Publications by authors named "Ricardo Ramiro"

Pemphigus foliaceus (PF) is a multifactorial skin disease. Substantial evidence for microbiota dysbiosis in skin disorders was gradually revealed. In PF patients' skin lesions, we characterized the profile of microbial communities and the expression of microbial peptides.

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Rands devastates forest species worldwide, causing significant ecological and economic impacts. The European chestnut () is susceptible to this hemibiotrophic oomycete, whereas the Asian chestnuts ( and ) are resistant and have been successfully used as resistance donors in breeding programs. The molecular mechanisms underlying the different disease outcomes among chestnut species are a key foundation for developing science-based control strategies.

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Article Synopsis
  • Severe malaria can cause serious conditions like severe anemia, coma, organ failure, and respiratory issues, leading to high mortality rates.
  • Research using rodent models indicates that the host's microbiota plays a role in developing malaria-related respiratory distress syndrome.
  • The anti-inflammatory response to fight tissue damage can weaken the body's ability to control bacteria, worsening lung disease, but using antibiotics like linezolid can help prevent fatal outcomes.
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Switching from a low-fat and high-fiber diet to a Western-style high-fat and high-sugar diet causes microbiota imbalances that underlay many pathological conditions (i.e., dysbiosis).

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New evidence shows that host-microbiota crosstalk can be modulated via endogenous miRNAs. We have previously reported that miR-21 ablation protects against liver injury in cholestasis. In this study, we investigated the role of miR-21 in modulating the gut microbiota during cholestasis and its effects in liver dysfunction.

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Most microbes live in spatially confined subpopulations. Under spatial structure conditions, the efficacy of natural selection is often reduced (relative to homogeneous conditions) due to the increased importance of genetic drift and local competition. Additionally, under spatial structure conditions, the fittest genotype may not always be the one with better access to the heterogeneous distribution of nutrients.

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Bacteria generally live in species-rich communities, such as the gut microbiota. Yet little is known about bacterial evolution in natural ecosystems. Here, we followed the long-term evolution of commensal Escherichia coli in the mouse gut.

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The evolution of new strains within the gut ecosystem is poorly understood. We used a natural but controlled system to follow the emergence of intraspecies diversity of commensal Escherichia coli, during three rounds of adaptation to the mouse gut (∼1,300 generations). We previously showed that, in the first round, a strongly beneficial phenotype (loss-of-function for galactitol consumption; gat-negative) spread to >90% frequency in all colonized mice.

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Hundreds of different bacterial species inhabit our intestines and contribute to our health status, with significant loss of species diversity typically observed in disease conditions. Within each microbial species a great deal of diversity is hidden and such intra-specific variation is also key to the proper homeostasis between the host and its microbial inhabitants. Indeed, it is at this level that new mechanisms of antibiotic resistance emerge and pathogenic characteristics evolve.

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The relative role of drift versus selection underlying the evolution of bacterial species within the gut microbiota remains poorly understood. The large sizes of bacterial populations in this environment suggest that even adaptive mutations with weak effects, thought to be the most frequently occurring, could substantially contribute to a rapid pace of evolutionary change in the gut. We followed the emergence of intra-species diversity in a commensal Escherichia coli strain that previously acquired an adaptive mutation with strong effect during one week of colonization of the mouse gut.

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Small-colony variants (SCVs) are commonly observed in evolution experiments and clinical isolates, being associated with antibiotic resistance and persistent infections. We recently observed the repeated emergence of Escherichia coli SCVs during adaptation to the interaction with macrophages. To identify the genetic targets underlying the emergence of this clinically relevant morphotype, we performed whole-genome sequencing of independently evolved SCV clones.

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A major challenge in disease ecology is to understand how co-infecting parasite species interact. We manipulate in vivo resources and immunity to explain interactions between two rodent malaria parasites, Plasmodium chabaudi and P. yoelii.

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Sexual reproduction is an obligate step in the life cycle of many parasites, including the causative agents of malaria (Plasmodium). Mixed-species infections are common in nature and consequently, interactions between heterospecific gametes occur. Given the importance of managing gene flow across parasite populations, remarkably little is understood about how reproductive isolation between species is maintained.

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Antagonistic interactions are likely important driving forces of the evolutionary process underlying bacterial genome complexity and diversity. We hypothesized that the ability of evolved bacteria to escape specific components of host innate immunity, such as phagocytosis and killing by macrophages (MΦ), is a critical trait relevant in the acquisition of bacterial virulence. Here, we used a combination of experimental evolution, phenotypic characterization, genome sequencing and mathematical modeling to address how fast, and through how many adaptive steps, a commensal Escherichia coli (E.

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Background: Over the last 6 decades, rodent Plasmodium species have become key model systems for understanding the basic biology of malaria parasites. Cell and molecular parasitology have made much progress in identifying genes underpinning interactions between malaria parasites, hosts, and vectors. However, little attention has been paid to the evolutionary genetics of parasites, which provides context for identifying potential therapeutic targets and for understanding the selective forces shaping parasites in natural populations.

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Malaria parasites must undergo a round of sexual reproduction in the blood meal of a mosquito vector to be transmitted between hosts. Developing a transmission-blocking intervention to prevent parasites from mating is a major goal of biomedicine, but its effectiveness could be compromised if parasites can compensate by simply adjusting their sex allocation strategies. Recently, the application of evolutionary theory for sex allocation has been supported by experiments demonstrating that malaria parasites adjust their sex ratios in response to infection genetic diversity, precisely as predicted.

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Adaptive phenotypic plasticity in life history traits, behaviours, and strategies is ubiquitous in biological systems. It is driven by variation in selection pressures across environmental gradients and operates under constraints imposed by trade-offs. Phenotypic plasticity has been thoroughly documented for multicellular taxa, such as insects, birds and mammals, and in many cases the underlying selective pressures are well understood.

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