Long-term dietary intake influences the structure and activity of the trillions of microorganisms residing in the human gut, but it remains unclear how rapidly and reproducibly the human gut microbiome responds to short-term macronutrient change. Here we show that the short-term consumption of diets composed entirely of animal or plant products alters microbial community structure and overwhelms inter-individual differences in microbial gene expression. The animal-based diet increased the abundance of bile-tolerant microorganisms (Alistipes, Bilophila and Bacteroides) and decreased the levels of Firmicutes that metabolize dietary plant polysaccharides (Roseburia, Eubacterium rectale and Ruminococcus bromii). Microbial activity mirrored differences between herbivorous and carnivorous mammals, reflecting trade-offs between carbohydrate and protein fermentation. Foodborne microbes from both diets transiently colonized the gut, including bacteria, fungi and even viruses. Finally, increases in the abundance and activity of Bilophila wadsworthia on the animal-based diet support a link between dietary fat, bile acids and the outgrowth of microorganisms capable of triggering inflammatory bowel disease. In concert, these results demonstrate that the gut microbiome can rapidly respond to altered diet, potentially facilitating the diversity of human dietary lifestyles.

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Diet rapidly and reproducibly alters the human gut microbiome

Antibiotics have always been considered one of the wonder discoveries of the 20th century. This is true, but the real wonder is the rise of antibiotic resistance in hospitals, communities, and the environment concomitant with their use. The extraordinary genetic capacities of microbes have benefitted from man's overuse of antibiotics to exploit every source of resistance genes and every means of horizontal gene transmission to develop multiple mechanisms of resistance for each and every antibiotic introduced into practice clinically, agriculturally, or otherwise. This review presents the salient aspects of antibiotic resistance development over the past half-century, with the oft-restated conclusion that it is time to act. To achieve complete restitution of therapeutic applications of antibiotics, there is a need for more information on the role of environmental microbiomes in the rise of antibiotic resistance. In particular, creative approaches to the discovery of novel antibiotics and their expedited and controlled introduction to therapy are obligatory.

Origins and Evolution of Antibiotic Resistance

The two primary human inflammatory bowel diseases, Crohn's disease (CD) and ulcerative colitis (UC), are idiopathic relapsing disorders characterized by chronic inflammation of the intestinal tract. Although several lines of reasoning suggest that gastrointestinal (GI) microbes influence inflammatory bowel disease (IBD) pathogenesis, the types of microbes involved have not been adequately described. Here we report the results of a culture-independent rRNA sequence analysis of GI tissue samples obtained from CD and UC patients, as well as non-IBD controls. Specimens were obtained through surgery from a variety of intestinal sites and included both pathologically normal and abnormal states. Our results provide comprehensive molecular-based analysis of the microbiota of the human small intestine. Comparison of clone libraries reveals statistically significant differences between the microbiotas of CD and UC patients and those of non-IBD controls. Significantly, our results indicate that a subset of CD and UC samples contained abnormal GI microbiotas, characterized by depletion of commensal bacteria, notably members of the phyla Firmicutes and Bacteroidetes. Patient stratification by GI microbiota provides further evidence that CD represents a spectrum of disease states and suggests that treatment of some forms of IBD may be facilitated by redress of the detected microbiological imbalances.

https://www.pnas.org/content/pnas/104/34/13780.full.pdf

Molecular-phylogenetic characterization of microbial community imbalances in human inflammatory bowel diseases

The causes of antibiotic resistance are complex and include human behaviour at many levels of society; the consequences affect everybody in the world. Similarities with climate change are evident. Many efforts have been made to describe the many different facets of antibiotic resistance and the interventions needed to meet the challenge. However, coordinated action is largely absent, especially at the political level, both nationally and internationally. Antibiotics paved the way for unprecedented medical and societal developments, and are today indispensible in all health systems. Achievements in modern medicine, such as major surgery, organ transplantation, treatment of preterm babies, and cancer chemotherapy, which we today take for granted, would not be possible without access to effective treatment for bacterial infections. Within just a few years, we might be faced with dire setbacks, medically, socially, and economically, unless real and unprecedented global coordinated actions are immediately taken. Here, we describe the global situation of antibiotic resistance, its major causes and consequences, and identify key areas in which action is urgently needed.

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Antibiotic resistance—the need for global solutions

Gut microbiota is an assortment of microorganisms inhabiting the length and width of the mammalian gastrointestinal tract. The composition of this microbial community is host specific, evolving throughout an individual's lifetime and susceptible to both exogenous and endogenous modifications. Recent renewed interest in the structure and function of this "organ" has illuminated its central position in health and disease. The microbiota is intimately involved in numerous aspects of normal host physiology, from nutritional status to behavior and stress response. Additionally, they can be a central or a contributing cause of many diseases, affecting both near and far organ systems. The overall balance in the composition of the gut microbial community, as well as the presence or absence of key species capable of effecting specific responses, is important in ensuring homeostasis or lack thereof at the intestinal mucosa and beyond. The mechanisms through which microbiota exerts its beneficial or detrimental influences remain largely undefined, but include elaboration of signaling molecules and recognition of bacterial epitopes by both intestinal epithelial and mucosal immune cells. The advances in modeling and analysis of gut microbiota will further our knowledge of their role in health and disease, allowing customization of existing and future therapeutic and prophylactic modalities.

Gut Microbiota in Health and Disease



Familial Mediterranean fever (FMF) is an autoinflammatory disease, which is prevalent in populations of the Mediterranean ancestry. Traditionally, FMF was considered as an autosomal recessive genetic disorder; however, several studies showed that a heterozygote state might also result in disease. Mutations responsible for the disease are located in the MEFV gene encoding a protein called pyrin/marenostrin/TRIM20. FMF is characterised by seemingly unprovoked periodic activation of innate immunity, with fever and serosal inflammation. Among more than 300 mutations in the MEFV gene, five mutations (M694V, V726A, M680I, M694I and E148Q) are the most common in classically affected populations (Armenians, Arabs, Jews and Turks). Disease severity depends on specific MEFV mutations and also on a number of other genetic or environmental modifiers. Certain evolutionary aspects of the disease were intensively investigated including the origin of major MEFV mutations, structure-and-function and evolution of pyrin and potential selective advantage of heterozygous carriage.



Key Concepts 

Familial Mediterranean fever (FMF, MIM 249100) is an autoinflammatory genetic disease, and it is prevalent in populations of Mediterranean origin.
The highest incidence of the disorder is documented in four ethnic groups Armenians, Arabs, Jews and Turks, which are considered as ‘classically affected populations’.
Clinical manifestations of FMF include periodic occurrence of fever and inflammation in the peritoneum, synovium or pleura. Renal amyloidosis is the most serious complication of the disease.
The disease is caused by mutations in the MEFV (MEditerraneanFeVer) gene, which is composed of 10 exons and located on chromosome 16 (16p13.3).
MEFV encodes a protein named pyrin or marenostrin or TRIM20, which is a key component of innate immunity.
Presently, more than 300 MEFV mutations have been identified. Five mutations (M694V, V726A, M680I and M694I in exon 10 and E148Q in exon 2) are most frequent in classically affected populations.
Severity of FMF depends on specific MEFV mutations as well as on a number of other genetic and environmental modifiers.
The most common MEFV mutations display a relatively ancient origin, with the subsequent penetration to other populations following migratory and interbreeding processes.
The high carriage rate of MEFV mutations in classically affected populations may be explained by a potential selection for the heterozygote genotype, which may have conferred some sort of selective advantage for populations in the area but currently there is no proof for this.




Keywords:

Familial Mediterranean fever;
MEFV;
Mediterranean basin;
pyrin;
evolution of pyrin

Molecular Genetics of Familial Mediterranean Fever

Microbial and Environmental Factors in Autoimmune and Inflammatory Diseases

Antibiotic Resistance in Commensal Escherichia coli in Armenia

COPYRIGHT © 2023 Yang, Aminov, Franco, de la Fuente-Nunez and Wang. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms. Editorial: Community series in antimicrobial peptides: Molecular design, structure function relationship and biosynthesis optimization

Editorial: Community series in antimicrobial peptides: Molecular design, structure function relationship and biosynthesis optimization

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Rustam Aminov

Papers

Molecular Genetics of Familial Mediterranean Fever

Microbial and Environmental Factors in Autoimmune and Inflammatory Diseases

Antibiotic Resistance in Commensal Escherichia coli in Armenia

Editorial: Community series in antimicrobial peptides: Molecular design, structure function relationship and biosynthesis optimization

Multidrug-resistance and presence of class 1 integrons in clinical isolates of Salmonella enterica serotype Enteritidis, circulating in Armenia