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Journals
Biomolecules
Special Issues
Inflammation as Target treatment for Chronic Diseases
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Inflammation as Target treatment for Chronic Diseases

A special issue of Biomolecules (ISSN 2218-273X). This special issue belongs to the section "Cellular Biochemistry".

Deadline for manuscript submissions: closed (31 March 2020) | Viewed by 14198

Special Issue Editors

Dr. Palanivel Ganesan

E-Mail Website
Guest Editor
Department of Integrated Bioscience-Biomedical Chemistry, Nanotechnology Research Center, College of Bio-medical and Health Science, Konkuk University Glocal campus, Chungju 27413, Korea
Interests: functional foods; nanotechnology; neuroinflammation; bioactive compounds; nanodelivery systems; phyto bioactive compounds; parkinsons
Special Issues, Collections and Topics in MDPI journals
Dr. Palanisamy Arulselvan

E-Mail Website
Guest Editor
Centre for Materials Engineering and Regenerative Medicine, Bharath Institute of Higher Education and Research, Chennai, Tamil Nadu, India
Interests: nanomedicine; cancer; natural products; pharmacology; inflammation

Special Issue Information

Dear Colleagues,

Inflammation is a process in which the immune system of our body generally responds to an infection or illness. It stimulates the expression of free radicals, cytokines, growth factors and chemokines inside the cells of essential organs (brain, liver, kidney, etc.), which further activates/inhibits several signaling pathways such as MAPK, NF-κB and STAT3, etc. The modulation of the signaling pathways and biomarkers leads to various non-communicable ailments such as type 2 diabetes, obesity, cancer, cardiovascular and other neurodegenerative disorders such as Parkinson’s and Alzheimer’s. Nowadays, several factors such as a sedentary life style, environmental conditions, microbial infections, chemical exposure and stress can turn acute inflammation into chronic inflammation. Up-regulating/down-regulating the altered biochemical pathways by targeting the inflammation with suitable drugs might contribute the eradication of various chronic diseases. Currently several bioactive compounds such as curcumin, quercetin, piperine and so on from natural sources are reported to play a vital role on the abolition of inflammation-linked chronic diseases. Nowadays, nanotechnology-based drug delivery systems are also applied in the treatment of inflammation-related chronic diseases by enhancing the bioavailability and kinetic parameters of the drugs. Thus, this Special Issue is focused on but not limited to articles covering inflammation-related chronic diseases.

This Special Issue is focused on but not limited to the following key topics:

  • Inflammation-based chronic diseases
  • Molecular pathways of chronic inflammation
  • Natural or synthetic compound-based therapy for neuro-inflammation
  • Drug delivery against inflammation such a biofilm, nano and micro-technology, etc.
  • Chemicals/toxins triggering inflammation
  • Biomolecules against inflammation
  • Cancer biology and inflammation

Dr. Palanivel Ganesan
Dr. Arulselvan Palanisamy
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Biomolecules is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • inflammation
  • bioactive compounds
  • chronic inflammation
  • nano-delivery
  • inflammatory pathways
  • diabetes
  • neuroinflammation
  • cancer
  • obesity
  • cardiovascular

Published Papers (3 papers)

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Research

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16 pages, 7223 KiB  
Article
Uric Acid Has Direct Proinflammatory Effects on Human Macrophages by Increasing Proinflammatory Mediators and Bacterial Phagocytosis Probably via URAT1
by Camilo P. Martínez-Reyes, Aarón N. Manjarrez-Reyna, Lucia A. Méndez-García, José A. Aguayo-Guerrero, Beatriz Aguirre-Sierra, Rafael Villalobos-Molina, Yolanda López-Vidal, Karen Bobadilla and Galileo Escobedo
Biomolecules 2020, 10(4), 576; https://doi.org/10.3390/biom10040576 - 09 Apr 2020
Cited by 17 | Viewed by 3684
Abstract
The relationship of uric acid with macrophages has not been fully elucidated. We investigated the effect of uric acid on the proinflammatory ability of human macrophages and then examined the possible molecular mechanism involved. Primary human monocytes were differentiated into macrophages for subsequent [...] Read more.
The relationship of uric acid with macrophages has not been fully elucidated. We investigated the effect of uric acid on the proinflammatory ability of human macrophages and then examined the possible molecular mechanism involved. Primary human monocytes were differentiated into macrophages for subsequent exposure to 0, 0.23, 0.45, or 0.9 mmol/L uric acid for 12 h, in the presence or absence of 1 mmol/L probenecid. Flow cytometry was used to measure proinflammatory marker production and phagocytic activity that was quantified as a percentage of GFP-labeled Escherichia coli positive macrophages. qPCR was used to measure the macrophage expression of the urate anion transporter 1 (URAT1). As compared to control cells, the production of tumor necrosis factor-alpha (TNF-alpha), toll-like receptor 4 (TLR4), and cluster of differentiation (CD) 11c was significantly increased by uric acid. In contrast, macrophages expressing CD206, CX3C-motif chemokine receptor 1 (CX3CR1), and C-C chemokine receptor type 2 (CCR2) were significantly reduced. Uric acid progressively increased macrophage phagocytic activity and downregulated URAT1 expression. Probenecid—a non-specific blocker of URAT1-dependent uric acid transport—inhibited both proinflammatory cytokine production and phagocytic activity in macrophages that were exposed to uric acid. These results suggest that uric acid has direct proinflammatory effects on macrophages possibly via URAT1. Full article
(This article belongs to the Special Issue Inflammation as Target treatment for Chronic Diseases)
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16 pages, 4378 KiB  
Article
An Adrenalectomy Mouse Model Reflecting Clinical Features for Chronic Fatigue Syndrome
by Jin-Seok Lee, Yoo-Jin Jeon, Samuel-Young Park and Chang-Gue Son
Biomolecules 2020, 10(1), 71; https://doi.org/10.3390/biom10010071 - 01 Jan 2020
Cited by 8 | Viewed by 4454
Abstract
Chronic fatigue syndrome (CFS) is one of the most intractable diseases and is characterized by severe central fatigue that impairs even daily activity. To date, the pathophysiological mechanisms are uncertain and no therapies exist. Therefore, a proper animal model reflecting the clinical features [...] Read more.
Chronic fatigue syndrome (CFS) is one of the most intractable diseases and is characterized by severe central fatigue that impairs even daily activity. To date, the pathophysiological mechanisms are uncertain and no therapies exist. Therefore, a proper animal model reflecting the clinical features of CFS is urgently required. We compared two CFS animal models most commonly used, by injection with lipopolysaccharide (LPS from Escherichia coli O111:B4) or polyinosinic: polycytidylic acid (poly I:C), along with bilateral adrenalectomy (ADX) as another possible model. Both LPS- and poly I:C-injected mice dominantly showed depressive behaviors, while ADX led to fatigue-like performances with high pain sensitivity. In brain tissues, LPS injection notably activated microglia and the 5-hydroxytryptamine (HT)1A receptor in the prefrontal cortex and hippocampus. Poly I:C-injection also remarkably activated the 5-HT transporter and 5-HT1A receptor with a reduction in serotonin levels in the brain. ADX particularly activated astrocytes and transforming growth factor beta (TGF-β) 1 in all brain regions. Our results revealed that LPS and poly I:C animal models approximate depressive disorder more closely than CFS. We suggest that ADX is a possible method for establishing a mouse model of CFS reflecting clinical features, especially in neuroendocrine system. Full article
(This article belongs to the Special Issue Inflammation as Target treatment for Chronic Diseases)
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Review

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19 pages, 2180 KiB  
Review
A Novel View of Human Helicobacter pylori Infections: Interplay between Microbiota and Beta-Defensins
by Raffaela Pero, Mariarita Brancaccio, Sonia Laneri, Margherita-Gabriella De Biasi, Barbara Lombardo and Olga Scudiero
Biomolecules 2019, 9(6), 237; https://doi.org/10.3390/biom9060237 - 18 Jun 2019
Cited by 41 | Viewed by 5599
Abstract
The gut microbiota is significantly involved in the preservation of the immune system of the host, protecting it against the pathogenic bacteria of the stomach. The correlation between gut microbiota and the host response supports human gastric homeostasis. Gut microbes may be shifted [...] Read more.
The gut microbiota is significantly involved in the preservation of the immune system of the host, protecting it against the pathogenic bacteria of the stomach. The correlation between gut microbiota and the host response supports human gastric homeostasis. Gut microbes may be shifted in Helicobacter pylori (Hp)-infected individuals to advance gastric inflammation and distinguished diseases. Particularly interesting is the establishment of cooperation between gut microbiota and antimicrobial peptides (AMPs) of the host in the gastrointestinal tract. AMPs have great importance in the innate immune reactions to Hp and participate in conservative co-evolution with an intricate microbiome. β-Defensins, a class of short, cationic, arginine-rich proteins belonging to the AMP group, are produced by epithelial and immunological cells. Their expression is enhanced during Hp infection. In this review, we discuss the impact of the gut microbiome on the host response, with particular regard to β-defensins in Hp-associated infections. In microbial infections, mostly in precancerous lesions induced by Hp infection, these modifications could lead to different outcomes. Full article
(This article belongs to the Special Issue Inflammation as Target treatment for Chronic Diseases)
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