Sterile post-traumatic immunosuppression

Md Nahidul Islam, Benjamin A Bradley, Rhodri Ceredig, Md Nahidul Islam, Benjamin A Bradley, Rhodri Ceredig

Abstract

After major trauma, the human immune system initiates a series of inflammatory events at the injury site that is later followed by suppression of local inflammation favoring the repair and remodeling of the damaged tissues. This local immune response involves complex interactions between resident cells such as macrophages and dendritic cells, soluble mediators such as cytokines and chemokines, and recruited cells such as neutrophils, monocytes and mesenchymal stromal cells. If of sufficient magnitude, these initial immune responses nevertheless have systemic consequences resulting in a state called post-traumatic immunosuppression (PTI). However, controversy exists regarding the exact immunological changes occurring in systemic compartments triggered by these local immune responses. PTI is one of the leading causes of post-surgical mortality and makes patients vulnerable to hospital-acquired infections, multiple organ failure and many other complications. In addition, hemorrhage, blood transfusion, immunesenescence and immunosuppressant drugs aggravate PTI. PTI has been intensively studied, but published results are frequently cloudy. The purpose of this review is to focus on the contributions made by different responsive modalities to immunosuppression following sterile trauma and to try to integrate these into an overall scheme of PTI.

Figures

Figure 1
Figure 1
Schematic representation of PTI after sterile trauma. This figure schematically illustrates the sequence of events following major trauma. In brief, at the local injury site, release of different DAMPs by the damaged tissues induces viable cells to secrete chemokines such as IL-8, MCP-1 and MIP-1α, and the immediate secretion of inflammatory cytokines such as TNF-α. DAMPs release results in IL-6 and TNF-α production that activate the HPE axis to release ACTH, cortisol and also PGE2. These events then trigger the secretion of anti-inflammatory biomolecules such as IL-1RA, IL-10 and sTNF-R. Later, IL-6, by the virtue of its ability to trigger the release of acute phase proteins (APPs) by the liver, indirectly involved in reducing the inflammatory events at the injured site. In parallel with the immediate release of DAMPs, inflammatory cytokines and the activities of resident immune cells, there is recruitment of neutrophils, monocytes and MSCs from the blood to the injured site. Bone marrow and spleen act as reservoirs for the egression of these cells to the site of injury via the blood. By releasing antimicrobial peptides and helping in hemostasis, damaged skin also activates inflammasomes to release DAMPs at the local site. On the other hand, ischemia–reperfusion injury associated with the surgical procedure increases HIF and ROS expression that also trigger the production of DAMPs, and thus have an additional role in recruiting immune cells to the injured site. The ultimate goal of the above events following a major trauma is tissue remodeling and promotion of wound healing.
Figure 2
Figure 2
Measuring immune status helps in choosing appropriate immunomodulatory drug. Measuring a patient's immune status based on particular profile of specific pro- and anti-inflammatory proteins will help to indicate if the patient: (i) has a stable immune status and medication is not necessary, (ii) is at the stage of cytokine storm following trauma or infection when both pro- and anti-inflammatory cytokines rise, (iii) requires immediate attention with treatment (either immunostimulatory or immunosuppressive drug will be administered) or (iv) is not in need of medication but requires monitoring over the coming days. Knowing immune status will provide information following trauma or sepsis that can be monitored throughout the patient's recovery, thereby preventing the risk of unnecessary danger from incorrect therapy.

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