scholarly journals The Strand Specific Regulation of miR-155-3p in Response to Lipopolysaccharide and Interleukin-10 Stimulation Requires FUBP1 Protein

2021 ◽  
Author(s):  
Jeff S. J. Yoon ◽  
Abdulwadood Baksh ◽  
Thomas C. Chamberlain ◽  
Alice L-F. Mui
Keyword(s):  
Inflammatory Cytokine ◽  
Inflammatory Responses ◽  
Interleukin 10 ◽  
Activated Macrophages ◽  
Anti Inflammatory ◽  
Specific Regulation ◽  
Anti Inflammatory Cytokine

MicroRNA-155 (miR-155) expression promotes inflammatory responses in macrophages. Activation of macrophages with lipopolysaccharide (LPS) elevates miR-155, while the anti-inflammatory cytokine interleukin-10 (IL10) reduces miR-155 levels. MiR-155 exists in two forms, miR-155-5p and miR-155-3p, produced from the precursor of miR-155 (pre-miR-155). MiR-155-5p is the most abundant strand in activated macrophages, but in response to LPS, the miR-155-3p level is upregulated first, followed by miR-155-5p later. We have previously identified CELF2 protein which interacts with pre-miR-155 and impairs miR-155-5p expression. We now show that CELF2 only regulates the miR-155-5p expression and that another protein FUBP1 controls miR-155-3p levels in response to LPS and IL10.

Time course of pro- and anti-inflammatory cytokine levels in patients with burns—Prognostic value of interleukin-10

Burns ◽  
2010 ◽  
Vol 36 (4) ◽  
pp. 483-494 ◽  
Author(s):  
C. Csontos ◽  
V. Foldi ◽  
L. Pálinkas ◽  
L. Bogar ◽  
E. Röth ◽  
...  
Keyword(s):  
Prognostic Value ◽  
Inflammatory Cytokine ◽  
Time Course ◽  
Interleukin 10 ◽  
Cytokine Levels ◽  
Anti Inflammatory ◽  
Anti Inflammatory Cytokine

Selective excretion of anti-inflammatory cytokine Interleukin-10 in a superantigen-inducing neonatal infectious disease

Cytokine ◽  
2009 ◽  
Vol 45 (1) ◽  
pp. 39-43 ◽  
Author(s):  
Naoto Takahashi ◽  
Hisaya Hasegawa ◽  
Mami Komiyama ◽  
Takehiro Ohki ◽  
Yukari Yada ◽  
...  
Keyword(s):  
Infectious Disease ◽  
Inflammatory Cytokine ◽  
Interleukin 10 ◽  
Anti Inflammatory ◽  
Anti Inflammatory Cytokine

scholarly journals An emerging role for the anti-inflammatory cytokine interleukin-10 in dengue virus infection

2013 ◽  
Vol 20 (1) ◽  
pp. 40 ◽  
Author(s):  
Tsung-Ting Tsai ◽  
Yi-Jui Chuang ◽  
Yee-Shin Lin ◽  
Shu-Wen Wan ◽  
Chia-Ling Chen ◽  
...  
Keyword(s):  
Virus Infection ◽  
Dengue Virus ◽  
Inflammatory Cytokine ◽  
Interleukin 10 ◽  
Dengue Virus Infection ◽  
Anti Inflammatory ◽  
Anti Inflammatory Cytokine

scholarly journals IL-10 based immunomodulation initiated at birth extends lifespan in a familial mouse model of amyotrophic lateral sclerosis

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Michael R. Strickland ◽  
Kristen R. Ibanez ◽  
Mariya Yaroshenko ◽  
Carolina Ceballos Diaz ◽  
David R. Borchelt ◽  
...  
Keyword(s):  
Amyotrophic Lateral Sclerosis ◽  
Mouse Model ◽  
Chemokine Receptor ◽  
Inflammatory Cytokine ◽  
Disease Onset ◽  
Interleukin 10 ◽  
Inflammatory Chemokines ◽  
Anti Inflammatory ◽  
Anti Inflammatory Cytokine ◽  
Lateral Sclerosis

AbstractInflammatory signaling is thought to modulate the neurodegenerative cascade in amyotrophic lateral sclerosis (ALS). We have previously shown that expression of Interleukin-10 (IL-10), a classical anti-inflammatory cytokine, extends lifespan in the SOD1-G93A mouse model of familial ALS. Here we test whether co-expression of the decoy chemokine receptor M3, that can scavenge inflammatory chemokines, augments the efficacy of IL-10. We found that recombinant adeno-associated virus (AAV)-mediated expression of IL-10, alone, or in combination with M3, resulted in modest extension of lifespan relative to control SOD1-G93A cohort. Interestingly neither AAV-M3 alone nor AAV-IL-10 + AAV-M3 extend survival beyond that of the AAV-IL-10 alone cohort. Focused transcriptomic analysis revealed induction of innate immunity and phagocytotic pathways in presymptomatic SOD1-G93A mice expressing IL-10 + M3 or IL-10 alone. Further, while IL-10 expression increased microglial burden, the IL-10 + M3 group showed lower microglial burden, suggesting that M3 can successfully lower microgliosis before disease onset. Our data demonstrates that over-expression of an anti-inflammatory cytokine and a decoy chemokine receptor can modulate inflammatory processes in SOD1-G93A mice, modestly delaying the age to paralysis. This suggests that multiple inflammatory pathways can be targeted simultaneously in neurodegenerative disease and supports consideration of adapting these approaches to treatment of ALS and related disorders.

scholarly journals Prototypical anti-inflammatory cytokine IL-10 prevents loss of IGF-I-induced myogenin protein expression caused by IL-1β

2008 ◽  
Vol 294 (4) ◽  
pp. E709-E718 ◽  
Author(s):  
Klemen Strle ◽  
Robert H. McCusker ◽  
Rodney W. Johnson ◽  
Samantha M. Zunich ◽  
Robert Dantzer ◽  
...  
Keyword(s):  
Inflammatory Cytokine ◽  
Muscle Wasting ◽  
Inflammatory Responses ◽  
Mapk Signaling ◽  
Protective Role ◽  
Igf I ◽  
Anti Inflammatory ◽  
Kinase Pathway ◽  
Anti Inflammatory Cytokine

Prolonged and excessive inflammation is implicated in resistance to the biological actions of IGF-I and contributes to the pathophysiology of neurodegenerative, metabolic, and muscle-wasting disorders. IL-10 is a critical anti-inflammatory cytokine that restrains inflammatory responses in macrophages and T cells by inhibiting cytokine and chemokine synthesis and reducing expression of their receptors. Here we demonstrate that IL-10 plays a protective role in nonhematopoietic cells by suppressing the ability of exogenous IL-1β to inhibit IGF-I-induced myogenin and myosin heavy chain expression in myoblasts. This action of IL-10 is not caused by impairment of IL-1β-induced synthesis of IL-6 or the ability of IL-1β to activate two members of the MAPK family, ERK1/2 and p38. Instead, this newly defined protective role of IL-10 occurs by specific reversal of IL-1β activation of the JNK kinase pathway. IL-10 blocks IL-1β-induced phosphorylation of JNK, but not ERK1/2 or p38, indicating that only the JNK component of the IL-1β-induced MAPK signaling pathway is targeted by IL-10. This conclusion is supported by the finding that a specific JNK inhibitor acts similarly to IL-10 to restore IGF-I-induced myogenin expression, which is suppressed by IL-1β. Collectively, these data demonstrate that IL-10 acts in a novel, nonclassical, protective manner in nonhematopoietic cells to inhibit the IL-1β receptor-induced JNK kinase pathway, resulting in prevention of IGF-I resistance.

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