Signaling Pathways in Alcohol Induced Inflammation

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cell Signaling".

Deadline for manuscript submissions: closed (30 July 2021) | Viewed by 3576

Special Issue Editor


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Guest Editor
Department of Physiology, College of Medicine, University of Tennessee Health Science Center, Memphis, TN 38163, USA
Interests: gut-liver-brain axis; microbiota; metagenomics; stress; ionization radiation; fetal alcohol

Special Issue Information

Dear Colleagues,

Acute and chronic alcohol exposure cause the increased production of reactive oxygen species (ROS) in cells; eventually, it associates with the state of oxidative stress and induces cell damage and death. Excessive alcohol consumption plays a notorious role in instigating inflammation in multiple organs, including vital organs. Chronic alcoholism results in liver inflammation and damage. It is necessary to explore the liver cell types involved in alcohol-mediated liver inflammation, oxidative stress leading to chronic hepatic ailments, as well as its pathogenesis, which involves various intracellular signaling pathways in different cell types. Ample research studies evidently show that the consumption of alcohol induces inflammation in the brain, acute or chronic, long-term alterations in brain functions, and contributes to neurodegeneration. Alcohol-induced neuroinflammation is the prime cause of intercellular and intracellular changes in the brain and, hence, molecular changes in the central nervous system. Alcohol disrupts the blood–brain barrier and affects brain functions. The gut microbiome also plays an important role in various neurological disorders and alcohol-induced inflammation. It is well known that the consumption of alcohol enhances gut-permeability and causes dysfunction, resulting in inflammation in the gastrointestinal tract. In other words, alcohol induces gut dysbiosis and causes endotoxemia, i.e., increased level of lipopolysaccharides (LPS). LPS binds to the TLR4 and triggers downstream signaling, ultimately increasing the inflammatory cytokines and eventually leading to organ damage. Therefore, it is important to understand how gut dysbiosis influences receptor-mediated signaling and affects brain functions. It is equally important to know the salient signaling pathways of alcohol-induced liver inflammation that apparently result in chronic hepatic diseases. This Special Issue aims to reveal the important signaling pathways in alcohol-induced inflammation. I am certain that this section will encompass the outstanding findings from scholarly  researchers in this area and will benefit the audience and the related science fraternity. We look forward to your significant contributions to uncover underlying signaling processes.

Dr. Pradeep K. Shukla
Guest Editor

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Keywords

  • alcohol
  • liver
  • inflammation
  • neurodegeneration
  • gut–brain axis
  • signaling pathways

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Published Papers (1 paper)

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Research

10 pages, 2957 KiB  
Article
Sex-Specific Whole-Transcriptome Analysis in the Cerebral Cortex of FAE Offspring
by Nitish K. Mishra, Pulastya Shrinath, Radhakrishna Rao and Pradeep K. Shukla
Cells 2023, 12(2), 328; https://doi.org/10.3390/cells12020328 - 15 Jan 2023
Cited by 4 | Viewed by 2955
Abstract
Fetal alcohol spectrum disorders (FASDs) are associated with systemic inflammation and neurodevelopmental abnormalities. Several candidate genes were found to be associated with fetal alcohol exposure (FAE)-associated behaviors, but a sex-specific complete transcriptomic analysis was not performed at the adult stage. Recent studies have [...] Read more.
Fetal alcohol spectrum disorders (FASDs) are associated with systemic inflammation and neurodevelopmental abnormalities. Several candidate genes were found to be associated with fetal alcohol exposure (FAE)-associated behaviors, but a sex-specific complete transcriptomic analysis was not performed at the adult stage. Recent studies have shown that they are regulated at the developmental stage. However, the sex-specific role of RNA in FAE offspring brain development and function has not been studied yet. Here, we carried out the first systematic RNA profiling by utilizing a high-throughput transcriptomic (RNA-seq) approach in response to FAE in the brain cortex of male and female offspring at adulthood (P60). Our RNA-seq data analysis suggests that the changes in RNA expression in response to FAE are marked sex-specific. We show that the genes Muc3a, Pttg1, Rec8, Clcnka, Capn11, and pnp2 exhibit significantly higher expression in the male offspring than in the female offspring at P60. FAE female mouse brain sequencing data also show an increased expression of Eno1, Tpm3, and Pcdhb2 compared to male offspring. We performed a pathway analysis using a commercial software package (Ingenuity Pathway Analysis). We found that the sex-specific top regulator genes (Rictor, Gaba, Fmri, Mlxipl) are highly associated with eIF2 (translation initiation), synaptogenesis (the formation of synapses between neurons in the nervous system), sirtuin (metabolic regulation), and estrogen receptor (involved in obesity, aging, and cancer) signaling. Taken together, our transcriptomic results demonstrate that FAE differentially alters RNA expression in the adult brain in a sex-specific manner. Full article
(This article belongs to the Special Issue Signaling Pathways in Alcohol Induced Inflammation)
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