Publisher Correction: Integrating respiratory microbiome and host immune response through machine learning for respiratory tract infection diagnosis
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Microbiome-based interventions to modulate gut ecology and the immune system
The gut microbiome lies at the intersection between the environment and the host, with the ability to modify host responses to disease-relevant exposures and stimuli. This is evident in how enteric microbes interact with the immune system, e.g., supporting immune maturation in early life, affecting drug efficacy via modulation of immune responses, or influencing development of immune cell populations and their mediators. Many factors modulate gut ecosystem dynamics during daily life and we are just beginning to realise the therapeutic and prophylactic potential of microbiome-based interventions. These approaches vary in application, goal, and mechanisms of action. Some modify the entire community, such as nutritional approaches or faecal microbiota transplantation, while others, such as phage therapy, probiotics, and prebiotics, target specific taxa or strains. In this review, we assessed the experimental evidence for microbiome-based interventions, with a particular focus on their clinical relevance, ecological effects, and modulation of the immune system.
Underscoring long-term host-microbiome interactions in a physiologically relevant gingival tissue model
The human body houses many distinct and interconnecting microbial populations with long-lasting systemic effects, where the oral cavity serves as a pathogens’ reservoir. The correlation of different disease states strongly supports the need to understand the interplay between the oral tissue niche and microbiome. Despite efforts, the recapitulation of gingival architecture and physiological characteristics of the periodontal niche has yet to be accomplished by traditional cultural strategies. Here, we are showing for the first time the investigation of host–microbiome interactions in healthy conditions within a human oral tissue model over seven days. Our results indicated long-term host and microbiome viability, host barrier integrity, phenotypic functional response, and preservation of healthy microbial populations and interbacterial dialogs. This in vitro platform can maintain tissue homeostasis at the interface of the periodontal niche, thus, offering opportunities to identify predictive disease biomarkers and to develop intervention strategies to promote oral and overall health.
A Consensus Statement on establishing causality, therapeutic applications and the use of preclinical models in microbiome research
The gut microbiome comprises trillions of microorganisms and profoundly influences human health by modulating metabolism, immune responses and neuronal functions. Disruption in gut microbiome composition is implicated in various inflammatory conditions, metabolic disorders and neurodegenerative diseases. However, determining the underlying mechanisms and establishing cause and effect is extremely difficult. Preclinical models offer crucial insights into the role of the gut microbiome in diseases and help identify potential therapeutic interventions. The Human Microbiome Action Consortium initiated a Delphi survey to assess the utility of preclinical models, including animal and cell-based models, in elucidating the causal role of the gut microbiome in these diseases. The Delphi survey aimed to address the complexity of selecting appropriate preclinical models to investigate disease causality and to study host–microbiome interactions effectively. We adopted a structured approach encompassing a literature review, expert workshops and the Delphi questionnaire to gather insights from a diverse range of stakeholders. Experts were requested to evaluate the strengths, limitations, and suitability of these models in addressing the causal relationship between the gut microbiome and disease pathogenesis. The resulting consensus statements and recommendations provide valuable insights for selecting preclinical models in future studies of gut microbiome-related diseases.
Moving beyond descriptive studies: harnessing metabolomics to elucidate the molecular mechanisms underpinning host-microbiome phenotypes
Advances in technology and software have radically expanded the scope of metabolomics studies and allow us to monitor a broad transect of central carbon metabolism in routine studies. These increasingly sophisticated tools have shown that many human diseases are modulated by microbial metabolism. Despite this, it remains surprisingly difficult to move beyond these statistical associations and identify the specific molecular mechanisms that link dysbiosis to the progression of human disease. This difficulty stems from both the biological intricacies of host-microbiome dynamics as well as the analytical complexities inherent to microbiome metabolism research. The primary objective of this review is to examine the experimental and computational tools that can provide insights into the molecular mechanisms at work in host–microbiome interactions and to highlight the undeveloped frontiers that are currently holding back microbiome research from fully leveraging the benefits of modern metabolomics.
Type 2 immunity in allergic diseases
Significant advancements have been made in understanding the cellular and molecular mechanisms of type 2 immunity in allergic diseases such as asthma, allergic rhinitis, chronic rhinosinusitis, eosinophilic esophagitis (EoE), food and drug allergies, and atopic dermatitis (AD). Type 2 immunity has evolved to protect against parasitic diseases and toxins, plays a role in the expulsion of parasites and larvae from inner tissues to the lumen and outside the body, maintains microbe-rich skin and mucosal epithelial barriers and counterbalances the type 1 immune response and its destructive effects. During the development of a type 2 immune response, an innate immune response initiates starting from epithelial cells and innate lymphoid cells (ILCs), including dendritic cells and macrophages, and translates to adaptive T and B-cell immunity, particularly IgE antibody production. Eosinophils, mast cells and basophils have effects on effector functions. Cytokines from ILC2s and CD4+ helper type 2 (Th2) cells, CD8 + T cells, and NK-T cells, along with myeloid cells, including IL-4, IL-5, IL-9, and IL-13, initiate and sustain allergic inflammation via T cell cells, eosinophils, and ILC2s; promote IgE class switching; and open the epithelial barrier. Epithelial cell activation, alarmin release and barrier dysfunction are key in the development of not only allergic diseases but also many other systemic diseases. Recent biologics targeting the pathways and effector functions of IL4/IL13, IL-5, and IgE have shown promising results for almost all ages, although some patients with severe allergic diseases do not respond to these therapies, highlighting the unmet need for a more detailed and personalized approach.
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