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Staphylococcus aureus vs. Osteoblast: Relationship and Consequences in Osteomyelitis.

Josse J, Velard F, Gangloff SC - Front Cell Infect Microbiol (2015)

Bottom Line: Bone cells, namely osteoblasts and osteoclasts work in concert and are responsible for bone extracellular matrix formation and resorption.This includes the over-production of chemokines, cytokines and growth factors, thus suggesting a role for these cells in both innate and adaptive immunity.The present review provides a survey of the relevant literature discussing the important aspects of S. aureus and osteoblast interaction as well as the ability for antimicrobial peptides to kill intra-osteoblastic S. aureus, hence emphasizing the necessity for new anti-infectious therapeutics.

View Article: PubMed Central - PubMed

Affiliation: EA 4691 Biomatériaux et inflammation en site osseux, Pôle Santé, Université de Reims Champagne-Ardenne Reims, France.

ABSTRACT
Bone cells, namely osteoblasts and osteoclasts work in concert and are responsible for bone extracellular matrix formation and resorption. This homeostasis is, in part, altered during infections by Staphylococcus aureus through the induction of various responses from the osteoblasts. This includes the over-production of chemokines, cytokines and growth factors, thus suggesting a role for these cells in both innate and adaptive immunity. S. aureus decreases the activity and viability of osteoblasts, by induction of apoptosis-dependent and independent mechanisms. The tight relationship between osteoclasts and osteoblasts is also modulated by S. aureus infection. The present review provides a survey of the relevant literature discussing the important aspects of S. aureus and osteoblast interaction as well as the ability for antimicrobial peptides to kill intra-osteoblastic S. aureus, hence emphasizing the necessity for new anti-infectious therapeutics.

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Staphylococcus aureus induction of inflammatory mediator production by osteoblasts and participation in the recruitment/activation of innate and adaptive immune cells. Staphylococcus aureus interaction with osteoblasts increases the expression of cytokines IL-1β, IL-18, TNF-α, the production and release of IL-6, IL-12 and the expression and release of chemokines CXCL2, CXCL8, CXCL10, CCL2, CCL3, CCL5 and growth factors G-CSF and GM-CSF. It also increases the expression and production of CD40 and MHC II. All of this participates to the recruitment and activation of innate (neutrophils, monocytes/macrophages) and adaptive (lymphocytes) immune cells.
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Figure 3: Staphylococcus aureus induction of inflammatory mediator production by osteoblasts and participation in the recruitment/activation of innate and adaptive immune cells. Staphylococcus aureus interaction with osteoblasts increases the expression of cytokines IL-1β, IL-18, TNF-α, the production and release of IL-6, IL-12 and the expression and release of chemokines CXCL2, CXCL8, CXCL10, CCL2, CCL3, CCL5 and growth factors G-CSF and GM-CSF. It also increases the expression and production of CD40 and MHC II. All of this participates to the recruitment and activation of innate (neutrophils, monocytes/macrophages) and adaptive (lymphocytes) immune cells.

Mentions: Following contact/internalization of S. aureus, the first line of defense of the osteoblasts is to secrete inflammatory factors like cytokines, chemokines and growth factors, all of which are able to activate and recruit immune cells from the innate or adaptive immune systems (Turner et al., 2014; Figure 3).


Staphylococcus aureus vs. Osteoblast: Relationship and Consequences in Osteomyelitis.

Josse J, Velard F, Gangloff SC - Front Cell Infect Microbiol (2015)

Staphylococcus aureus induction of inflammatory mediator production by osteoblasts and participation in the recruitment/activation of innate and adaptive immune cells. Staphylococcus aureus interaction with osteoblasts increases the expression of cytokines IL-1β, IL-18, TNF-α, the production and release of IL-6, IL-12 and the expression and release of chemokines CXCL2, CXCL8, CXCL10, CCL2, CCL3, CCL5 and growth factors G-CSF and GM-CSF. It also increases the expression and production of CD40 and MHC II. All of this participates to the recruitment and activation of innate (neutrophils, monocytes/macrophages) and adaptive (lymphocytes) immune cells.
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4660271&req=5

Figure 3: Staphylococcus aureus induction of inflammatory mediator production by osteoblasts and participation in the recruitment/activation of innate and adaptive immune cells. Staphylococcus aureus interaction with osteoblasts increases the expression of cytokines IL-1β, IL-18, TNF-α, the production and release of IL-6, IL-12 and the expression and release of chemokines CXCL2, CXCL8, CXCL10, CCL2, CCL3, CCL5 and growth factors G-CSF and GM-CSF. It also increases the expression and production of CD40 and MHC II. All of this participates to the recruitment and activation of innate (neutrophils, monocytes/macrophages) and adaptive (lymphocytes) immune cells.
Mentions: Following contact/internalization of S. aureus, the first line of defense of the osteoblasts is to secrete inflammatory factors like cytokines, chemokines and growth factors, all of which are able to activate and recruit immune cells from the innate or adaptive immune systems (Turner et al., 2014; Figure 3).

Bottom Line: Bone cells, namely osteoblasts and osteoclasts work in concert and are responsible for bone extracellular matrix formation and resorption.This includes the over-production of chemokines, cytokines and growth factors, thus suggesting a role for these cells in both innate and adaptive immunity.The present review provides a survey of the relevant literature discussing the important aspects of S. aureus and osteoblast interaction as well as the ability for antimicrobial peptides to kill intra-osteoblastic S. aureus, hence emphasizing the necessity for new anti-infectious therapeutics.

View Article: PubMed Central - PubMed

Affiliation: EA 4691 Biomatériaux et inflammation en site osseux, Pôle Santé, Université de Reims Champagne-Ardenne Reims, France.

ABSTRACT
Bone cells, namely osteoblasts and osteoclasts work in concert and are responsible for bone extracellular matrix formation and resorption. This homeostasis is, in part, altered during infections by Staphylococcus aureus through the induction of various responses from the osteoblasts. This includes the over-production of chemokines, cytokines and growth factors, thus suggesting a role for these cells in both innate and adaptive immunity. S. aureus decreases the activity and viability of osteoblasts, by induction of apoptosis-dependent and independent mechanisms. The tight relationship between osteoclasts and osteoblasts is also modulated by S. aureus infection. The present review provides a survey of the relevant literature discussing the important aspects of S. aureus and osteoblast interaction as well as the ability for antimicrobial peptides to kill intra-osteoblastic S. aureus, hence emphasizing the necessity for new anti-infectious therapeutics.

Show MeSH
Related in: MedlinePlus