were simulated. A maxilla model which Type IIb maxillary defect received five external hexagon implants (4.1 x 10 mm). An implant-supported palatal obturator prosthesis was simulated in three different materials: polyetheretherketone (PEEK), titanium (Ti:90%, Al:6%, V:4%) and Co-Cr (Co:60.6%, Cr:31.5%, Mo:6%) alloys. The model was imported into the analysis software and divided into a mesh composed of nodes and tetrahedral elements. Each material was assumed isotropic, elastic and homogeneous and all contacts were considered ideal. The bone was fixed and the load was applied in two different regions for each material: at the palatal face (cingulum area) of the central incisors (100 N magnitude at 45°); and at the occlusal surface of the first left molar (150 N magnitude normal to the surface). The microstrain and von-Mises stress were selected as criteria for analysis. The posterior load showed a higher strain concentration in the posterior peri-implant tissue, near the load application side for cortical and cancellous bone, regardless the simulated material. The anterior load showed a lower strain concentration with reduced magnitude and more implants involving in the load dissipation. The stress peak was calculated during posterior loading, which 77.7 MPa in the prosthetic screws and 2,686 με microstrain in the cortical bone. For bone tissue and bar, the material stiffness was inversely proportional to the calculated microstrain and stress. However, for the prosthetic screws and implants the PEEK showed higher stress concentration than the other materials. PEEK showed a promising behavior for the bone tissue and for the integrity of the bar and bar-clip attachments. However, the stress concentration in the prosthetic screws may represent an increase in failure risk. The use of Co-Cr alloy can reduce the stress in the prosthetic screw; however, it increases the bone strain; while the Titanium showed an intermediate behavior.

Dataset Information

Neutrophil Responses to Sterile Implant Materials.

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Neutrophil Responses to Sterile Implant Materials.

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