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Burger, E.

Publications and source records attributed to Burger, E..

2 recordsLinked to original sources

Microbial Influenced Corrosion: A Novel Initiator of In Vivo Spine Rod Fracture

ABSTRACTSpine rod catastrophic failure/rod fracture after implantation is estimated to occur in [~]10% of all cases worldwide with this rate remaining consistent for more than 20 years. To accommodate the spine mechanical environment, metal alloys such as austenitic stainless steels, cobalt-chromium-molybdenum alloys, and /{beta} type titanium alloys such are used as they have a high resistance to fatigue failure. The work presented herein addresses the gap in understanding about what happens in a laboratory environment versus what is happening in human patients that results in metal leaching into tissues as well as a shortened lifespan of a spine rod in a patient population that is not capable of breaking these spine rods from purely mechanical means. Eighty-five (N=85) patients (51 female - 62.9 {+/-} 13.5 years old, 34 male - 62.7 {+/-} 10.9 years old) who had spine revision surgery due to patient mechanical issues, such as loss of sagittal or coronal balance, pain, pedicle screw loosening, hardware associated infection were included in this study. All explanted rods had optical indications of surface modification that were not the result of mechanical damage, e.g. gouges, scratches, notches. The presence of Ti6Al4V rods increases the presence of local tissue concentrations of elemental Ti (190.98 {+/-} 207.84 g/g (ppm)) in all patients over the amount that would normally be present in patients who never had any titanium based orthopedic device implants (spinous muscle, 13.12 {+/-} 11.43 g/g). PQS, HHQ, and NHQ ToF-SIMS molecular signals were found co-located to corrosion pits as well with AHLs and palmitic acids indicating microbial presence and metabolism in all patients. This suggests that MIC can cause in vivo pitting corrosion resulting on rod failure.

bioengineering↗

ILC1-derived IFN-gamma mediates cDC1-dependent host resistance against Toxoplasma gondii

Host resistance against intracellular pathogens requires a rapid IFN-{gamma} mediated immune response. We reveal that T-bet-dependent production of IFN-{gamma} is essential for the maintenance of inflammatory DCs at the site of infection with a common protozoan parasite, Toxoplasma gondii. A detailed analysis of the cellular sources for T-bet-dependent IFN-{gamma} identified that ILC1s, but not NK or TH1 cells, were involved in the regulation of inflammatory DCs via IFN-{gamma}. Mechanistically, we established that T-bet dependent ILC1-derived IFN-{gamma} is critical for the induction of IRF8, an essential transcription factor for cDC1s. Failure to upregulate IRF8 in DCs resulted in acute susceptibility to T. gondii infection. Our data identifies that ILC1-derived IFN-{gamma} is indispensable for host resistance against intracellular infection via maintaining IRF8+ inflammatory DCs at the site of infection. Author SummaryMounting a robust type I innate immune response is essential for resistance against numerous intracellular pathogens. The type I immune response is characterized by the production of IFN-{gamma}, a central cytokine required for multiple non-redundant effector functions against bacterial, viral, and parasitic pathogens. Previous work has shown that group 1 innate lymphocyte cells (ILC1s) together with NK and CD4+ T cells play an indispensable IFN-{gamma} mediated protective role against Toxoplasma gondii infection; yet, the pathway of how IFN-{gamma} produced by ILC1s defend against T. gondii remains unknown. In this work we identified that early production of IFN-{gamma} by ILC1 is essential for maintaining dendritic cells (DCs) during infection. Mechanistically, we reveal that ILC1-derived IFN-{gamma} is indispensable for inducing the transcription factor IRF8 that is critical for sustaining inflammatory DCs. Finally, we demonstrate that IRF8+ DCs are critical for parasite elimination.

immunology↗