scholarly journals microRNA-210 and microRNA-3570 Negatively Regulate NF-κB-Mediated Inflammatory Responses by Targeting RIPK2 in Teleost Fish

2021 ◽  
Vol 12 ◽  
Author(s):  
Hui Su ◽  
Renjie Chang ◽  
Weiwei Zheng ◽  
Yuena Sun ◽  
Tianjun Xu
Keyword(s):  
Immune Response ◽  
Signaling Pathway ◽  
Innate Immune Response ◽  
Inflammatory Responses ◽  
Innate Immune ◽  
Regulatory Role ◽  
Inflammatory Cytokine Production ◽  
Immune Genes ◽  
Lower Vertebrates ◽  
Antimicrobial Immunity

Pathogen infection can cause the production of inflammatory cytokines, which are key mediators that cause the host’s innate immune response. Therefore, proper regulation of immune genes associated with inflammation is essential for immune response. Among them, microRNAs (miRNAs) as gene regulator have been widely reported to be involved in the innate immune response of mammals. However, the regulatory network in which miRNAs are involved in the development of inflammation is largely unknown in lower vertebrates. Here, we identified two miRNAs from miiuy croaker (Miichthys miiuy), miR-210 and miR-3570, which play a negative regulatory role in host antibacterial immunity. We found that the expressions of miR-210 and miR-3570 were significantly upregulated under the stimulation of Gram-negative bacterium vibrio harveyi and LPS (lipopolysaccharide). Induced miR-210 and miR-3570 inhibit inflammatory cytokine production by targeting RIPK2, thereby avoiding excessive inflammation. In particular, we found that miR-210 and miR-3570 negatively regulate antimicrobial immunity by regulating the RIPK2-mediated NF-κB signaling pathway. The collective results indicated that both miRNAs are used as negative feedback regulators to regulate RIPK2-mediated NF-κB signaling pathway and thus play a regulatory role in bacteria-induced inflammatory response.

Differential modulation of innate immune response by epinephrine and estradiol

2017 ◽  
Vol 30 (3) ◽  
Author(s):  
Sona Margaryan ◽  
Armenuhi Hyusyan ◽  
Anush Martirosyan ◽  
Shushan Sargsian ◽  
Gayane Manukyan
Keyword(s):  
Immune Response ◽  
Innate Immune Response ◽  
Inflammatory Responses ◽  
Innate Immune ◽  
Dependent Manner ◽  
Induced Expression ◽  
Short Term Exposure ◽  
Tnf Α ◽  
Vitro Effect ◽  
Dose Dependent

AbstractBackgroundAlthough it is widely accepted that catecholamines and estrogens influence immunity and have consequences for health, their effect on innate immunity (e.g. monocytes and neutrophils) is still not fully investigated.Materials and methodsOur study aimed to analyze the production of tumor necrosis factor (TNF)-α, interleukin (IL)-1β, monocyte chemoattractant protein (MCP)-1 and IL-8 by whole blood cells following short-term exposure to epinephrine (Epi) and 17β-estradiol (E2) in the presence or absence of lipopolysaccharide (LPS). We also evaluated the in vitro effect of these hormones on expression of β2 integrin (CD11b/CD18) and L-selectin (CD62L) by circulating neutrophils and monocytes in the blood of healthy subjects.ResultsEpi has shown a potential to modulate the production of pro-inflammatory mediators. Its exposure resulted in significantly increased production of IL-8 in a dose-dependent manner. On the contrary, a dose-dependent suppression of LPS-induced production of IL-1β, IL-8, and MCP-1 by Epi was observed. In neutrophils, a modest rise in CD11b expression was observed after Epi exposure. Simultaneously, Epi suppressed LPS-induced expression of CD11b and CD18. In monocytes, Epi suppressed LPS-induced expression of C11b. E2 inhibited LPS-induced TNF-α production and caused a significant decrease in CD62L expression in both cell populations. No significant changes were observed after double exposure of cells with Epi and E2.ConclusionsThus, our results show that Epi and E2 differentially modulate the innate immune response and have a dual effect on cytokine modulation. The findings suggest that the observed immunoregulatory role of Epi and E2 may influence the outcome in endotoxin responses and can be critical in the regulation of inflammatory responses.

scholarly journals Multi-walled carbon nanotubes enhanced fungal colonization and suppressed innate immune response to fungal infection in nematodes

2016 ◽  
Vol 5 (2) ◽  
pp. 492-499 ◽  
Author(s):  
Shumaila Shakoor ◽  
Lingmei Sun ◽  
Dayong Wang
Keyword(s):  
Carbon Nanotubes ◽  
Immune Response ◽  
Fungal Infection ◽  
Signaling Pathway ◽  
Innate Immune Response ◽  
Mapk Signaling ◽  
Innate Immune ◽  
Fungal Colonization ◽  
Multi Walled Carbon Nanotubes ◽  
Walled Carbon Nanotubes

MWCNTs require the involvement of p38 MAPK signaling pathway to enhance toxicity of fungal infection.

The Regulatory Role of Dendritic Cells in the Innate Immune Response

2014 ◽  
pp. 95-109 ◽  
Author(s):  
F. Granucci ◽  
S. Feau ◽  
I. Zanoni ◽  
G. Raimondi ◽  
N. Pavelka ◽  
...  
Keyword(s):  
Immune Response ◽  
Dendritic Cells ◽  
Innate Immune Response ◽  
Innate Immune ◽  
Regulatory Role

scholarly journals The Threshold Effect: Lipopolysaccharide-Induced Inflammatory Responses in Primary Macrophages Are Differentially Regulated in an iRhom2-Dependent Manner

2021 ◽  
Vol 10 ◽  
Author(s):  
Joseph Skurski ◽  
Garima Dixit ◽  
Carl P. Blobel ◽  
Priya D. Issuree ◽  
Thorsten Maretzky
Keyword(s):  
Immune Response ◽  
Innate Immune Response ◽  
Immune Cells ◽  
Regulatory Mechanism ◽  
Inflammatory Responses ◽  
Genetic Model ◽  
Innate Immune ◽  
High Dose ◽  
Dependent Manner ◽  
Low Levels

A well-controlled innate immune response is characterized by a rapid yet self-limiting inflammatory response. Although much is known about the range of inflammatory stimuli capable of triggering an innate immune response, the mechanisms which govern the degree of inflammation induced by inflammatory insults and the mechanisms in place to reset or maintain homeostasis are poorly understood. Tumor necrosis factor (TNF) is a potent early response pro-inflammatory cytokine produced by immune cells following a broad range of insults spanning autoimmunity and metabolic diseases to pathogenic infections. Previous studies have shown that a disintegrin and metalloproteinase (ADAM) 17 controls the release of soluble TNF and epidermal growth factor receptor signaling. Utilizing a genetic model of ADAM17 deficiency through the deletion of its regulator, the inactive rhomboid 2 (iRhom2), we show that loss of ADAM17 activity in innate immune cells leads to decreased expression of various cytokines in response to low levels of pathogen-associated molecular pattern (PAMP) stimulation but not at high-dose stimulation. In addition, TNF receptor (TNFR) 1/2-deficient bone marrow-derived macrophages yielded significantly reduced TNF expression following low levels of PAMP stimulation, suggesting that signaling through the TNFRs in immune cells drives a feed-forward regulatory mechanism wherein low levels of TNF allow sustained enhancement of TNF expression in an iRhom2/ADAM17-dependent manner. Thus, we demonstrate that inflammatory expression of TNF and IL1β is differentially regulated following high or low doses of PAMP stimulation, invoking the activation of a previously unknown regulatory mechanism of inflammation.

scholarly journals Inflammation drives alternative first exon usage to regulate immune genes including a novel iron regulated isoform of Aim2

eLife ◽  
2021 ◽  
Vol 10 ◽  
Author(s):  
Elektra Kantzari Robinson ◽  
Pratibha Jagannatha ◽  
Sergio Covarrubias ◽  
Matthew Cattle ◽  
Valeriya Smaliy ◽  
...  
Keyword(s):  
Immune Response ◽  
Gene Regulation ◽  
Innate Immune Response ◽  
Translational Regulation ◽  
Mrna Translation ◽  
Innate Immune ◽  
Immune Genes ◽  
Transcription Start Sites ◽  
Oxford Nanopore ◽  
Responsive Element

Determining the layers of gene regulation within the innate immune response is critical to our understanding of the cellular responses to infection and dysregulation in disease. We identified a conserved mechanism of gene regulation in human and mouse via changes in alternative first exon (AFE) usage following inflammation, resulting in changes to isoform usage. Of these AFE events, we identified 50 unannotated transcription start sites (TSS) in mice using Oxford Nanopore native RNA sequencing, one of which is the cytosolic receptor for dsDNA and known inflammatory inducible gene, Aim2. We show that this unannotated AFE isoform of Aim2 is the predominant isoform transcribed during inflammation and contains an iron-responsive element in its 5′UTR enabling mRNA translation to be regulated by iron levels. This work highlights the importance of examining alternative isoform changes and translational regulation in the innate immune response and uncovers novel regulatory mechanisms of Aim2.

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