Environmental Factors Impacting Bone-Relevant Chemokines

Our plain-English summary of Environmental Factors Impacting Bone-Relevant Chemokines, by J.T. Smith, A.D. Schneider, K.M. Katchko, et al (Frontiers in Endocrinology, 2017).

The study

• Authors: J.T. Smith, A.D. Schneider, K.M. Katchko, C. Yun, E.L. Hsu
• Journal: Frontiers in Endocrinology
• Published: 2017;8:22
• Cited by: 23 articles, as counted by NIH iCite
• Read it: PubMed · Publisher · Free full text

Abstract

Chemokines play an important role in normal bone physiology and the pathophysiology of many bone diseases. The recent increased focus on the individual roles of this class of proteins in the context of bone has shown that members of the two major chemokine subfamilies-CC and CXC-support or promote the formation of new bone and the remodeling of existing bone in response to a myriad of stimuli. These chemotactic molecules are crucial in orchestrating appropriate cellular homing, osteoblastogenesis, and osteoclastogenesis during normal bone repair. Bone healing is a complex cascade of carefully regulated processes, including inflammation, progenitor cell recruitment, differentiation, and remodeling. The extensive role of chemokines in these processes and the known links between environmental contaminants and chemokine expression/activity leaves ample opportunity for disruption of bone healing by environmental factors. However, despite increased clinical awareness, the potential impact of many of these environmental factors on bone-related chemokines is still ill defined. A great deal of focus has been placed on environmental exposure to various endocrine disruptors (bisphenol A, phthalate esters, etc.), volatile organic compounds, dioxins, and heavy metals, though mainly in other tissues. Awareness of the impact of other less well-studied bone toxicants, such as fluoride, mold and fungal toxins, asbestos, and chlorine, is also reviewed. In many cases, the literature on these toxins in osteogenic models is lacking. However, research focused on their effects in other tissues and cell lines provides clues for where future resources could be best utilized. This review aims to serve as a current and exhaustive resource detailing the known links between several classes of high-interest environmental pollutants and their interaction with the chemokines relevant to bone healing.

In plain English

This article, published as a 'Hypothesis and Theory' paper, was a review of published research on how environmental pollutants affect chemokines. Chemokines are signaling proteins that help guide bone healing. The review covered endocrine disruptors, volatile organic compounds, dioxins, metals and prosthetic wear particles, along with less-studied agents including fluoride, mold toxins, asbestos and chlorine. For asbestos, the authors summarized other studies. Those studies reported lower CXCR3 levels in CD4+ T-cells, including in patients with asbestos-related lung disease, and raised inflammatory markers in asbestos-exposed persons. The authors found no literature connecting asbestos to chemokine levels in the context of bone. They also reported their own laboratory work in rat bone marrow stromal cells. Dioxin and dioxin-like compounds significantly reduced CXCL12 in all treatment groups and reduced CXCR4 in most. All compounds except PCB-118 reduced the cells' movement toward CXCL12. The authors concluded that little literature links most of the reviewed compounds to bone-relevant chemokines. They said it remains to be determined whether asbestos has any impact on bone-related chemokines.

We wrote this plain-English summary from the full article with the help of AI, and a second AI model checked each sentence against the article. It is not the authors' wording; the abstract and the article are their own account.

What the study did and found

• Design: Review of published literature (labeled 'Hypothesis and Theory'), with some original laboratory data on dioxins in rat cells
• Who was studied: Published studies in cell lines, animal models and humans. The authors' own experiments used primary rat bone marrow stromal cells (BMSC). No dates or numbers of studies reviewed are given.
• Exposure: Environmental pollutants: endocrine disruptors, volatile organic compounds, dioxins and dioxin-like compounds, metals and prosthetic wear particles, plus fluoride, mold and fungal toxins, asbestos (no fiber type specified), and chlorine
• Main results:
  • The authors found no published literature connecting asbestos to BMP, IL-8, or other chemokine levels in the context of bone.
  • From other studies cited in the review: CXCR3 levels were reported to be decreased in CD4+ T-cells, including in patients with asbestos-related lung disease.
  • From other studies cited in the review: systemic inflammatory markers (IgE, IgA, IL-6, IL-8, ICAM-1) were found elevated in asbestos-exposed persons.
  • In the authors' own experiments in rat BMSC, CXCL12 was significantly reduced for all dioxin and dioxin-like treatment groups, under both standard and osteogenic conditions.
  • In the authors' own experiments, CXCR4 expression in rat BMSC was significantly decreased under both conditions for all treatment groups except PCB-118, PCB-126 and PCB-156.
  • In the authors' own experiments, movement of rat BMSC toward CXCL12 was significantly reduced in cells pretreated with every compound except PCB-118.
• The authors' conclusion: The authors concluded that there is little literature on the relationship between most of the environmental compounds reviewed and chemokines relevant to bone.
• Limitations the authors state:
  • The authors stated that for many of these toxins, the literature in bone-forming (osteogenic) models is lacking.
  • The authors stated that it remains to be determined whether asbestos affects growth factor signaling in bone or has any impact on bone-related chemokines.

Topics

Medical terms in this study, explained in our Lexicon: Inflammation, Environmental Exposure.

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