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 mononuclear cells via direct physical contact, a mechanism potentially explaining increased IL-1 secretion in patients with high-turnover osteoporosis.

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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 direct physical contact between monocytes and bone particles, as well as specific matrix components like collagen fragments and hydroxyproline, significantly increased IL-1 secretion in a dose-dependent manner. Conversely, lymphocytes lacking monocytes did not respond, and the effect was inhibited by agents that block bone binding or by antibodies targeting the alpha 2 beta 1-integrin 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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