Current opinion in microbiology最新文献

Microbial ecology is moving away from purely descriptive analyses to experiments that can determine the underlying mechanisms driving changes in community assembly and function. More species-rich microbial communities generally have higher functional capabilities depending on if there is positive selection of certain species or complementarity among different species. When building synthetic communities or laboratory enrichment cultures, there are specific choices that can increase the number of species able to coexist. Higher resource complexity or the addition of physical niches are two of the many factors leading to greater biodiversity and associated increases in functional capabilities. We can use principles from community ecology and knowledge of microbial physiology to generate improved microbiomes for use in medicine, agriculture, or environmental management.

Microbial communities are fundamental to every ecosystem on Earth and hold great potential for biotechnological applications. However, their complex nature hampers our ability to study and understand them. A common strategy to tackle this complexity is to abstract the community into a network of interactions between its members — a phenomenological description that captures the overall effects of various chemical and physical mechanisms that underpin these relationships. This approach has proven useful for numerous applications in microbial ecology, including predicting community dynamics and stability and understanding community assembly and evolution. However, care is required in quantifying and interpreting interactions. Here, we clarify the concept of an interaction and discuss when interaction measurements are useful despite their context-dependent nature. Furthermore, we categorize different approaches for quantifying interactions, highlighting the research objectives each approach is best suited for.

Resource colimitation — the dependence of growth on multiple resources simultaneously — has become an important topic in microbiology due both to the development of systems approaches to cell physiology and ecology and to the relevance of colimitation to environmental science, biotechnology, and human health. Empirical tests of colimitation in microbes suggest that it may be common in nature. However, recent theoretical and empirical work has demonstrated the need for systematic measurements across resource conditions, in contrast to the factorial supplementation experiments used in most previous studies. The mechanistic causes of colimitation remain unclear in most cases and are an important challenge for future work, but we identify the alignment of resource consumption with the environment, interactions between resources, and biological and environmental heterogeneity as major factors. On the other hand, the consequences of colimitation are widespread for microbial physiology and ecology, especially the prediction and control of microbial growth, motivating continued consideration of this state in microbiology.

Epithelial cells orchestrate immune responses against fungal pathogens. This review highlights advances in integrating epithelial cells in immune responses against inhaled molds and dimorphic fungi, and against Candida species that colonize mucosal surfaces. In the lung, epithelial cells respond to interleukin-1 (IL-1) and interferon signaling to regulate effector cell influx and fungal killing. In the alimentary and vulvovaginal tracts, epithelial cells modulate fungal commensalism, invasive growth, and local immune tone, in part by responding to damage caused by candidalysin, a C. albicans peptide toxin, and through IL-17-dependent release of antimicrobial peptides that contribute to Candida colonization resistance. Understanding fungal–epithelial interactions in mammalian models of disease is critical to predict vulnerabilities and to identify opportunities for immune-based strategies to treat fungal infections.

Candida auris, a newly emergent fungal species, has been spreading in health care systems and causing life-threatening infections. Intact innate immunity is essential for protection against many invasive fungal infections, including candidiasis. Here, we highlight recent studies exploring immune interactions with C. auris, including investigations using animal models and ex vivo immune cells. We summarize innate immune studies comparing C. auris and the common fungal pathogen Candida albicans. We also discuss how structures of the C. auris cell wall influence immune recognition, the role of soluble host factors in immune recognition, and areas of future study.

The human microbiota is a complex microbial ecosystem populated by bacteria, fungi, viruses, protists, and archaea. The coexistence of fungi alongside with many billions of bacteria, especially in the gut, involves complex interactions, ranging from antagonistic to beneficial, between the members of these two kingdoms. Bacteria can impact fungi through various means, such as physical interactions, secretion of metabolites, or alteration of the host immune response, thereby affecting fungal growth and virulence. This review summarizes recent progress in this field, delving into the latest understandings of bacterial–fungal–immune interactions and innovative therapeutic approaches addressing the challenges of treating fungal infections associated with microbiota imbalances.

Commensal bacteria are residents of the human airway where they interact with both colonizing pathogens and host respiratory epithelial cells of this mucosal surface. It is here that commensals exert their influence through host signaling cascades, host transcriptional responses and host immunity, all of which are rooted in chromatin remodeling and histone modifications. Recent studies show that airway commensals impact host chromatin, but compared the what is known for gut commensals, the field remains in its infancy. The mechanisms by which airway commensals regulate respiratory health and homeostasis through chromatin modifications is of increasing interest, specifically since their displacement precedes the increased potential for respiratory disease. Herein we will discuss recent advances and intriguing avenues of future work aimed at deciphering how airway commensals protect and influence respiratory health.

Candida auris is an emerging fungal pathogen with several concerning qualities. First recognized in 2009, it has arisen in multiple geographically distinct genomic clades nearly simultaneously. C. auris strains are typically multidrug resistant and colonize the skin much better than most other pathogenic fungi; it also persists on abiotic surfaces, enabling outbreaks due to transmission in health care facilities. All these suggest a biology substantially different from the ‘model’ fungal pathogen, Candida albicans and support intensive investigation of C. auris biology directly. To uncover novel virulence mechanisms in this species requires the development of appropriate animal infection models. Various studies using mice, the definitive model, are inconsistent due to differences in mouse and fungal strains, immunosuppressive regimes, doses, and outcome metrics. At the same time, developing models of skin colonization present a route to new insights into an aspect of fungal pathogenesis that has not been well studied in other species. We also discuss the growing use of nonmammalian model systems, including both vertebrates and invertebrates, such as zebrafish, C. elegans, Drosophila, and Galleria mellonella, that have been productively employed in virulence studies with other fungal species. This review will discuss progress in developing appropriate animal models, outline current challenges, and highlight opportunities in demystifying this curious species.

Legionella species are Gram-negative intracellular bacteria that evolved in soil and freshwater environments, where they infect and replicate within various unicellular protozoa. The primary virulence factor of Legionella is the expression of a type IV secretion system (T4SS), which contributes to the translocation of effector proteins that subvert biological processes of the host cells. Because of its evolution in unicellular organisms, T4SS effector proteins are not adapted to subvert specific mammalian signaling pathways and immunity. Consequently, Legionella pneumophila has emerged as an interesting infection model for investigating immune responses against pathogenic bacteria in multicellular organisms. This review highlights recent advances in our understanding of mammalian innate immunity derived from studies involving L. pneumophila. This includes recent insights into inflammasome-mediated mechanisms restricting bacterial replication in macrophages, mechanisms inducing cell death in response to infection, induction of effector-triggered immunity, activation of specific pulmonary cell types in mammalian lungs, and the protective role of recruiting monocyte-derived cells to infected lungs.