Markers of Tissue Deterioration and Pain on Earth and in Space

Abstract

Purpose

Pain is an understudied physiological effect of spaceflight. Changes in inflammatory and tissue degradation markers are often associated with painful conditions. Our aim was to evaluate the changes in markers associated with tissue deterioration after a short-term spaceflight.

Patients and Methods

Plasma levels of markers for systemic inflammation and tissue degeneration markers were assessed in two astronauts before and within 24 h after the 17-day Axiom Space AX-1 mission.

Results

After the spaceflight, C-reactive protein (CRP) was reduced in both astronauts, while INFγ, GM-CSF, TNFα, BDNF, and all measured interleukins were consistently increased. Chemokines demonstrated variable changes, with consistent positive changes in CCL3, 4, 8, 22 and CXCL8, 9, 10, and consistent negative change in CCL8. Markers associated with tissue degradation and bone turnover demonstrated consistent increases in MMP1, MMP13, NTX and OPG, and consistent decreases in MMP3 and MMP9.

Conclusion

Spaceflight induced changes in the markers of systemic inflammation, tissue deterioration, and bone resorption in two astronauts after a short, 17-day, which were often consistent with those observed in painful conditions on Earth. However, some differences, such as a consistent decrease in CRP, were noted. All records for the effect of space travel on human health are critical for improving our understanding of the effect of this unique environment on humans.

Keywords:

• spaceflight
• astronaut
• cytokine
• interleukin
• chemokine
• bone turnover

Abbreviations

AP, abdominal pain; BDNF, brain derived neurotrophic factor; BFM, bone formation markers; BP, back pain; BRM, bone resorption markers; CCL24, myeloid progenitor inhibitory factor 2; CCL3, macrophage inflammatory protein 1-alpha; CCL4, macrophage inflammatory protein 1-beta; CMP, chronic malignant pain; CNMP, chronic non-malignant pain; CP, chest pain; CRP, c-reactive protein; CRP, C-reactive protein; CXCL5, epithelial-derived neutrophil-activating peptide 7; CXCL6, granulocyte chemotactic protein-2; CXCL9, monokine induced by gamma IFN; GM-CSF, granulocyte-macrophage colony-stimulating factor; HNP, head and neck pain; IFN, interferon; IL-1 alpha, hematopoietin 1; IL-1 beta, lymphocyte activating factor; IL, interleukins; IP-10/CXCL10, IFN gamma-induced protein 10; IRB, Institutional Review Board; LIGHT, TNF superfamily member 14; MCP, monocyte chemoattractant protein; MDC/CCL22, macrophage-derived chemokine; MFI, Median fluorescence intensity; MMP, matrix metalloproteinase; MSP, musculoskeletal pain; NGF-beta, beta nerve growth factor; NTX, human cross linked N-telopeptide of type I collagen; OA, osteoarthritis; OPG, osteoprotegerin; PICP, human procollagen I C-terminal; PP, pelvic pain; RANKL, receptor activator of nuclear factor κB ligand; RANTES/CCL5, normal T cell expressed and secreted; TGF, transforming growth factor; TNF, tumor necrosis factor.

Acknowledgments

This work was supported by the Montreal Children’s Hospital Foundation.

Disclosure

Dr Jean Ouellet reports grants from AO North America, outside the submitted work. The author reports no other conflicts of interest in this work.