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Gut Microbiota and Chronic Diseases
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Gut Microbiota and Chronic Diseases

A special issue of Applied Sciences (ISSN 2076-3417). This special issue belongs to the section "Applied Microbiology".

Deadline for manuscript submissions: closed (10 May 2023) | Viewed by 8533

Special Issue Editors

Dr. Kaijian Hou

E-Mail Website
Guest Editor
School of Nursing, Anhui University of Chinese Medicine, Hefei 230001, China
Interests: FM; microorganism; gut microbiota; chronic diseases
Dr. Barkat Khan

E-Mail Website
Guest Editor
Faculty of Pharmacy, Gomal University, Dera Ismail Khan, Pakistan
Interests: cosmeceuticals; skin formulations; biophysical evaluation of skin formulations; rheology; transdermal patches; emulgels
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Prediction and intervention of risk factors for chronic noncommunicable diseases are an important issue and previous studies have focused on environmental, genetic, and psychosocial factors. Gut microbiota, known as the second genome of the host, have been shown to play an important role in the development of a variety of chronic diseases, including but not limited to inflammatory bowel disease, neoplasms, cardiovascular disease, immune-related diseases, and psychiatric and neurological-related disorders.

Gut microbiota influence the development of chronic diseases through multiple pathways, including small-molecule metabolites, cell wall components, and direct interactions with live bacteria. Further understanding of the association between gut microbiota composition and chronic diseases in multiple countries and regions will help to explore the role of intestinal flora in chronic diseases and provide useful clues for further research.

This Special Issue is dedicated to exploring new evidence on the association between gut microbiota and chronic diseases.

The topics discussed in this Special Issue will not only focus on the correlation of gut microbiota composition to chronic diseases, but will also further focus on and support the exploration of validation studies of gut microbiota in animals or humans and welcome the related molecular mechanism studies.

Dr. Kaijian Hou
Dr. Barkat Khan
Guest Editors

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Keywords

  • chronic noncommunicable diseases
  • gut microbiota
  • molecular mechanisms
  • intestinal microecology
  • tumors
  • inflammatory bowel disease
  • immune-related diseases
  • psychiatric disorders

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Published Papers (3 papers)

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Research

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14 pages, 2696 KiB  
Communication
Development of a Simple Protocol for Zymogram-Based Isolation and Characterization of Gingipains from Porphyromonas gingivalis: The Causative Agent of Periodontitis
by Eng Sze Wei, Ramasamy Kavitha, Mohammad Auwal Sa’ad, Pattabhiraman Lalitha, Neeraj Kumar Fuloria, Manickam Ravichandran and Shivkanya Fuloria
Appl. Sci. 2023, 13(7), 4314; https://doi.org/10.3390/app13074314 - 29 Mar 2023
Cited by 2 | Viewed by 1854
Abstract
Gingipains (RgpA, RgpB, and Kgp) are major virulence factors of the periodontitis-causing bacterium Porphyromonas gingivalis. Isolation of gingipains from the crude protein sample of P. gingivalis is critical for studying the underlying invasion mechanism that contributes to periodontitis, Alzheimer’s disease, and cardiovascular [...] Read more.
Gingipains (RgpA, RgpB, and Kgp) are major virulence factors of the periodontitis-causing bacterium Porphyromonas gingivalis. Isolation of gingipains from the crude protein sample of P. gingivalis is critical for studying the underlying invasion mechanism that contributes to periodontitis, Alzheimer’s disease, and cardiovascular disease (CVD). Chromatographic processes and molecular cloning are two standard techniques often used for gingipains isolation, which are time-consuming and costly. In this study, considerably easier methods based on passive-mediated diffusion gel elution and gelatin zymogram were used to isolate and characterize gingipains. Importantly, proteins eluted from Native-PAGE showed enzymatic activity for both Rgp and Kgp. In gelatin zymography, the proteins with a molecular size of ~50 kDa and above 245 kDa were suggested as arginine-specific gingipains. The passive diffusion-mediated gel elution method is a simpler technique to isolate gingipains from crude protein samples of P. gingivalis. By using covalent and highly specific gingipain inhibitors, gelatin zymography enabled an individual characterization of gingipain activity and inhibition. Finally, this protocol can be easily extended by adding the isoelectric focusing to further improve the protein separation and characterization. Full article
(This article belongs to the Special Issue Gut Microbiota and Chronic Diseases)
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12 pages, 2686 KiB  
Article
Comparative Analysis of the Effect of Different Concentrations of Dextran Sodium Sulfate on the Severity and Extent of Inflammation in Experimental Ulcerative Colitis
by Abdulmajeed G. Almutary, Abdullah M. Alnuqaydan, Saleh A. Almatroodi and Murtaza M. Tambuwala
Appl. Sci. 2023, 13(5), 3233; https://doi.org/10.3390/app13053233 - 2 Mar 2023
Cited by 6 | Viewed by 2077
Abstract
Several chemicals, such as dextran sulfate sodium (DSS), oxazolone, acetic acid, and trinitrobenzene sulphonic acid (TNBS), have been used for establishing animal models of ulcerative colitis. These animal models help us to study or explore several factors involved in the etiology or pathogenesis [...] Read more.
Several chemicals, such as dextran sulfate sodium (DSS), oxazolone, acetic acid, and trinitrobenzene sulphonic acid (TNBS), have been used for establishing animal models of ulcerative colitis. These animal models help us to study or explore several factors involved in the etiology or pathogenesis of ulcerative colitis. They are also useful tools to design and develop effective drug delivery strategies. DSS is the most widely used tool to induce colitis in animals. The model of ulcerative colitis developed by this method effectively mimics the colitis condition in humans. The amount of DSS in drinking water can be adjusted to control the severity of colitis, such as acute or chronic inflammation. However, a miscalculation in the amount of DSS produces severe inflammation, which may lead to the death of mice. DSS has been shown to rupture the epithelial lining and induce infiltration of inflammatory markers such as TNF, interferons, and interleukins. The current study aims to study the effects of different amounts of DSS on weight loss, changes in colon length, and histological scoring. Furthermore, the main objective of this study was to find an optimum concentration of DSS to establish a mouse model for ulcerative colitis. Based on the disease index, weight loss, bleeding, histological studies, and colon length, 2.5% w/v DSS for 7 days in water was found to be adequate for the DSS-induced colitis model for a moderate level of colitis, and 3.5% w/v DSS could be used to study severe experimental colitis. Full article
(This article belongs to the Special Issue Gut Microbiota and Chronic Diseases)
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Review

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33 pages, 2645 KiB  
Review
Neuromyelitis Optica Spectrum Disorders: Clinical Perspectives, Molecular Mechanisms, and Treatments
by Subramanian Thangaleela, Bhagavathi Sundaram Sivamaruthi, Arumugam Radha, Periyanaina Kesika and Chaiyavat Chaiyasut
Appl. Sci. 2023, 13(8), 5029; https://doi.org/10.3390/app13085029 - 17 Apr 2023
Cited by 2 | Viewed by 3187
Abstract
Neuromyelitis optica (NMO) is a rare autoimmune inflammatory disorder affecting the central nervous system (CNS), specifically the optic nerve and the spinal cord, with severe clinical manifestations, including optic neuritis (ON) and transverse myelitis. Initially, NMO was wrongly understood as a condition related [...] Read more.
Neuromyelitis optica (NMO) is a rare autoimmune inflammatory disorder affecting the central nervous system (CNS), specifically the optic nerve and the spinal cord, with severe clinical manifestations, including optic neuritis (ON) and transverse myelitis. Initially, NMO was wrongly understood as a condition related to multiple sclerosis (MS), due to a few similar clinical and radiological features, until the discovery of the AQP4 antibody (NMO-IgG/AQP4-ab). Various etiological factors, such as genetic-environmental factors, medication, low levels of vitamins, and others, contribute to the initiation of NMO pathogenesis. The autoantibodies against AQP4 target the AQP4 channel at the blood–brain barrier (BBB) of the astrocyte end feet, which leads to high permeability or leakage of the BBB that causes more influx of AQP4-antibodies into the cerebrospinal fluid (CSF) of NMO patients. The binding of AQP4-IgG onto the AQP4 extracellular epitopes initiates astrocyte damage through complement-dependent cytotoxicity (CDC) and antibody-dependent cellular cytotoxicity (ADCC). Thus, a membrane attack complex is formed due to complement cascade activation; the membrane attack complex targets the AQP4 channels in the astrocytes, leading to astrocyte cell damage, demyelination of neurons and oligodendrocytes, and neuroinflammation. The treatment of NMOSD could improve relapse symptoms, restore neurological functions, and alleviate immunosuppression. Corticosteroids, apheresis therapies, immunosuppressive drugs, and B cell inactivating and complement cascade blocking agents have been used to treat NMOSD. This review intends to provide all possible recent studies related to molecular mechanisms, clinical perspectives, and treatment methodologies of the disease, particularly focusing on recent developments in clinical criteria and therapeutic formulations. Full article
(This article belongs to the Special Issue Gut Microbiota and Chronic Diseases)
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