The Initial Inflammatory Response to Bioactive Implants Is Characterized by NETosis

Abstract

Implants trigger an inflammatory response, which is important for osseointegration. Here we studied neutrophil extracellular trap (NET) release of human neutrophils in response to sandblasted large-grit acid etched (SLA) implants using fluorescent, confocal laser scanning and scanning electron microscopy. Our studies demonstrate that human neutrophils rapidly adhered to SLA surfaces, which triggered histone citrullination and NET release. Further studies showed that albumin or acetylsalicylic acid had no significant effects on the inflammatory response to SLA surfaces. In contrast to bioinert materials, which do not osseointegrate, the bioactivity of SLA surfaces is coupled with the ability to release NETs. Further investigations are necessary for clarifying the role of NETosis for osseointegration.

Hydrophilic titanium surfaces reduce neutrophil inflammatory response and NETosis

“…While a recent study identified a NETotic response to roughened Ti implant surfaces, 40 our study demonstrates that the neutrophil response depends on the type of surface modification and that these cues alter neutrophil inflammatory response. We have previously demonstrated a similar effect in macrophages, which respond to roughness and hydrophilicity with an enhanced anti-inflammatory profile.…”

Combating Implant Infections: Shifting Focus from Bacteria to Host

“…[27,82] Second, increasing data show that the normal function of neutrophils is influenced by inherent biomaterial surface features. [43,83,84] Under ideal noninfected conditions, the presence of neutrophils around a biomaterial is confined to only a few days, as they should be quickly replaced by cells capable of dampening inflammation and initiating tissue regeneration. [85] When the neutrophil replacement mechanism fails, the sustained arsenal of antimicrobial effectors employed by neutrophils can be the cause of an undesired local immune milieu.…”

“…Specifically, the roles of neutrophils and macrophages in the host defense and inflammatory responses are highlighted, as the fate of the biomaterial is thought to be largely dependent on the initial reaction of these crucial innate immune cell players. [40][41][42][43] Based on the premise that appropriate immune-protection by the host is key, surface properties can be precisely modified to influence the biomaterial-host interactions, for which the effect of surface biophysical cues can be used as an example. Moreover, strategies for biomaterial surface functionalization with systems for delivery of immunomodulatory therapeutics-including host defense peptides, metallic nanoparticles, quorum sensing (QS) inhibitors, and therapeutic adjuvants-are discussed.…”

Mechanical shear stress and leukocyte phenotype and function: Implications for ventricular assist device development and use

“…The pre-existing inflammatory state of the recipient might prime neutrophils for exacerbated activation upon exposure to mechanical shear stress. Such excessive stimulation of neutrophils by MCS might contribute to the occurrence of sepsis, multiple organ failure (16), the formation of thrombosis (17).…”

“…As the first line of defence against foreign bodies such as VADs, granulocytes are predisposed to upregulation and expression of activation markers. Macrophage antigen-1 (MAC-1) is a granulocyte marker for systemic inflammation and has been used as a biomarker in CPB and sepsis [16,17]. MAC-1 expression on granulocytes was increased significantly in HMII at POD 14 and did not return to pre-operative levels until POD 120 (35).…”