Elastic Compression Attenuates Inflammatory Response in a Model of Acute Subcutaneous Abdominal Inflammation

Acute inflammation, when unresolved, can lead to complications that impair tissue repair and therapeutic outcomes.

In this study, we employed a model of lipopolysaccharide (LPS)-induced acute subcutaneous abdominal inflammation in mice to investigate the modulatory effects of elastic compression.

LPS administration elicited a robust inflammatory response, characterized by increased leukocyte infiltration, edema, and upregulation of pro-inflammatory mediators. Elastic compression significantly attenuated this response, reducing leukocyte counts in subcutaneous lavage, histological inflammatory infiltrates, and the expression of key pro-inflammatory genes and proteins, including NF-κB, IL-1β, and TNF-α, at both 24 and 72 hours post-induction. Mechanistically, these effects may result from the compressive force altering microvascular dynamics and modulating macrophage polarization and mechanotransduction pathways, including TLR4 and integrin signaling. Additionally, compression preserved redox homeostasis, as indicated by stable oxidative stress markers and antioxidant responses. To our knowledge, this is the first study to demonstrate that elastic compression modulates inflammation at molecular, cellular, and tissue levels in an acute inflammation model.

These findings support the therapeutic potential of elastic compression as a non-pharmacological strategy for managing acute inflammation, with possible applications in postoperative care, traumatic edema, and other soft tissue inflammatory conditions.

Further translational and clinical studies are warranted to validate these outcomes and guide evidence-based application protocols.

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