Bone matrix constituents stimulate interleukin-1 release from human blood mononuclear cells.

Pacifici R, Carano A, Santoro SA, Rifas L, Jeffrey JJ, Malone JD, McCracken R, Avioli LV
The Journal of clinical investigation · 1991 · doi:10.1172/jci114975 · PMID:1845868 · PMC295032
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Bone matrix constituents, particularly collagen fragments, stimulate interleukin-1 release from human peripheral blood mononuclear cells through direct physical contact mediated by alpha 2 beta 1-integrins.

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This study investigated whether bone matrix constituents stimulate interleukin-1 release from human peripheral blood mononuclear cells. The researchers found that co-culturing monocytes with bone particles or specific matrix components like collagen fragments and hydroxyproline significantly increased IL-1 activity, whereas lymphocytes alone did not respond. Physical contact between the cells and the bone surface was required for this stimulation, a process partially inhibited by antibodies targeting the alpha 2 beta 1-integrin collagen receptor. The paper does not explicitly discuss endometriosis or adenomyosis; it was included in the corpus via a keyword match in the upstream search index.

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Abstract

To test the hypothesis that mononuclear cells are stimulated to release interleukin 1 (IL-1) by bone fragments released in the bone microenvironment during the remodeling cycle, we have investigated the effects of bone matrix and some of its constituents on IL-1 secretin from peripheral blood mononuclear cells (PBMC). Increases in IL-1 activity were observed when either PBMC or adherent monocytes, but not lymphocytes depleted of monocytes, were co-cultured with either human or rat bone particles but not with latex particles of similar size. Co-culture of PBMC with bone particles in a transwell system where the cells were physically separated from the bone particles, or with osteoblast- or osteoclast-covered bone particles, did not stimulate IL-1 release, indicating that a physical contact between PBMC and the bone surface is required for eliciting IL-1 release. This was confirmed by the finding of a lower stimulatory effect of bone particles pretreated with etidronate, a bisphosphonate which decreases the bone binding capacity of PBMC. Constituents of bone matrix, such as collagen fragments, hydroxyproline, and, to a lesser extent, transforming growth factor-beta, but not osteocalcin, alpha 2HS glycoprotein, fragments of either bone sialoprotein or osteopontin, and fibronectin, stimulated PBMC IL-1 release in a dose-dependent fashion. Collagen-stimulated IL-1 release was partially and specifically inhibited by a monoclonal antibody directed against the alpha 2 beta 1-integrin cell surface collagen receptor. These data demonstrate that products of bone resorption, known to be chemotactic for mononuclear cells, stimulate PBMC IL-1 activity. These findings may help explain previous documentation of increased IL-1 secretion by circulating monocytes obtained from patients with high turnover osteoporosis.
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Advertisement Research Article Free access | 10.1172/JCI114975 Division of Bone and Mineral Metabolism, Washington University School of Medicine and Medical Center, St. Louis, Missouri. Find articles by Pacifici, R. in: PubMed | Google Scholar Division of Bone and Mineral Metabolism, Washington University School of Medicine and Medical Center, St. Louis, Missouri. Find articles by Carano, A. in: PubMed | Google Scholar Division of Bone and Mineral Metabolism, Washington University School of Medicine and Medical Center, St. Louis, Missouri. Find articles by Santoro, S. in: PubMed | Google Scholar Division of Bone and Mineral Metabolism, Washington University School of Medicine and Medical Center, St. Louis, Missouri. Find articles by Rifas, L. in: PubMed | Google Scholar Division of Bone and Mineral Metabolism, Washington University School of Medicine and Medical Center, St. Louis, Missouri. Find articles by Jeffrey, J. in: PubMed | Google Scholar Division of Bone and Mineral Metabolism, Washington University School of Medicine and Medical Center, St. Louis, Missouri. Find articles by Malone, J. in: PubMed | Google Scholar Division of Bone and Mineral Metabolism, Washington University School of Medicine and Medical Center, St. Louis, Missouri. Find articles by McCracken, R. in: PubMed | Google Scholar Division of Bone and Mineral Metabolism, Washington University School of Medicine and Medical Center, St. Louis, Missouri. Find articles by Avioli, L. in: PubMed | Google Scholar Published January 1, 1991 - More info Published in Volume 87, Issue 1 on January 1, 1991 J Clin Invest. 1991;87(1):221–228. https://doi.org/10.1172/JCI114975. © 1991 The American Society for Clinical Investigation J Clin Invest. 1991;87(1):221–228. https://doi.org/10.1172/JCI114975. © 1991 The American Society for Clinical Investigation Published January 1, 1991 - Version history - Abstract To test the hypothesis that mononuclear cells are stimulated to release interleukin 1 (IL-1) by bone fragments released in the bone microenvironment during the remodeling cycle, we have investigated the effects of bone matrix and some of its constituents on IL-1 secretin from peripheral blood mononuclear cells (PBMC). Increases in IL-1 activity were observed when either PBMC or adherent monocytes, but not lymphocytes depleted of monocytes, were co-cultured with either human or rat bone particles but not with latex particles of similar size. Co-culture of PBMC with bone particles in a transwell system where the cells were physically separated from the bone particles, or with osteoblast- or osteoclast-covered bone particles, did not stimulate IL-1 release, indicating that a physical contact between PBMC and the bone surface is required for eliciting IL-1 release. This was confirmed by the finding of a lower stimulatory effect of bone particles pretreated with etidronate, a bisphosphonate which decreases the bone binding capacity of PBMC. Constituents of bone matrix, such as collagen fragments, hydroxyproline, and, to a lesser extent, transforming growth factor-beta, but not osteocalcin, alpha 2HS glycoprotein, fragments of either bone sialoprotein or osteopontin, and fibronectin, stimulated PBMC IL-1 release in a dose-dependent fashion. Collagen-stimulated IL-1 release was partially and specifically inhibited by a monoclonal antibody directed against the alpha 2 beta 1-integrin cell surface collagen receptor. These data demonstrate that products of bone resorption, known to be chemotactic for mononuclear cells, stimulate PBMC IL-1 activity. These findings may help explain previous documentation of increased IL-1 secretion by circulating monocytes obtained from patients with high turnover osteoporosis. Images. - Version history - Version 1 (January 1, 1991): No description Advertisement Advertisement Copyright © 2026 American Society for Clinical Investigation ISSN: 0021-9738 (print), 1558-8238 (online)

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