Critical Reviews in Microbiology最新文献

Microbial communities thrive through interactions and communication, which are challenging to study as most microorganisms are not cultivable. To address this challenge, researchers focus on the extracellular space where communication events occur. Exometabolomics and interactome analysis provide insights into the molecules involved in communication and the dynamics of their interactions. Advances in sequencing technologies and computational methods enable the reconstruction of taxonomic and functional profiles of microbial communities using high-throughput multi-omics data. Network-based approaches, including community flux balance analysis, aim to model molecular interactions within and between communities. Despite these advances, challenges remain in computer-assisted biosynthetic capacities elucidation, requiring continued innovation and collaboration among diverse scientists. This review provides insights into the current state and future directions of computer-assisted biosynthetic capacities elucidation in studying microbial communities.

The classical microbiology techniques have inherent limitations in unraveling the complexity of microbial communities, necessitating the pivotal role of sequencing in studying the diversity of microbial communities. Whole genome sequencing (WGS) enables researchers to uncover the metabolic capabilities of the microbial community, providing valuable insights into the microbiome. Herein, we present an overview of the rapid advancements achieved thus far in the use of WGS in microbiome research. There was an upsurge in publications, particularly in 2021 and 2022 with the United States, China, and India leading the metagenomics research landscape. The Illumina platform has emerged as the widely adopted sequencing technology, whereas a significant focus of metagenomics has been on understanding the relationship between the gut microbiome and human health where distinct bacterial species have been linked to various diseases. Additionally, studies have explored the impact of human activities on microbial communities, including the potential spread of pathogenic bacteria and antimicrobial resistance genes in different ecosystems. Furthermore, WGS is used in investigating the microbiome of various animal species and plant tissues such as the rhizosphere microbiome. Overall, this review reflects the importance of WGS in metagenomics studies and underscores its remarkable power in illuminating the variety and intricacy of the microbiome in different environments.

Pseudomonas aeruginosa is an opportunistic pathogen that is responsible for infections in people living with chronic respiratory conditions, such as cystic fibrosis (CF) and non-CF bronchiectasis (NCFB). Traditionally, in people with chronic respiratory disorders, P. aeruginosa infection has been managed with a combination of inhaled and intravenous antibiotic therapies. However, due in part to the prolonged use of antibiotics in these people, the emergence of multi-drug resistant P. aeruginosa strains is a growing concern. The development of anti-virulence therapeutics may provide a new means of treating P. aeruginosa lung infections whilst also combatting the AMR crisis, as these agents are presumed to exert reduced pressure for the emergence of drug resistance as compared to antibiotics. However, the pipeline for developing anti-virulence therapeutics is poorly defined, and it is currently unclear as to whether in vivo and in vitro models effectively replicate the complex pulmonary environment sufficiently to enable development and testing of such therapies for future clinical use. Here, we discuss potential targets for P. aeruginosa anti-virulence therapeutics and the effectiveness of the current models used to study them. Focus is given to the difficulty of replicating the virulence gene expression patterns of P. aeruginosa in the CF and NCFB lung under laboratory conditions and to the challenges this poses for anti-virulence therapeutic development.

Pseudomonas aeruginosa can efficiently adapt to changing environmental conditions due to its ubiquitous nature, intrinsic/acquired/adaptive resistance mechanisms, high metabolic versatility, and the production of numerous virulence factors. As a result, P. aeruginosa becomes an opportunistic pathogen, causing chronic infection in the lungs and several organs of patients suffering from cystic fibrosis. Biofilm established by P. aeruginosa in host tissues and medical device surfaces has been identified as a major obstruction to antimicrobial therapy. P. aeruginosa is very likely to be closely associated with the various microorganisms in the host tissues or organs in a pathogenic or nonpathogenic behavior. Aside from host-derived molecules, other beneficial and pathogenic microorganisms produce a diverse range of secondary metabolites that either directly or indirectly favor the persistence of P. aeruginosa. Thus, it is critical to understand how P. aeruginosa interacts with different molecules and ions in the host and abiotic environment to produce extracellular polymeric substances and virulence factors. Thus, the current review discusses how various natural and synthetic molecules in the environment induce biofilm formation and the production of multiple virulence factors.

Acute respiratory infections (ARIs) are amongst the leading causes of death and disability, and the greatest burden of disease impacts children, pregnant women, and the elderly. Respiratory viruses account for the majority of ARIs. The unfolded protein response (UPR) is a host homeostatic defence mechanism primarily activated in response to aberrant endoplasmic reticulum (ER) resident protein accumulation in cell stresses including viral infection. The UPR has been implicated in the pathogenesis of several respiratory diseases, as the respiratory system is particularly vulnerable to chronic and acute activation of the ER stress response pathway. Many respiratory viruses therefore employ strategies to modulate the UPR during infection, with varying effects on the host and the pathogens. Here, we review the specific means by which respiratory viruses affect the host UPR, particularly in association with the high production of viral glycoproteins, and the impact of UPR activation and subversion on viral replication and disease pathogenesis. We further review the activation of UPR in common co-morbidities of ARIs and discuss the therapeutic potential of modulating the UPR in virally induced respiratory diseases.

The abundance of gut commensals has historically been associated with health-promoting effects despite the fact that the definition of good or bad microbiota remains condition-specific. The beneficial or pathogenic nature of microbiota is generally dictated by the dimensions of host-microbiota and microbe-microbe interactions. With the increasing popularity of gut microbiota in human health and disease, emerging evidence suggests opportunistic infections promoted by those gut bacteria that are generally considered beneficial. Therefore, the current review deals with the opportunistic nature of the gut commensals and aims to summarise the concepts behind the occasional commensal-to-pathogenic transformation of the gut microbes. Specifically, relevant clinical and experimental studies have been discussed on the overgrowth and bacteraemia caused by commensals. Three key processes and their underlying mechanisms have been summarised to be responsible for the opportunistic nature of commensals, viz. improved colonisation fitness that is dictated by commensal-pathogen interactions and availability of preferred nutrients; pathoadaptive mutations that can trigger the commensal-to-pathogen transformation; and evasion of host immune response as a survival and proliferation strategy of the microbes. Collectively, this review provides an updated concept summary on the underlying mechanisms of disease causative events driven by gut commensal bacteria.

Perturbations in microbial abundance or diversity in the intestinal lumen leads to intestinal inflammation and disruption of intestinal membrane which eventually facilitates the translocation of microbial metabolites or whole microbes to the liver and other organs through portal vein. This process of translocation finally leads to multitude of health disorders. In this review, we are going to focus on the mechanisms by which gut metabolites like SCFAs, tryptophan (Trp) metabolites, bile acids (BAs), ethanol, and choline can either cause the development/progression of non-alcoholic fatty liver disease (NAFLD) or serves as a therapeutic treatment for the disease. Alterations in some metabolites like SCFAs, Trp metabolites, etc., can serve as biomarker molecules whereas presence of specific metabolites like ethanol definitely leads to disease progression. Thus, proper understanding of these mechanisms will subsequently help in designing of microbiome-based therapeutic approaches. Furthermore, we have also focussed on the role of dysbiosis on the mucosal immune system. In addition, we would also compile up the microbiome-based clinical trials which are currently undergoing for the treatment of NAFLD and non-alcoholic steatohepatitis (NASH). It has been observed that the use of microbiome-based approaches like prebiotics, probiotics, symbiotics, etc., can act as a beneficial treatment option but more research needs to be done to know how to manipulate the composition of gut microbes.

People with diabetes mellitus (DM) are at an increased risk for developing dry eye disease (DED). However, the mechanisms underlying this phenomenon remain unclear. Recent studies have found that the ocular surface microbiota (OSM) differs significantly between patients with DED and healthy people, suggesting that OSM dysbiosis may contribute to the pathogenesis of DED. This hypothesis provides a new possible explanation for why diabetic patients have a higher prevalence of DED than healthy people. The high-glucose environment and the subsequent pathological changes on the ocular surface can cause OSM dysbiosis. The unbalanced microbiota then promotes ocular surface inflammation and alters tear composition, which disturbs the homeostasis of the ocular surface. This "high glucose-OSM dysbiosis" pathway in the pathogenesis of DED with DM (DM-DED) is discussed in this review.

The microbial aetiology for periodontitis has been widely studied and deciphered for more than a century. The evolving and changing concepts about periodontal microbiology can be attributed to continuously developing laboratory techniques. The current sequencing platforms have not only expanded the catalog of periodontal pathogens but have also facilitated the understanding of functional interactions of the ecological framework. However, the translation of this new knowledge to advance periodontal therapeutics is minimal. We contend that novel clinical interventions directed beyond conventional therapies need to be emphasized. A clear understanding of the structural and functional dynamics of subgingival microbiota is a pre-requisite for developing any microbiome-based interventions for applications in periodontal health care. In this review, we discuss the 16 s-rRNA gene sequencing-based knowledge of the subgingival microbial community structure, its interactions and functions, and our perspective on the potential to engineer it for periodontal therapeutics. Harnessing this next-generation sequencing-based knowledge, microbiome modulation therapies are poised to change microbiome therapeutics' face.