International Journal of Molecular Sciences

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Dear Colleagues,

Inflammation is a defense response of the living body to harmful stimuli, for example, pathogens or injuries. Inflammation removes the cause of cell damage and goes through the steps of removing dead cells and tissues due to injury and inflammatory response; then, it goes through the stage of initial repair, which restores cells or tissues to their original state. Chronic inflammation has a longer course than acute inflammation, and the causes of it are complex and involve the severity of tissue disorders, repetition of inflammatory stimuli, and the reactivity of the body. There are five typical signs: fever, pain, redness, swelling and loss of function. Inflammatory pain is especially characterized by increased sensitivity due to the inflammatory response associated with tissue damage, resulting in increased activity of primary afferent nerves, which, in turn, results in spontaneous pain, hyperalgesia, and allodynia.

Therefore, detailed research is needed to elucidate the exact mechanism for more effective inflammation management and development of anti-inflammatory and analgesic treatment methods for inflammatory pain patients.

The purpose of this Special Issue is to bring together experts in the field of inflammation and pain to investigate precise molecular mechanisms. This Special Issue welcomes original research and review articles.

Dr. Suk-Yun Kang
Guest Editor

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Keywords

inflammation
inflammatory pain
molecular mechanism
central sensitization

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9 pages, 1502 KiB

Open AccessBrief Report

Soft Tissue Manipulation Alters RANTES/CCL5 and IL-4 Cytokine Levels in a Rat Model of Chronic Low Back Pain

by Carmela L. Marciano, Taylor A. Hiland, Krista L. Jackson, Sierra Street, Carson Maris, Andrew Ehrsam, Julia M. Hum, Mary Terry Loghmani, Tien-Min G. Chu, Kyung S. Kang and Jonathan W. Lowery

Int. J. Mol. Sci. 2023, 24(18), 14392; https://doi.org/10.3390/ijms241814392 - 21 Sep 2023

Viewed by 1041

Abstract

Low back pain (LBP) is a common musculoskeletal complaint that can impede physical function and mobility. Current management often involves pain medication, but there is a need for non-pharmacological and non-invasive interventions. Soft tissue manipulation (STM), such as massage, has been shown to be effective in human subjects, but the molecular mechanisms underlying these findings are not well understood. In this paper, we evaluated potential changes in the soft tissue levels of more than thirty pro- or anti-inflammatory cytokines following instrument-assisted STM (IASTM) in rats with chronic, induced LBP using Complete Freund’s Adjuvant. Our results indicate that IASTM is associated with reduced soft tissue levels of Regulated on Activation, Normal T cell Expressed and Secreted (RANTES)/Chemokine (C-C motif) ligand 5 (CCL5) and increased soft tissue levels of Interleukin (IL)-4, which are pro-inflammatory and anti-inflammatory factors, respectively, by 120 min post-treatment. IASTM was not associated with tissue-level changes in C-X-C Motif Chemokine Ligand (CXCL)-5/Lipopolysaccharide-Induced CXC Chemokine (LIX)–which is the murine homologue of IL-8, CXCL-7, Granulocyte-Macrophage-Colony Simulating Factor (GM-CSF), Intercellular Adhesion Molecule (ICAM)-1, IL1-Receptor Antagonist (IL-1ra), IL-6, Interferon-Inducible Protein (IP)-10/CXCL-10, L-selectin, Tumor Necrosis Factor (TNF)-α, or Vascular Endothelial Growth Factor (VEGF) at either 30 or 120 min post-treatment. Combined, our findings raise the possibility that IASTM may exert tissue-level effects associated with improved clinical outcomes and potentially beneficial changes in pro-/anti-inflammatory cytokines in circulation and at the tissue level. Full article

(This article belongs to the Special Issue Molecular Mechanisms and Therapeutic Strategies of Inflammatory Pain)

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