Mycobacterium avium in Crohn’s Disease and Other Inflammatory Diseases

A special issue of Microorganisms (ISSN 2076-2607). This special issue belongs to the section "Medical Microbiology".

Deadline for manuscript submissions: closed (31 October 2021) | Viewed by 3589

Special Issue Editors


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Guest Editor
Centre for Digestive Diseases, Five Dock, Australia
Interests: fecal microbiota transplantation (fmt) inflammatory disease; infection digestive diseases

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Guest Editor
Burnett School of Biomedical Sciences, College of Medicine, University of Central Florida, Orlando, FL 32816, USA
Interests: investigation of the role of Mycobacterium avium subsp. paratuberculosis (MAP) in the etiology of Crohn's disease, Rheumatoid Arthritis and Type I Diabetes; development of nested PCR molecular diagnostics for detection of MAP in clinical samples; investigation the role of single nucleotide polymorphisms (SNPs) in disease-specific genes in patients with Crohn's disease, Rheumatoid Arthritis and Type I Diabetes; validation of antibiotics therapy for treatment of human infected with MAP; investigation of environmental triggers including diet and smoking in patients with autoimmune diseases

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Guest Editor
School of Veterinary Medicine, University of Wisconsin, Madison, WI, USA
Interests: Mycobacterium avium subsp. paratuberculosis; Johne’s disease; diagnosis; epidemiology

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Guest Editor
Microbiology, Otakaro Pathways, Christchurch, New Zealand
Interests: antimicrobial resistance; emerging bacterial infectious diseases

Special Issue Information

Dear Colleagues,

For many decades, the question of the involvement of Mycobacterium avium paratuberculosis (MAP) in Crohn’s Disease has confounded scientists continually. However, rapidly developing technologies and rediscoveries of old thinking and methods has helped accelerate investigations into this association. We are learning it is not a simple cause (infection) and effect (disease) model but involves critical components of the host-microbe response, sensitivities, and microbiome profiling, with immunological and macrophage responses at play.

Microbiome studies are rapidly evolving, and new discoveries are changing the way we think about the composition and effects on the host, signalling mechanisms and molecules, inflammatory contribution, biology of organisms and their interactions with the local and systemic environment, availability of resources, and synergistic relationships with commensal, opportunistic, and pathogenic organisms. New applications for the use of microbes and commercial opportunities are being created. A greater understanding of the gut microbiome will lead to new strategies for treatment of Crohn’s Disease and other chronic inflammatory diseases.

It is fortunate that there is already an animal model present for comparison and analysis in the form of Johne’s Disease. However, there are current limitations and restrictions in direct comparisons to an infection in humans. The main criticism levelled as to whether MAP is a pathogenic or opportunistic micro-organism in humans is the lack of a reliable diagnostic assay, specificity markers to Crohn’s Disease, and treatment curative benefits, according to currently desired phase III Randomised Control Trials.

This Special Issue of Microorganisms will be dedicated to the following themes: MAP in Crohn’s Disease and other inflammatory diseases that have been proposed such as sarcoidosis and psoriasis; the microbiome in Crohn’s disease; the microbiome effects on the human host and dysbiosis consequences; functional analysis, manipulating and treating the microbiome to suppress pathogens; challenges and tools of microbiome and mycobacteria research (standardization, taxonomy, data analysis); treatment effects and challenges of M.avium and critically; whether there is a relationship between MAP and dysbiosis of the gut microbiome in Crohn’s Disease. Other desired topics will address culture and diagnoses of Mycobacteria avium, Johne’s disease parallels and epidemiology, and the evidence for a zoonotic disease.

We hope you’ll be curious and excited to submit your innovative research and proposals on this microorganism.

Dr. Gaurav Agrawal
Dr. Thomas Borody
Prof. Dr. Saleh A. Naser
Dr. Michael. T. Collins
Dr. John Aitken
Guest Editors

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Published Papers (1 paper)

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Research

11 pages, 1380 KiB  
Article
Nicotine Increases Macrophage Survival through α7nAChR/NF-κB Pathway in Mycobacterium avium paratuberculosis Infection
by Dania AlQasrawi, Ebraheem Naser and Saleh A. Naser
Microorganisms 2021, 9(5), 1086; https://doi.org/10.3390/microorganisms9051086 - 18 May 2021
Cited by 6 | Viewed by 2722
Abstract
Recently, we reported that nicotine plays a role in the failure of the macrophage in the clearance of Mycobacterium avium subspecies paratuberculosis (MAP) during infection in Crohn’s disease smokers. We also demonstrated that nicotine enhances macrophages cellular survival during MAP infection. Blocking α7 [...] Read more.
Recently, we reported that nicotine plays a role in the failure of the macrophage in the clearance of Mycobacterium avium subspecies paratuberculosis (MAP) during infection in Crohn’s disease smokers. We also demonstrated that nicotine enhances macrophages cellular survival during MAP infection. Blocking α7 nicotinic acetylcholine receptor (α7nAChR) with the pharmacological antagonist—mecamylamine—subverted the anti-inflammatory effect of nicotine in macrophages. Yet, it is still unknown how α7nAChR is involved in the modulation of the macrophage response during MAP infection. Here, we studied the mechanistic role of nicotine-α7nAChR interaction in modulating NF-ĸB survival pathway, autophagy, and effect on cathelicidin production in MAP-infected macrophages using THP-1 cell lines. Our results showed that nicotine upregulated α7nAChR expression by 5-folds during MAP infection compared to controls. Bcl-2 expression was also significantly increased after nicotine exposure. Moreover, Nicotine inhibited autophagosome formation whereas infection with MAP in absence of nicotine has significantly increased LC-3b in macrophages. Nicotine also further upregulated NF-ĸB subunits expression including Rel-B and p100, and increased nuclear translocation of p52 protein. We also discovered that cathelicidin production was significantly suppressed in MAP-infected macrophages, treatment with nicotine showed no effect. Overall, the study provides new insight toward understanding the cellular role of nicotine through α7nAChR/NF-ĸB p100/p52 signaling pathway in inducing anti-apoptosis and macrophage survival during MAP infection in Crohn’s disease smokers. Full article
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