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Advances in Experimental Medicine and... 2020Calcium (Ca) is a universal signaling ion, whose major informational role shaped the evolution of signaling pathways, enabling cellular communications and responsiveness... (Review)
Review
Calcium (Ca) is a universal signaling ion, whose major informational role shaped the evolution of signaling pathways, enabling cellular communications and responsiveness to both the intracellular and extracellular environments. Elaborate Ca regulatory networks have been well characterized in eukaryotic cells, where Ca regulates a number of essential cellular processes, ranging from cell division, transport and motility, to apoptosis and pathogenesis. However, in bacteria, the knowledge on Ca signaling is still fragmentary. This is complicated by the large variability of environments that bacteria inhabit with diverse levels of Ca. Yet another complication arises when bacterial pathogens invade a host and become exposed to different levels of Ca that (1) are tightly regulated by the host, (2) control host defenses including immune responses to bacterial infections, and (3) become impaired during diseases. The invading pathogens evolved to recognize and respond to the host Ca, triggering the molecular mechanisms of adhesion, biofilm formation, host cellular damage, and host-defense resistance, processes enabling the development of persistent infections. In this review, we discuss: (1) Ca as a determinant of a host environment for invading bacterial pathogens, (2) the role of Ca in regulating main events of host colonization and bacterial virulence, and (3) the molecular mechanisms of Ca signaling in bacterial pathogens.
Topics: Bacteria; Bacterial Infections; Calcium; Host Microbial Interactions; Humans; Virulence
PubMed: 31646536
DOI: 10.1007/978-3-030-12457-1_33 -
Fungal Genetics and Biology : FG & B Sep 2017Fungi, like other organisms, actively sense the environmental light conditions in order to drive adaptive responses, including protective mechanisms against the... (Review)
Review
Fungi, like other organisms, actively sense the environmental light conditions in order to drive adaptive responses, including protective mechanisms against the light-associated stresses, and to regulate development. Ecological niches are characterized by different light regimes, for instance light is absent underground, and light spectra from the sunlight are changed underwater or under the canopy of foliage due to the absorption of distinct wavelengths by bacterial, algal and plant pigments. Considering the fact that fungi have evolved to adapt to their habitats, the complexities of their 'visual' systems may vary significantly. Fungi that are pathogenic on plants experience a special light regime because the host always seeks the optimum light conditions for photosynthesis - and the pathogen has to cope with this environment. When the pathogen lives under the canopy and is indirectly exposed to sunlight, it is confronted with an altered light spectrum enriched for green and far-red light. Botrytis cinerea, the gray mold fungus, is an aggressive plant pathogen mainly infecting the above-ground parts of the plant. As outlined in this review, the Leotiomycete maintains a highly sophisticated light signaling machinery, integrating (near)-UV, blue, green, red and far-red light signals by use of at least eleven potential photoreceptors to trigger a variety of responses, i.e. protection (pigmentation, enzymatic systems), morphogenesis (conidiation, apothecial development), entrainment of a circadian clock, and positive and negative tropism of multicellular (conidiophores, apothecia) and unicellular structures (conidial germ tubes). In that sense, 'looking through the eyes' of this plant pathogen will expand our knowledge of fungal photobiology.
Topics: Botrytis; Circadian Clocks; Cryptochromes; Light; Photoreceptors, Microbial; Phototropism; Plant Components, Aerial; Signal Transduction; Virulence
PubMed: 28648816
DOI: 10.1016/j.fgb.2017.06.002 -
The ISME Journal Aug 2016Many micro-organisms employ a parasitic lifestyle and, through their antagonistic interactions with host populations, have major impacts on human, agricultural and... (Review)
Review
Many micro-organisms employ a parasitic lifestyle and, through their antagonistic interactions with host populations, have major impacts on human, agricultural and natural ecosystems. Most pathogens are likely to host parasites of their own, that is, hyperparasites, but how nested chains of parasites impact on disease dynamics is grossly neglected in the ecological and evolutionary literature. In this minireview we argue that the diversity and dynamics of micro-hyperparasites are an important component of natural host-pathogen systems. We use the current literature from a handful of key systems to show that observed patterns of pathogen virulence and disease dynamics may well be influenced by hyperparasites. Exploring these factors will shed light on many aspects of microbial ecology and disease biology, including resistance-virulence evolution, apparent competition, epidemiology and ecosystem stability. Considering the importance of hyperparasites in natural populations will have applied consequences for the field of biological control and therapeutic science, where hyperparastism is employed as a control mechanism but not necessarily ecologically understood.
Topics: Animals; Biological Evolution; Ecology; Ecosystem; Host-Pathogen Interactions; Humans; Parasites; Virulence
PubMed: 26784356
DOI: 10.1038/ismej.2015.247 -
Frontiers in Cellular and Infection... 2019During infection, bacterial pathogens successfully sense, respond and adapt to a myriad of harsh environments presented by the mammalian host. This exquisite level of... (Review)
Review
During infection, bacterial pathogens successfully sense, respond and adapt to a myriad of harsh environments presented by the mammalian host. This exquisite level of adaptation requires a robust modulation of their physiological and metabolic features. Additionally, virulence determinants, which include host invasion, colonization and survival despite the host's immune responses and antimicrobial therapy, must be optimally orchestrated by the pathogen at all times during infection. This can only be achieved by tight coordination of gene expression. A large body of evidence implicate the prolific roles played by bacterial regulatory RNAs in mediating gene expression both at the transcriptional and post-transcriptional levels. This review describes mechanistic and regulatory aspects of bacterial regulatory RNAs and highlights how these molecules increase virulence efficiency in human pathogens. As illustrative examples, , the uropathogenic strain of , and have been selected.
Topics: Animals; Bacterial Infections; Bacterial Physiological Phenomena; Gene Expression Regulation, Bacterial; Host-Pathogen Interactions; Humans; RNA, Bacterial; Species Specificity; Virulence; Virulence Factors
PubMed: 31649894
DOI: 10.3389/fcimb.2019.00337 -
Proceedings of the National Academy of... Nov 2023The expansion and intensification of livestock production is predicted to promote the emergence of pathogens. As pathogens sometimes jump between species, this can...
The expansion and intensification of livestock production is predicted to promote the emergence of pathogens. As pathogens sometimes jump between species, this can affect the health of humans as well as livestock. Here, we investigate how livestock microbiota can act as a source of these emerging pathogens through analysis of , a ubiquitous component of the respiratory microbiota of pigs that is also a major cause of disease on pig farms and an important zoonotic pathogen. Combining molecular dating, phylogeography, and comparative genomic analyses of a large collection of isolates, we find that several pathogenic lineages of emerged in the 19th and 20th centuries, during an early period of growth in pig farming. These lineages have since spread between countries and continents, mirroring trade in live pigs. They are distinguished by the presence of three genomic islands with putative roles in metabolism and cell adhesion, and an ongoing reduction in genome size, which may reflect their recent shift to a more pathogenic ecology. Reconstructions of the evolutionary histories of these islands reveal constraints on pathogen emergence that could inform control strategies, with pathogenic lineages consistently emerging from one subpopulation of and acquiring genes through horizontal transfer from other pathogenic lineages. These results shed light on the capacity of the microbiota to rapidly evolve to exploit changes in their host population and suggest that the impact of changes in farming on the pathogenicity and zoonotic potential of is yet to be fully realized.
Topics: Animals; Humans; Swine; Streptococcal Infections; Farms; Swine Diseases; Virulence; Streptococcus suis; Livestock
PubMed: 37963246
DOI: 10.1073/pnas.2307773120 -
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 -
Microbiology Spectrum Oct 2014Gram-positive bacteria are leading causes of many types of human infection, including pneumonia, skin and nasopharyngeal infections, as well as urinary tract and... (Review)
Review
Gram-positive bacteria are leading causes of many types of human infection, including pneumonia, skin and nasopharyngeal infections, as well as urinary tract and surgical wound infections among hospitalized patients. These infections have become particularly problematic because many of the species causing them have become highly resistant to antibiotics. The role of mobile genetic elements, such as plasmids, in the dissemination of antibiotic resistance among Gram-positive bacteria has been well studied; less well understood is the role of mobile elements in the evolution and spread of virulence traits among these pathogens. While these organisms are leading agents of infection, they are also prominent members of the human commensal ecology. It appears that these bacteria are able to take advantage of the intimate association between host and commensal, via virulence traits that exacerbate infection and cause disease. However, evolution into an obligate pathogen has not occurred, presumably because it would lead to rejection of pathogenic organisms from the host ecology. Instead, in organisms that exist as both commensal and pathogen, selection has favored the development of mechanisms for variability. As a result, many virulence traits are localized on mobile genetic elements, such as virulence plasmids and pathogenicity islands. Virulence traits may occur within a minority of isolates of a given species, but these minority populations have nonetheless emerged as a leading problem in infectious disease. This chapter reviews virulence plasmids in nonsporulating Gram-positive bacteria, and examines their contribution to disease pathogenesis.
Topics: Animals; Bacterial Infections; Gene Transfer, Horizontal; Gram-Positive Bacteria; Humans; Plasmids; Virulence; Virulence Factors
PubMed: 25544937
DOI: 10.1128/microbiolspec.PLAS-0002-2013 -
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 -
Virulence 2014Until quite recently and since the late 19(th) century, medical microbiology has been based on the assumption that some micro-organisms are pathogens and others are not.... (Review)
Review
Until quite recently and since the late 19(th) century, medical microbiology has been based on the assumption that some micro-organisms are pathogens and others are not. This binary view is now strongly criticized and is even becoming untenable. We first provide a historical overview of the changing nature of host-parasite interactions, in which we argue that large-scale sequencing not only shows that identifying the roots of pathogenesis is much more complicated than previously thought, but also forces us to reconsider what a pathogen is. To address the challenge of defining a pathogen in post-genomic science, we present and discuss recent results that embrace the microbial genetic diversity (both within- and between-host) and underline the relevance of microbial ecology and evolution. By analyzing and extending earlier work on the concept of pathogen, we propose pathogenicity (or virulence) should be viewed as a dynamical feature of an interaction between a host and microbes.
Topics: Animals; Bacteria; Biological Evolution; Fungi; Genetic Variation; Host-Parasite Interactions; Host-Pathogen Interactions; Humans; Virulence; Viruses
PubMed: 25483864
DOI: 10.4161/21505594.2014.960726 -
Nature Microbiology May 2022Fungal pathogens cause more than a billion human infections every year, resulting in more than 1.6 million deaths annually. Understanding the natural history and... (Review)
Review
Fungal pathogens cause more than a billion human infections every year, resulting in more than 1.6 million deaths annually. Understanding the natural history and evolutionary ecology of fungi is helping us understand how disease-relevant traits have repeatedly evolved. Different types and mechanisms of genetic variation have contributed to the evolution of fungal pathogenicity and specific genetic differences distinguish pathogens from non-pathogens. Insights into the traits, genetic elements, and genetic and ecological mechanisms that contribute to the evolution of fungal pathogenicity are crucial for developing strategies to both predict emergence of fungal pathogens and develop drugs to combat them.
Topics: Fungi; Humans; Life Style; Virulence
PubMed: 35508719
DOI: 10.1038/s41564-022-01112-0