The role of IL‐3 in bone

Soysa, Niroshani Surangika; Alles, Neil

doi:10.1002/jcb.27956

Cited by 7 publications

(3 citation statements)

References 59 publications

(172 reference statements)

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“…Through this signaling pathway, IL-3 promotes basophil growth and differentiation, which are involved in allergic rhinitis. 27,28 Additionally, IL-3 has strong hematopoietic effects, promoting the production of granulocytes, monocytes, mast cells, basophils, and macrophages, which could also promote airway inflammation 29 in response to air pollution.…”

Section: Discussionmentioning

confidence: 99%

Air pollution exposure is associated with rhinitis in older US adults via specific immune mechanisms

Scussiatto

Wroblewski

Pagel

et al. 2023

Int Forum Allergy Rhinol

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BackgroundPathophysiology of rhinitis in older adults is largely unknown. We tested whether air pollution is associated with this condition and how immune mechanisms may play a role in this relationship.MethodsWe analyzed cross‐sectional data from the National Social Life, Health, and Aging Project, a nationally representative study of older adults born between 1920 and 1947. Particulate matter ≤2.5 μm (PM2.5) air pollution exposure estimates were generated using validated spatiotemporal models. Presence of rhinitis was defined based on medication use (≥1: intranasal medications: steroids, antihistamines, lubricants, and/or decongestants, and/or oral medications: antihistamines and/or decongestants). K‐means cluster analysis (Jaccard method) was used to group 13 peripheral blood cytokines into 3 clusters to facilitate functional determination. We fitted multivariate logistic regressions to correlate PM2.5 exposure with presence of rhinitis, controlling for confounders, and then determined the role of cytokines in this relationship.ResultsLong‐ (but not short‐) term exposure to PM2.5 was associated with presence of rhinitis: 3‐year exposure window, odds ratio (OR) = 1.32, 95% confidence interval (CI): 0.98, 1.80, per 1 standard deviation (SD) PM2.5 increase. Inclusion of cytokine cluster in the model led to a modestly stronger effect of PM2.5 exposure on rhinitis (OR = 1.37; 95% CI: 1.00, 1.87; 3‐year exposure window). The particular immune profile responsible for this result was composed of elevated IL‐3, IL‐12, and IFN‐γ (OR = 4.86, 95% CI: 1.10, 21.58, immune profile–PM2.5 exposure interaction term).ConclusionWe show for the first time that IL‐3, IL‐12, and IFN‐γ explain in part the relationship between PM2.5 exposure and rhinitis in older US adults. If confirmed, these immune pathways may be used as therapeutic targets.

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Section: Discussionmentioning

confidence: 99%

Air pollution exposure is associated with rhinitis in older US adults via specific immune mechanisms

Scussiatto

Wroblewski

Pagel

et al. 2023

Int Forum Allergy Rhinol

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“…IL-3, also known as multicolony stimulation factor (multi-CSF), is a member of the βc family due to the fact that its receptor shares the signaling subunit βc with granulocyte/macrophage colony-stimulating factor (GM-CSF) and IL-5 ( 134 ). Activated T lymphocytes, mast cells, and osteoblasts are the primary secretors ( 135 ).…”

Section: Interleukinsmentioning

confidence: 99%

The effect of cytokines on osteoblasts and osteoclasts in bone remodeling in osteoporosis: a review

et al. 2023

Front. Immunol.

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The complicated connections and cross talk between the skeletal system and the immune system are attracting more attention, which is developing into the field of Osteoimmunology. In this field, cytokines that are among osteoblasts and osteoclasts play a critical role in bone remodeling, which is a pathological process in the pathogenesis and development of osteoporosis. Those cytokines include the tumor necrosis factor (TNF) family, the interleukin (IL) family, interferon (IFN), chemokines, and so on, most of which influence the bone microenvironment, osteoblasts, and osteoclasts. This review summarizes the effect of cytokines on osteoblasts and osteoclasts in bone remodeling in osteoporosis, aiming to providing the latest reference to the role of immunology in osteoporosis.

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“…IL-1-has been shown to induce OC survival by acting through the PI 3-kinase/Akt and ERK signaling pathways and by reducing caspase-3 activity (Lee et al, 2002). It has been shown that OCPs and mature OCs express IL-3R which is necessary for OCP survival and commitment to OC lineage, whereas its role in OC differentiation has not been fully delineated yet (Soysa and Alles, 2018). IL-6 is a known activator of OC bone resorption activity.…”

Section: Interleukins (Ils)mentioning

confidence: 99%

Positive and negative regulators of osteoclast apoptosis

Soysa

Alles

2019

Bone Reports

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Survival and apoptosis are of major importance in the osteoclast life cycle. As osteoclasts have short lifespan, any alteration that prolongs their viability may cause enhanced osteoclast activity. Hence, the regulation of OC apoptosis has been recognized as a critical factor in bone remodeling. An imbalance in bone remodeling due to increased osteoclast activity leads to most adult bone diseases such as osteoporosis, rheumatoid arthritis and multiple myeloma. Therefore, manipulating osteoclast death would be a viable therapeutic approach in ameliorating bone diseases, with accelerated resorption. Over the last few decades we have witnessed the unraveling of many of the intracellular mechanisms responsible for osteoclast apoptosis. Thus, an understanding of the underlying mechanisms by which osteoclasts undergo programmed cell death and the regulators that modulate that activity will undoubtedly provide an insight into the development of pharmacological agents to treat such pathological bone diseases.

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The role of IL‐3 in bone

Cited by 7 publications

References 59 publications

Air pollution exposure is associated with rhinitis in older US adults via specific immune mechanisms

Air pollution exposure is associated with rhinitis in older US adults via specific immune mechanisms

The effect of cytokines on osteoblasts and osteoclasts in bone remodeling in osteoporosis: a review

Positive and negative regulators of osteoclast apoptosis

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