Effects of inflammation on stem cells: together they strive?
Inflammation entails a complex set of defense mechanisms acting in concert to restore the homeostatic balance in organisms after damage or pathogen invasion. This immune response consists of the activity of various immune cells in a highly complex manner. Inflammation is a double-edged sword as it is reported to have both detrimental and beneficial consequences. In this review, we discuss the effects of inflammation on stem cell activity, focusing primarily on neural stem/progenitor cells in mammals and zebrafish. We also give a brief overview of the effects of inflammation on other stem cell compartments, exemplifying the positive and negative role of inflammation on stemness. The majority of the chronic diseases involve an unremitting phase of inflammation due to improper resolution of the initial pro-inflammatory response that impinges on the stem cell behavior. Thus, understanding the mechanisms of crosstalk between the inflammatory milieu and tissue-resident stem cells is an important basis for clinical efforts. Not only is it important to understand the effect of inflammation on stem cell activity for further defining the etiology of the diseases, but also better mechanistic understanding is essential to design regenerative therapies that aim at micromanipulating the inflammatory milieu to offset the negative effects and maximize the beneficial outcomes.
German Centre for Neurodegenerative Diseases (DZNE) Dresden within the Helmholtz Association, Dresden, Germany DFG-Center for Regenerative Therapies Dresden, Cluster of Excellence (CRTD) of the Technische Universität Dresden, Dresden, Germany caghan.kizil@dzne.de michael.brand@biotec.tu-dresden.de.
Caghan
C
Kizil
DFG-Center for Regenerative Therapies Dresden, Cluster of Excellence (CRTD) of the Technische Universität Dresden, Dresden, Germany.
Nikos
N
Kyritsis
DFG-Center for Regenerative Therapies Dresden, Cluster of Excellence (CRTD) of the Technische Universität Dresden, Dresden, Germany caghan.kizil@dzne.de michael.brand@biotec.tu-dresden.de.
Michael
M
Brand
D000209:Acute-Phase Proteins / Q000235:genetics / Q000378:metabolism; D000818:Animals; D049109:Cell Proliferation; D016207:Cytokines / Q000235:genetics / Q000378:metabolism; D005786:Gene Expression Regulation; D006801:Humans; D007249:Inflammation / Q000235:genetics / Q000378:metabolism* / Q000473:pathology; D009416:Nerve Regeneration / Q000502:physiology; D009419:Nerve Tissue Proteins / Q000235:genetics / Q000378:metabolism*; D009420:Nervous System / Q000378:metabolism* / Q000473:pathology; D058953:Neural Stem Cells / Q000378:metabolism* / Q000473:pathology; D015398:Signal Transduction; D055153:Stem Cell Niche / Q000235:genetics; D015027:Zebrafish
D000209:Acute-Phase Proteins; D016207:Cytokines; D009419:Nerve Tissue Proteins
disease; inflammation; neural stem cell; proliferation; regeneration