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Genes Jul 2021RNA modifications are involved in numerous biological processes and are present in all RNA classes. These modifications can be constitutive or modulated in response to... (Review)
Review
RNA modifications are involved in numerous biological processes and are present in all RNA classes. These modifications can be constitutive or modulated in response to adaptive processes. RNA modifications play multiple functions since they can impact RNA base-pairings, recognition by proteins, decoding, as well as RNA structure and stability. However, their roles in stress, environmental adaptation and during infections caused by pathogenic bacteria have just started to be appreciated. With the development of modern technologies in mass spectrometry and deep sequencing, recent examples of modifications regulating host-pathogen interactions have been demonstrated. They show how RNA modifications can regulate immune responses, antibiotic resistance, expression of virulence genes, and bacterial persistence. Here, we illustrate some of these findings, and highlight the strategies used to characterize RNA modifications, and their potential for new therapeutic applications.
Topics: Bacteria; Host Adaptation; Host-Pathogen Interactions; RNA Processing, Post-Transcriptional; RNA, Bacterial; Virulence
PubMed: 34440299
DOI: 10.3390/genes12081125 -
Nature Communications Jan 2023Host bottlenecks prevent many infections before the onset of disease by eliminating invading pathogens. By monitoring the diversity of a barcoded population of the...
Host bottlenecks prevent many infections before the onset of disease by eliminating invading pathogens. By monitoring the diversity of a barcoded population of the diarrhea causing bacterium Citrobacter rodentium during colonization of its natural host, mice, we determine the number of cells that found the infection by establishing a replicative niche. In female mice the size of the pathogen's founding population scales with dose and is controlled by a severe yet slow-acting bottleneck. Reducing stomach acid or changing host genotype modestly relaxes the bottleneck without breaking the fractional relationship between dose and founders. In contrast, disrupting the microbiota causes the founding population to no longer scale with the size of the inoculum and allows the pathogen to infect at almost any dose, indicating that the microbiota creates the dominant bottleneck. Further, in the absence of competition with the microbiota, the diversity of the pathogen population slowly contracts as the population is overtaken by bacteria having lost the critical virulence island, the locus of enterocyte effacement (LEE). Collectively, our findings reveal that the mechanisms of protection by colonization bottlenecks are reflected in and can be generally defined by the impact of dose on the pathogen's founding population.
Topics: Female; Animals; Mice; Virulence; Bacteria; Virulence Factors; Enterocytes; Diarrhea; Citrobacter rodentium; Enterobacteriaceae Infections
PubMed: 36709326
DOI: 10.1038/s41467-023-36162-3 -
Virulence Dec 2022is an important opportunistic pathogen widely distributed in the environment. In this study, we reported the isolation and characterization of a isolate, MB1, from the...
is an important opportunistic pathogen widely distributed in the environment. In this study, we reported the isolation and characterization of a isolate, MB1, from the Challenger Deep of the Mariana Trench. MB1 is aerobic, motile, and able to form endospores. It possesses 5966 genes distributed on a circular chromosome and two plasmids. The MB1 genome contains 14 sets of 23S, 5S, and 16S ribosomal RNA operons, 106 tRNA genes, 4 sRNA genes, 12 genomic islands, 13 prophages, and 302 putative virulence genes, including enterotoxins and cytolysins. Infection studies showed that MB1 was able to cause acute and lethal infection in fish and mice, and was highly toxic to mammalian cells. MB1 induced, in a dose-dependent manner, pyroptotic cell death, characterized by activation of caspase-1, cleavage of gasdermin D, and release of IL-1β and IL-18. MB1 spores exhibited swimming and haemolytic capacity, but were severely attenuated in pathogenicity, which, however, was regained to the full extent when the spores germinated under suitable conditions. Taken together, these results provide new insights into the biological and pathogenic mechanism of deep sea .
Topics: Animals; Bacillus cereus; Mammals; Mice; Operon; Plasmids; RNA, Ribosomal, 16S; Virulence
PubMed: 35733351
DOI: 10.1080/21505594.2022.2088641 -
Environmental Pollution (Barking, Essex... Jun 2022Pollinating bees are stressed by highly variable environmental conditions, malnutrition, parasites and pathogens, but may also by getting in contact with microorganisms... (Review)
Review
Impact of microorganisms and entomopathogenic nematodes used for plant protection on solitary and social bee pollinators: Host range, specificity, pathogenicity, toxicity, and effects of experimental parameters.
Pollinating bees are stressed by highly variable environmental conditions, malnutrition, parasites and pathogens, but may also by getting in contact with microorganisms or entomopathogenic nematodes that are used to control plant pests and diseases. While foraging for water, food, or nest material social as well as solitary bees have direct contact or even consume the plant protection product with its active substance (e.g., viruses, bacteria, fungi, etc.). Here, we summarize the results of cage, microcolony, observation hive assays, semi-field and field studies using full-size queen-right colonies. By now, some species and subspecies of the Western and Eastern honey bee (Apis mellifera, A. cerana), few species of bumble bees, very few stingless bee species and only a single species of leafcutter bees have been studied as non-target host organisms. Survival and reproduction are the major criteria that have been evaluated. Especially sublethal effects on the bees' physiology, immune response and metabolisms will be targets of future investigations. By studying infectivity and pathogenic mechanisms, individual strains of the microorganism and impact on different bee species are future challenges, especially under field conditions. Overall, it became evident that honey bees, bumble bees and few stingless bee species may not be suitable surrogate species to make general conclusions for biological mechanisms of bee-microorganism interactions of other social bee species. Solitary bees have been studied on leafcutter bees (Megachile rotundata) only, which shows that this huge group of bees (∼20,000 species worldwide) is right at the beginning to get an insight into the interaction of wild pollinators and microbial plant protection organisms.
Topics: Animals; Bees; Host Specificity; Nematoda; Plants; Reproduction; Virulence
PubMed: 35219794
DOI: 10.1016/j.envpol.2022.119051 -
American Journal of Respiratory and... Jul 2022
Topics: Bacterial Proteins; Humans; Hypoxia; Inflammation; Mycobacterium tuberculosis; Virulence
PubMed: 35442854
DOI: 10.1164/rccm.202203-0432ED -
Molecular Plant Pathology Jan 2022Pseudomonas viridiflava is a gram-negative pseudomonad that is phylogenetically placed within the Pseudomonas syringae species complex. P. viridiflava has a wide host...
UNLABELLED
Pseudomonas viridiflava is a gram-negative pseudomonad that is phylogenetically placed within the Pseudomonas syringae species complex. P. viridiflava has a wide host range and causes a variety of symptoms in different plant parts, including stems, leaves, and blossoms. Outside of its role as a pathogen, P. viridiflava also exists as an endophyte, epiphyte, and saprophyte. Increased reports of P. viridiflava causing disease on new hosts in recent years coincide with increased research on its genetic variability, virulence, phylogenetics, and phenotypes. There is high variation in its core genome, virulence factors, and phenotypic characteristics. The main virulence factors of this pathogen include the enzyme pectate lyase and virulence genes encoded within one or two pathogenicity islands. The delineation of P. viridiflava in the P. syringae complex has been investigated using several molecular approaches. P. viridiflava comprises its own species, within the complex. While seemingly an outsider to the complex as a whole due to differences in the core genome and virulence genes, low average nucleotide identity to other of P. syringae complex members, and some phenotypic traits, it remains as part of the complex. Defining phylogenetic, phenotypic, and genomic characteristics of P. viridiflava in comparison to other P. syringae members is important to understanding this pathogen and for the development of disease resistance and management practices.
TAXONOMY
Kingdom Bacteria; Phylum Proteobacteria; Class Gammaproteobacteria; Family Pseudomonadaceae; Genus Pseudomonas; Species Pseudomonas syringae species complex, Genomospecies 6, Phylogroup 7 and 8.
MICROBIOLOGICAL PROPERTIES
Gram-negative, fluorescent, aerobic, motile, rod-shaped, oxidase negative, arginine dihydrolase negative, levan production negative (or positive), potato rot positive (or negative), tobacco hypersensitivity positive.
GENOME
There are two complete genomes, five chromosome-level genomes, and 1,540 genomes composed of multiple scaffolds of P. viridiflava available in the National Center for Biotechnology Information Genome database. The median total length of these assemblies is 5,975,050 bp, the median number of protein coding genes is 5,208, and the median G + C content is 59.3%.
DISEASE SYMPTOMS
P. viridiflava causes a variety of disease symptoms, including spots, streaks, necrosis, rots, and more in above- and below-ground plant parts on at least 50 hosts.
EPIDEMIOLOGY
There have been several significant disease outbreaks on field and horticultural crops caused by P. viridiflava since the turn of the century. P. viridiflava has been reported as a pathogen, epiphyte, endophyte, and saprophyte. This species has been isolated from a variety of environmental sources, including asymptomatic wild plants, snow, epilithic biofilms, and icepacks.
Topics: Phylogeny; Plant Diseases; Pseudomonas; Pseudomonas syringae; Virulence
PubMed: 34463014
DOI: 10.1111/mpp.13133 -
Molecular Microbiology Mar 2020The universe of Molecular Microbial Pathogenesis is filled with many female and male stars. But there are two particularly bright shining supernovae-like stars: the late...
The universe of Molecular Microbial Pathogenesis is filled with many female and male stars. But there are two particularly bright shining supernovae-like stars: the late Stanley Falkow and the very lively and creative Pascale Cossart. These two outstanding luminaries, surrounded by numerous planets, do not only belong to different scientific generations but their splendor also comes from very different scientific concepts. Stanley Falkow, often referred to as the 'Father of Molecular Microbial Pathogenesis', made many groundbreaking contributions to this field by addressing almost all important bacterial pathogens. Pascale Cossart, who could be called in analogy the 'Queen of Modern Molecular Microbial Pathogenesis' by combining the Microbiology and Cell Biology, concentrates in her similarly impressive scientific work essentially on a single bacterial species which she studied and still studies in great depth: the facultative intracellular bacterial pathogen Listeria monocytogenes-and the vast majority of her most prominent publications deals with this pathogen in almost all facets. It is certainly not an exaggeration to say that she together with her co-workers and collaborators developed this model bacterium into a paradigm among the intracellular bacterial pathogens.
Topics: Female; History, 20th Century; History, 21st Century; Host-Pathogen Interactions; Humans; Listeria monocytogenes; Listeriosis; Virulence; Virulence Factors
PubMed: 32185837
DOI: 10.1111/mmi.14450 -
Science Advances Jun 2023Animals evolved two defense strategies to survive infections. Antagonistic strategies include immune resistance mechanisms that operate to kill invading pathogens....
Animals evolved two defense strategies to survive infections. Antagonistic strategies include immune resistance mechanisms that operate to kill invading pathogens. Cooperative or physiological defenses mediate host adaptation to the infected state, limiting physiological damage and disease, without killing the pathogen, and have been shown to cause asymptomatic carriage and transmission of lethal pathogens. Here, we demonstrate that physiological defenses cooperate with the adaptive immune response to generate long-term asymptomatic carriage of the lethal enteric murine pathogen, . Asymptomatic carriage of genetically virulent provided immune resistance against subsequent infections. Immune protection was dependent on systemic antibody responses and pathogen virulence behavior rather than the recognition of specific virulent antigens. Last, we demonstrate that an avirulent strain of in the field has background mutations in genes that are important for LPS structure. Our work reveals insight into how asymptomatic infections can arise mechanistically with immune resistance, mediating exclusion of phenotypically virulent enteric pathogen to promote asymptomatic carriage.
Topics: Animals; Mice; Enterobacteriaceae Infections; Virulence; Intestine, Small
PubMed: 37352357
DOI: 10.1126/sciadv.adg8719 -
Frontiers in Cellular and Infection... 2019
Topics: Host-Pathogen Interactions; Mycobacterium tuberculosis; Tuberculosis; Virulence
PubMed: 31649893
DOI: 10.3389/fcimb.2019.00331 -
Journal of Mathematical Biology Jul 2022This study explores the coevolutionary dynamics of host-pathogen interaction based on a susceptible-infected population model with density-dependent mortality. We assume...
This study explores the coevolutionary dynamics of host-pathogen interaction based on a susceptible-infected population model with density-dependent mortality. We assume that both the host's resistance and the pathogen's virulence will adaptively evolve, but there are inevitable costs in terms of host birth rate and disease-related mortality rate. Particularly, it is assumed that both the host resistance and pathogen virulence can affect the transmission rate. By using the approach of adaptive dynamics and numerical simulation, we find that the finally coevolutionary outcome depends on the strength of host-pathogen asymmetric interaction, the curvature of trade-off functions, and the intensity of density-dependent natural mortality. To be specific, firstly, we find that if the strengths of host-pathogen asymmetric interaction and disease-related mortality are relatively weak, or the density-dependent natural mortality is relatively strong, then the host resistance and pathogen virulence will evolve to a continuously stable strategy. However, if the strength of host-pathogen asymmetric interaction and disease-related mortality becomes stronger, then the host resistance and pathogen virulence will evolve periodically. Secondly, we find that if the intensities of both the birth rate trade-off function and the density-dependent natural mortality are relatively weak, but the strength of host-pathogen asymmetric interaction becomes relatively strong, then the evolution of host resistance will have a relatively strongly accelerating benefit, the evolutionary branching of host resistance will first arise. However, if the strength of host-pathogen asymmetric interaction is relatively weak, but the intensity of the trade-off function of disease-related mortality becomes relatively strong, then the evolution of pathogen virulence will have a relatively strongly decelerating cost, and the evolutionary branching of pathogen virulence will first arise. Thirdly, after the evolutionary branching of host resistance and pathogen virulence, we further study the coevolutionary dynamics of two-hosts-one-pathogen interaction and one-host-two-pathogens interaction. We find that if the evolutionary branching of host resistance arises firstly, then the finally evolutionary outcome contains a dimorphic host and a monomorphic pathogen population. If the evolutionary branching of pathogen virulence arises firstly, then the finally evolutionary outcome may contain a monomorphic host and a dimorphic pathogen population.
Topics: Biological Evolution; Computer Simulation; Host-Pathogen Interactions; Models, Biological; Virulence
PubMed: 35877051
DOI: 10.1007/s00285-022-01782-8