Critical Reviews in Microbiology最新文献

Pseudomonas aeruginosa (PA), an opportunistic human pathogen that is frequently linked with chronic infections in immunocompromised individuals, is also metabolically versatile, and thrives in diverse environments. Additionally, studies report that PA can interact with other microorganisms, such as bacteria, and fungi, producing unique metabolites that can modulate the host immune response, and contribute to disease pathogenesis. This review summarizes the current knowledge related to the metabolic interactions of PA with other microorganisms (Staphylococcus, Acinetobacter, Klebsiella, Enterococcus, and Candida) and human hosts, and the importance of these interactions in a polymicrobial context. Further, we highlight the potential applications of studying these metabolic interactions toward designing better diagnostic tools, and therapeutic strategies to prevent, and treat infections caused by this pathogen.

Periodontal diseases, chronic inflammatory conditions initiated by dysbiotic microbial communities, are predominantly driven by the "red complex" pathogens. This review explores how glycosylation on surface molecules of Tannerella forsythia, Porphyromonas gingivalis, and Treponema denticola modulate their pathogenesis. Research reveal glycosylation profoundly impacts synthesis, stability and functionality of major virulence factors like gingipains, fimbriae and surface layer proteins in these keystone pathogens. Distinct glycan motifs facilitate immune evasion by masking antigenic epitopes, subverting immune recognition and skewing inflammatory responses. Remarkably, glycosylation signatures influence crucial virulence traits such as biofilm formation, host adhesion and invasion, potentiating persistence. Through evaluating current literature, this review unravels the interplay between glycosylation pathways and virulence expression, elucidating mechanisms underpinning glycan-mediated host-pathogen interactions and pathology progression. Emerging prospects of exploiting glycosylation as a diagnostic, therapeutic target and vaccine candidate are discussed. Synthesizing cutting-edge findings, this comprehensive review illuminates glycosylation's central role in periodontal pathogenesis.

Mycotoxin contamination of food and feed is a major global concern. Chronic or acute dietary exposure to contaminated food and feed can negatively affect both human and animal health. Contamination occurs through plant infection by toxigenic fungi, primarily Aspergillus and Fusarium spp., either before or after harvest. Despite the application of various management strategies, controlling these pathogens remains a major challenge primarily because of their ability to adapt to environmental changes and selection pressures. Understanding the genetic structure of plant pathogen populations is pivotal for gaining new insights into their biology and epidemiology, as well as for understanding the mechanisms behind their adaptability. Such deeper understanding is crucial for developing effective and preemptive management strategies tailored to the evolving nature of pathogenic populations. This review focuses on the population-level variations within the two most economically significant toxigenic fungal genera according to space, host, and pathogenicity. Outcomes in terms of migration patterns, gene flow within populations, mating abilities, and the potential for host jumps are examined. We also discuss effective yet often underutilized applications of population genetics and genomics to address practical challenges in the epidemiology and disease control of toxigenic fungi.

Prevotella intermedia is a Gram-negative anaerobic bacterium that is a common pathogen of periodontitis. Recent studies have revealed that P. intermedia is closely associated with a variety of diseases involving multiple systems. Under the action of its virulence factors such as cysteine protease and adhesins, P. intermedia has the ability to bind and invade various host cells including gingival fibroblasts. It can also copolymerize a variety of pathogenic bacteria, leading to interference with the host's immune inflammatory response and causing various diseases. In this article, we review the progress of research on P. intermedia virulence factors and bacterial pathogenesis, and the correlation between P. intermedia and various diseases.

Carotenoids are isoprenoid pigments that are largely responsible for the red, pink, orange, and yellow pigmentation in bacteria. Despite their structural diversity, they share a similar general chemical structure. Carotenogenesis is a complex, multistep process, mediated by the crt gene products. The crt genes encode enzymes that catalyze a wide array of reactions within the carotenogenic pathways, sometimes showcasing broad substrate specificity. These enzymes are involved in processes such as condensation, desaturation, oxygenation, cyclization, hydroxylation, ketolation, glycosylation, acylation, elongation, and methylation of carotenoid intermediates. Some crt genes do not encode enzymes, but rather regulators of carotenogenesis. This review provides an in-depth exploration of the multitude of crt genes identified in various bacteria, emphasizing the pivotal role of Crt enzymes, their diverse functions within the different carotenogenic pathways and some of the reactions they catalyze. Additionally, the biosynthetic pathways of C30, C40, C45, and C50 carotenoids, as well as the production of certain rare carotenoids in bacteria, are explored. Overall, this review highlights the importance of crt gene products in the diverse and tightly regulated biosynthesis pathways of bacterial carotenoids.

The gut microbiota produces a variety of metabolites that are crucial for regulating host health and physiological homeostasis. Indole-3-acetic acid (IAA), a microbial metabolite of tryptophan, exhibits diverse biological activities including anti-inflammatory, anti-tumor, anti-obesity, hepatoprotective, enteroprotective, and neuromodulatory effects. Accumulating evidence has demonstrated its therapeutic potential against metabolic, inflammatory, and neurological disorders. Emerging evidence suggests that IAA exerts beneficial effects on mammalian health through multiple mechanisms, including modulation of gut microbiota composition, enhancement of intestinal barrier integrity, immune regulation, attenuation of bone loss, and improvement of glucose and lipid homeostasis. This review systematically summarizes current knowledge regarding IAA sources, elucidates recent advances in understanding its biological functions, and integrates existing evidence on its mechanisms of action in mammalian systems. Collectively, this synthesis provides a framework for future investigations and translational applications of IAA.

Brevibacillus laterosporus is a ubiquitous bacterium that has been isolated from a wide range of abiotic and biotic habitats. Especially, it has been reported from various insects which supported the development of its mutualistic or pathogenic interaction with diverse insect species under co-evolutionary force. In the recent past, different B. laterosporus strains reported to produce multiple bioactive agents including antimicrobial peptides (AMPs) and antibiotics with diverse antimicrobial and antitumor activities. Further, whole genome sequencing of this bacterium revealed biosynthetic gene clusters which suggested its potential to produce multiple polyketides, non-ribosomal peptides, and bacteriocins. All these facts strongly suggest B. laterosporus as a potential bio-pesticidal or bio-control agent against a diverse species of insects and phytopathogens including bacteria and fungi which may lead to its application in the agricultural industry. Further, broad-spectrum antimicrobial action against drug-resistant and pathogenic bacteria along with antitumor activities suggested the potential for the development of bioactive molecules produced by B. laterosporus in the pharmaceutical and biotechnology industry including agriculture and food preservation. Overall, the present review is focused on the co-evolution of B. laterosporus with its diverse hosts that result in a diverse array of bioactive agents for various agricultural and therapeutic applications.

Type IV pili are filamentous surface structures found in diverse bacterial species that provide specialized functions to bacteria, such as initiating cell aggregation via attachment to host cells. The structural filament is made up of polymers of pilin subunits. Gene expression of major pilins is typically the major factor deciding the timing of Type IV pilus filament assembly. Therefore, the regulation of pilin genes is often independent from other pilus biogenesis genes even when they are located within the same cluster. Such strictly regulated pilin transcription ensures that the pilus filament is expressed only when the bacterial cells require it, such as precise timing for a specialized function, or preventing potentially adverse situations like clearing by host defense systems or cell death by phage infection. This review will focus on the transcriptional regulation of Type IV major pilins found in bacteria, and speculate on the evolution of such regulatory systems by identifying similarities and differences across different bacterial phyla.

Infection with H. pylori induces chronic gastric inflammation, progressing to peptic ulcer and stomach adenocarcinoma. Macrophages function as innate immune cells and play a vital role in host immune defense against bacterial infection. However, the distinctive mechanism by which H. pylori evades phagocytosis allows it to colonize the stomach and further aggravate gastric preneoplastic pathology. H. pylori exacerbates gastric inflammation by promoting oxidative stress, resisting macrophage phagocytosis, and inducing M1 macrophage polarization. M2 macrophages facilitate the proliferation, invasion, and migration of gastric cancer cells. Various molecular mechanisms governing macrophage function in the pathogenesis of H. pylori infection have been identified. In this review, we summarize recent findings of macrophage interactions with H. pylori infection, with an emphasis on the regulatory mechanisms that determine the clinical outcome of bacterial infection.

Mycobacterium tuberculosis (Mtb) is the causative pathogen of tuberculosis, the most lethal infectious disease resulting in 1.3 million deaths annually. Treatments against Mtb are increasingly impaired by the growing prevalence of antimicrobial drug resistance, which necessitates the development of new antibiotics or alternative therapeutic approaches. Upon infecting host cells, predominantly macrophages, Mtb becomes critically dependent on lipids as a source of nutrients. Additionally, Mtb produces numerous lipid-based virulence factors that contribute to the pathogen's ability to interfere with the host's immune responses and to create a lipid rich environment for itself. As lipids, lipid metabolism and manipulating host lipid metabolism play an important role for the virulence of Mtb, this review provides a state-of-the-art overview of mycobacterial lipid metabolism and concomitant role of host metabolism and host-pathogen interaction therein. While doing so, we will emphasize unexploited bacteria-directed and host-directed drug targets, and highlight potential synergistic drug combinations that hold promise for the development of new therapeutic interventions.