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Fibrosis Related Inflammatory Mediators: Role of the IL-10 Cytokine Family.

Sziksz E, Pap D, Lippai R, Béres NJ, Fekete A, Szabó AJ, Vannay Á - Mediators Inflamm. (2015)

Bottom Line: Independently of their etiology the common hallmark of FDs is chronic inflammation.Abnormal amount of ECM disturbs the original organ architecture leading to the decline of function.Although our knowledge is rapidly expanding, we still have neither a diagnostic tool to detect nor a drug to specifically target fibrosis.

View Article: PubMed Central - PubMed

Affiliation: MTA-SE, Pediatrics and Nephrology Research Group, Bokay Janos Street 53-54, Budapest 1083, Hungary ; 1st Department of Pediatrics, Semmelweis University, Bokay Janos Street 53-54, Budapest 1083, Hungary.

ABSTRACT
Importance of chronic fibroproliferative diseases (FDs) including pulmonary fibrosis, chronic kidney diseases, inflammatory bowel disease, and cardiovascular or liver fibrosis is rapidly increasing and they have become a major public health problem. According to some estimates about 45% of all deaths are attributed to FDs in the developed world. Independently of their etiology the common hallmark of FDs is chronic inflammation. Infiltrating immune cells, endothelial, epithelial, and other resident cells of the injured organ release an orchestra of inflammatory mediators, which stimulate the proliferation and excessive extracellular matrix (ECM) production of myofibroblasts, the effector cells of organ fibrosis. Abnormal amount of ECM disturbs the original organ architecture leading to the decline of function. Although our knowledge is rapidly expanding, we still have neither a diagnostic tool to detect nor a drug to specifically target fibrosis. Therefore, there is an urgent need for the more comprehensive understanding of the pathomechanism of fibrosis and development of novel diagnostic and therapeutic strategies. In the present review we provide an overview of the common key mediators of organ fibrosis highlighting the role of interleukin-10 (IL-10) cytokine family members (IL-10, IL-19, IL-20, IL-22, IL-24, and IL-26), which recently came into focus as tissue remodeling-related inflammatory cytokines.

No MeSH data available.


Related in: MedlinePlus

Hypothetical origin of myofibroblasts.
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Related In: Results  -  Collection


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fig1: Hypothetical origin of myofibroblasts.

Mentions: MFs, as the main effector cells of organ fibrosis, are α-smooth muscle actin (α-SMA) positive, spindle, or stellate-shaped cells lacking the epithelial or endothelial markers, such as cytokeratins or cluster of differentiation (CD) 31 [10, 11]. Although the origin of MFs is controversial, they may arise by the phenoconversion of different cell types including fibroblasts [12], pericytes [13], stellate [14], smooth muscle [15], epithelial [16], endothelial [17], and stem cells or circulating progenitors [18–20] (Figure 1). After their activation MFs proliferate and produce an excessive amount of different ECM components including fibrillar collagens including collagens I, III and glycoproteins such as fibronectin, fibrillin, elastin, and proteoglycans [10] and nonfibrillar collagens including collagen IV, a main component of the basal membranes [21]. However, the relative contribution of the different infiltrating and inherent cell types in the injured organ to the formation of MFs is still not clear.


Fibrosis Related Inflammatory Mediators: Role of the IL-10 Cytokine Family.

Sziksz E, Pap D, Lippai R, Béres NJ, Fekete A, Szabó AJ, Vannay Á - Mediators Inflamm. (2015)

Hypothetical origin of myofibroblasts.
© Copyright Policy - open-access
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC4495231&req=5

fig1: Hypothetical origin of myofibroblasts.
Mentions: MFs, as the main effector cells of organ fibrosis, are α-smooth muscle actin (α-SMA) positive, spindle, or stellate-shaped cells lacking the epithelial or endothelial markers, such as cytokeratins or cluster of differentiation (CD) 31 [10, 11]. Although the origin of MFs is controversial, they may arise by the phenoconversion of different cell types including fibroblasts [12], pericytes [13], stellate [14], smooth muscle [15], epithelial [16], endothelial [17], and stem cells or circulating progenitors [18–20] (Figure 1). After their activation MFs proliferate and produce an excessive amount of different ECM components including fibrillar collagens including collagens I, III and glycoproteins such as fibronectin, fibrillin, elastin, and proteoglycans [10] and nonfibrillar collagens including collagen IV, a main component of the basal membranes [21]. However, the relative contribution of the different infiltrating and inherent cell types in the injured organ to the formation of MFs is still not clear.

Bottom Line: Independently of their etiology the common hallmark of FDs is chronic inflammation.Abnormal amount of ECM disturbs the original organ architecture leading to the decline of function.Although our knowledge is rapidly expanding, we still have neither a diagnostic tool to detect nor a drug to specifically target fibrosis.

View Article: PubMed Central - PubMed

Affiliation: MTA-SE, Pediatrics and Nephrology Research Group, Bokay Janos Street 53-54, Budapest 1083, Hungary ; 1st Department of Pediatrics, Semmelweis University, Bokay Janos Street 53-54, Budapest 1083, Hungary.

ABSTRACT
Importance of chronic fibroproliferative diseases (FDs) including pulmonary fibrosis, chronic kidney diseases, inflammatory bowel disease, and cardiovascular or liver fibrosis is rapidly increasing and they have become a major public health problem. According to some estimates about 45% of all deaths are attributed to FDs in the developed world. Independently of their etiology the common hallmark of FDs is chronic inflammation. Infiltrating immune cells, endothelial, epithelial, and other resident cells of the injured organ release an orchestra of inflammatory mediators, which stimulate the proliferation and excessive extracellular matrix (ECM) production of myofibroblasts, the effector cells of organ fibrosis. Abnormal amount of ECM disturbs the original organ architecture leading to the decline of function. Although our knowledge is rapidly expanding, we still have neither a diagnostic tool to detect nor a drug to specifically target fibrosis. Therefore, there is an urgent need for the more comprehensive understanding of the pathomechanism of fibrosis and development of novel diagnostic and therapeutic strategies. In the present review we provide an overview of the common key mediators of organ fibrosis highlighting the role of interleukin-10 (IL-10) cytokine family members (IL-10, IL-19, IL-20, IL-22, IL-24, and IL-26), which recently came into focus as tissue remodeling-related inflammatory cytokines.

No MeSH data available.


Related in: MedlinePlus