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In vitro modulatory effects of electrical field on fibroblasts
Published in Ze Zhang, Mahmoud Rouabhia, Simon E. Moulton, Conductive Polymers, 2018
Fibroblast is a source of different cytokines and chemokines, such as IL-1β, IL-6, IL-8, IL-33, transforming growth factor β1 (TGFβ1), and CXC and CC chemokines (Feghali and Wright 1997; Gharaee-Kermani et al. 2012). These mediators have different roles. As an example, TGFβ promotes cell proliferation, migration, extracellular matrix production, and fibroblast differentiation to myofibroblasts. Inhibition of TGFβ secretion prevents fibrosis (Bonniaud et al. 2005). As another example, fibroblasts produce IL-1β, a potent pro-inflammatory cytokine (Feghali and Wright 1997). IL-1β is involved in the production of profibrotic cytokines such as PDGF and TGFβ. Fibroblasts play an important role in angiogenesis by producing VEGF, which acts on VEGF receptors expressed on endothelial cells to promote angiogenesis by stimulating mitogenesis and migration, for example (Kajihara et al. 2013; Newman et al. 2011). Fibroblasts regulate wound healing through the secretion of matrix metalloproteinases (MMPs), including MMP-1 and MMP-3 (Zhang et al. 2014). Growth factors such as FGF1 and FGF2 are required for fibroblast growth and interaction with neighbor cells. Growth factors and cytokines are therefore critical players in tissue repair (Powers et al. 2000; Komi-Kuramochi et al. 2005).
Pro- and Anti-Inflammatory Cytokine Signaling within 3D Tissue Models
Published in Karen J.L. Burg, Didier Dréau, Timothy Burg, Engineering 3D Tissue Test Systems, 2017
Stephen L. Rego, Tian McCann, Didier Dréau
Cytokines are soluble signaling peptides that elicit responses by binding to their cognate receptors (Leonard and Lin 2000). Although there are many different classification systems used for cytokines, most recently they have been grouped into superfamilies based on their structural and sequence similarities. The tumor necrosis factor (TNF)/TNF receptor superfamily includes TNFα, lymphotoxins, CD40L, and CD95. The TNF superfamily modulates immune cell phenotype, migration, or survival (stimulate apoptosis) (Locksley et al. 2001). The interleukin 1 (IL1)/IL1 receptor superfamily contains IL1α, IL1β, IL-receptor antagonist, IL-18, IL-33, and Toll-like receptors (TLRs). Those cytokines mediate host-defense function and microbial recognition (Pantschenko et al. 2003; Rifkin et al. 2005; Marshak-Rothstein 2006). In this chapter, cytokines are grouped functionally based on their ability to elicit (1) inflammatory immune responses or (2) anti-inflammatory (wound healing) immune responses.
Role of Histone Methyltransferase in Breast Cancer
Published in Meenu Gupta, Rachna Jain, Arun Solanki, Fadi Al-Turjman, Cancer Prediction for Industrial IoT 4.0: A Machine Learning Perspective, 2021
Surekha Manhas, Zaved Ahmed Khan
TGF-β makes it critical to express CD103 and IL-17A/F in Treg and Th17 cells by downregulation, the expression of GFI1 up to that extent [81]. Furthermore, it also inhibits CD73 and CD39 ectonucleotidase expressions [82]. For the activation reduction of methylation marks, lysine demethylae LSD1 recruitment is carried out by GFI1 to the mentioned genetic loci. Upon TGF-β stimulation, gene expression of GFI1 gets reduced, which allows the cellular differentiation of Treg and Th17 cells optimally. T cells that lack GFI1 display an increase in IL-17A production and an increase in the expression of FOXP3 in response to transforming growth factor-beta (TGF-β) that shows similarities with G9a-deficient lymphocytes, specifically T cells [14]. As dysregulated IL-17A expression was observed in Th2 cells with a lack of G9a, the same was observed with GFI1, which is basically required to silence the expression of IL-17A found in lymphocytes [15,81]. Consequently, it is very interesting to specifically hypothesize about interactions between GFI1–G9a. Specifically, they are more critical in restraining the cellular-based responses of Treg cells along with Th17 cells, resulting in repression in the transcriptional mechanism that leads to epigenetic gene inactivation or gene silencing. For the type 11 innate lymphoid cell (ILC2) development and cellular functions, GFI1 usually acts as an important potent regulator [83]. GFI1 expression is correlated to the ST2-based receptor IL-33 expression (Il1rl1, ST2), along with the expression of GATA3. GFI1 loss in ILC2s results in the impairment of GATA3 expressions and IL-17A expression upregulation, too. It is reminiscent of the specified G9a role in ILC biology, where G9a is needed to repress the actions of genes specifically related to ILC during the development of ILC2 [69], although, unlike T cells, the GFI1 effect and potentially G9a seem to be reliant on methyltransferase-dependent repressive activity of the specific gene. By analyzing all the available dates, which suggest G9a–GFI1 are critical to performing functions in ILCs and T cells, future studies defining these interactions on the basis of molecular level might open new ways for novel therapeutics that might inhibit the dysregulated responses of Th2 cell-related to other diseases like allergies and asthma.
Early life exposure to particulate matter and childhood asthma in Beijing, China: a case–control study
Published in International Journal of Environmental Health Research, 2022
Meimei Xu, Mingjun Shao, Yuzhi Chen, Chuanhe Liu
Few studies have examined the effect of exposure to particulate matter during specific periods of pregnancy on childhood asthma. A study conducted in Boston (MA, USA) examined the effect of weekly exposures to PM2.5 during pregnancy on the development of asthma among 736 full-term children and found that PM2.5 exposure during the second trimester was associated with childhood asthma, but only among boys (Hsu et al. 2015; Lee et al. 2018). In a study conducted in Ontario, Canada among 761 172 births, exposure to increased levels of PM2.5 during the second trimester was associated with the development of asthma (Lavigne et al. 2018). Our study also found that the sensitive window of PM2.5 exposure during the pregnancy was the second trimester, which is consistent with the prior literature. The identified sensitive window of PM2.5 exposure was the period in which the canalicular stages of fetal lung development occurred (Kajekar 2007; Lee et al. 2018). In this stage, perturbation may affect distal airway formation and proximal to distal airway epithelial differentiation that implicate in asthma. Airway epithelium is a major source of innate immune molecules (IL-25, IL-33, and thymic stromal lymphopoietin) that could mediate inflammatory airway diseases such as asthma (Moffatt et al. 2010; Yao et al. 2016).
Genetic variants affecting chemical mediated skin immunotoxicity
Published in Journal of Toxicology and Environmental Health, Part B, 2022
Isisdoris Rodrigues de Souza, Patrícia Savio de Araujo-Souza, Daniela Morais Leme
Th2 cells are the primary IL-31 source in the skin (Saleem et al. 2017). However, this cytokine is also expressed by keratinocytes, fibroblasts, DCs, monocytes/macrophages, mast cells, cutaneous lymphocyte antigen (CLA)+ CD45RO+ memory T cells (Akdis et al. 2016; Bilsborough et al. 2006), and activated eosinophils (Saleem et al. 2017). IL-31 may be released after skin exposure to pathogens or following physical damage to skin tissues by UVB rays, H2O2, or staphylococcus enterotoxin B (Cheung et al. 2010; Cornelissen et al. 2011; Kunsleben et al. 2015; Sonkoly et al. 2006). After skin tissue damage occurs, keratinocytes release IL-33 that, in synergy with IL-4, upregulates IL-31 expression through the NF-ĸB pathway (Maier et al. 2014). Although, in AD, nonlesional skin also express elevated IL-31 mRNA levels (Sonkoly et al. 2006). IL-31 binds to heterodimeric IL-31 receptor A (IL-31RA) and the oncostatin M receptor (OSMR) – a receptor that enhances IL-31 binding affinity to IL-31RA (Akdis et al. 2016; Hermanns 2015). These receptors are found in T cells, keratinocytes, DCs, eosinophils, basophils, macrophages, activated monocytes, and dorsal root ganglia cells (DRG), sensory neurons responsible for the induction of itching (Akdis et al. 2016; Gibbs, Patsinakidis, and Raap 2019).
Exposure to lead on expression levels of brain immunoglobulins, inflammatory cytokines, and brain-derived neurotropic factor in fetal and postnatal mice with autism-like characteristics
Published in Journal of Toxicology and Environmental Health, Part A, 2021
KyeongMin Shin, GyeongDong Lim, Young-Seoub Hong, SoNam Kim, SoRyeon Hwang, JaeHee Lee, SoJung Sin, AhRang Cho, YeonGyeong Kim, Ravi Gautam, JiHun Jo, Manju Acharya, Anju Maharjan, DaEun Lee, Pramod B. K C, ChangYul Kim, Yong Heo, Hyoung-Ah Kim
IL-33 is a key cytokine that plays a predominant role in TH2 immunity (Drake and Kita 2017; Shen et al. 2020). IL-33 expression in postnatal brains was significantly higher in BTBR-C compared to FVB-C mice. Brain IL-33 expression was also elevated in BTBR relative to C57BL/6 animals (Heo et al. 2011). Pb exposure did not significantly influence brain IL-33 levels in BTBR mice.