Search bioRxiv⌕ Search

Biology subjects

Jarquin-Diaz, V. H.

Publications and source records attributed to Jarquin-Diaz, V. H..

12 recordsLinked to original sources

A nutrient-derived dietary gradient links gut microbiome composition, network structure, and host physiology

Diet is an important determinant of gut microbiome composition and host physiology. However, dietary exposure is often represented using categorical groups that may not fully capture variation in nutrient intake or its associations with gut microbiome and host biomarkers. Here, we analyzed diet-microbiome-host physiology relationships in healthy adults with long-term adherence ([≥]2 years) to omnivore, vegetarian, or vegan diets. We integrated four-day weighed dietary records, blood biomarkers, and 16S rRNA gene sequencing to characterize dietary intake, host physiology, and gut microbiome composition. We derived nutrient intake gradients by dimensionality reduction of representative nutrients and identified the second nutrient intake gradient (NIG2) as a quantitative axis reflecting variation between animal- and plant-leaning nutrient profiles, broadly recapitulating categorical dietary groups. While NIG2 showed no association with microbiome within-sample diversity, it explained gut microbiome compositional variation that was not detected using categorical dietary groups. Mediation analyses identified nominal candidate microbiome-mediated diet-biomarker relationships involving thyroid-related, hematological, and vitamin-related biomarkers. Network analyses of NIG2-defined animal-leaning and plant-leaning subsets identified subset-specific microbial associations and differences in microbial community structure and potential interactions. Overall, this continuous nutrient-derived dietary gradient provides a quantitative exposure metric for characterizing diet-microbiome-host physiology relationships. Graphical Abstract O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=97 SRC="FIGDIR/small/740531v1_ufig1.gif" ALT="Figure 1"> View larger version (23K): org.highwire.dtl.DTLVardef@104a825org.highwire.dtl.DTLVardef@bb2b33org.highwire.dtl.DTLVardef@114171org.highwire.dtl.DTLVardef@df9c38_HPS_FORMAT_FIGEXP M_FIG C_FIG

microbiology↗

The elusive resistome: a global comparison reveals large discrepancies among detection pipelines

Identifying antibiotic resistance genes (ARGs) from metagenomic data is critical for studying antimicrobial resistance across microbial communities and pathogens. However, there is no standardized methodology for ARG annotation. Here, we compare ten commonly used ARG detection pipelines by analysing over 270 million prokaryotic genes from the Global Microbial Gene Catalogue across 13 distinct habitats. We observed up to a 45-fold difference in the number of reported ARGs, with a mean Jaccard index of only 16% between pipelines. Pipeline selection profoundly impacted downstream biological interpretations, with drastic changes to estimates of ARG relative abundance and richness, to the characterization of pan- and core-resistomes, and to the class-level composition of the inferred resistome. ARG detection pipelines make different, defensible trade-offs, and no single approach should be treated as authoritative. Therefore, users should justify and communicate choices carefully, as our analyses show that, taken uncritically, the same data can support conflicting biological and ecological interpretations.

bioinformatics↗

Anthropogenic land use exerts selection pressures on the resistome of a wild rodent

Antimicrobial resistance poses a significant global health challenge. However, the factors maintaining antimicrobial resistance genes (ARGs) in wildlife microbiomes remain unclear particularly in species inhabiting human-dominated landscapes. We analysed 875 gut metagenomes from wild house mice (Mus musculus) on German farms between 2016 and 2022 to identify environmental and host determinants of ARG occurrence. Using joint species distribution models, we quantified the influence of landscape, climate and mouse associated characteristics on the occurrence of individual ARGs and on trait dependence among genes. Environmental variables and livestock farming intensity explained more than 21% of ARG variation, whereas host characteristics accounted for less than 10%. Analysis of ARG traits revealed that agricultural land use and exposure to livestock increased the occurrence of mobile ARGs. Pig density was strongly associated with integron-encoded sulfonamide resistance genes and genes conferring tetracycline and beta-lactam resistance. Consistent with these findings, mouse resistomes closely resembled those of livestock manure. Taken together, our results show that landscape conditions, particularly farming intensity, shape the distribution of specific ARGs and mobile ARGs in house mice microbiomes. Understanding the factors impacting ARGs prevalence in wildlife is crucial for determining transmission of antimicrobial resistant microorganisms from animal and environmental reservoirs.

microbiology↗

Global analysis of infant gut microbiota revealed distinctive maturation dynamics across lifestyles

The infant gut microbiome develops during the first years of life and influences long-term health through its interaction with immune system development. However, our understanding of early-life microbiome assembly is biased by the predominance of infants with industrialized lifestyles from North America and Europe. Here, we address this bias by assembling a globally representative dataset of infant gut microbiomes to train a microbiome maturation model that can characterize lifestyle specific patterns of microbial maturation as a function of age. Models trained exclusively on industrialized infants perform poorly when applied to non-industrialized datasets. In contrast, more diverse models including individuals from both lifestyles achieve increased correlation between microbial and chronological age. We identified differences in relevant taxa associated with the maturation in the different lifestyles. Additionally, our modeling approach detects a delay in the microbial maturation of independent cohorts of severely malnourished and preterm infants compared to healthy ones. Our results underscore the relevance of global diversity in microbiome research and provide deeper insights into context-dependent maturation dynamics of the infant gut microbiome.

microbiology↗

Baseline microbiome composition impacts resilience to and recovery following antibiotics

The gut microbiome of healthy individuals naturally undergoes temporal changes linked to the dynamics of its community components1. These dynamics are only observable in longitudinal studies; they are particularly relevant to understanding ecosystem responses to external environment disturbances. External exposures, such as antibiotic treatment, significantly reshape the gut microbiome, impacting both pathogen and commensal microbes2. The gut microbiome plays pivotal roles in digestion, nutrient absorption, and mental health, influencing immune systems, obesity, and various diseases3-6. Consequently, beyond the short-term effects on the host gut microbiome dynamics, alterations resulting from antibiotic exposure also have enduring repercussions on human health and physiological equilibrium7. Therefore, enhancing gut microbiome resilience during antibiotic treatment is essential, with the goal of mitigating prolonged adverse effects. Here, we explored the impact of pre-antibiotic microbial and functional profiles on resilience, suggesting that specific baseline features exhibit greater resilience to antibiotics-induced changes. Our results identified an uncultured Faecalibacterium prausnitzii taxon as a species at baseline associated with diminished resilience. We demonstrated that this association could be linked to the role of this F. prausnitzii taxon as a keystone species. Additionally, we observed the influence of other commensal bacteria, such as Bifidobacterium animalis and Lactobacillus acidophilus, as well as functional modules, such as multidrug resistance efflux pump, on resilience. This lays the foundations for designing targeted strategies to promote a resilient gut microbiome before antibiotic treatment, alleviating possible prolonged effects on human health.

microbiology↗

Mucosal washes are useful for sampling intestinal mucus-associated microbiota despite low biomass

Exploring the dynamic relationship between mucus-associated microbiota and host health is pivotal, yet prevalent studies using stool samples may not accurately represent these bacteria. Here, we explored mucus-associated microbiota in the gastrointestinal tract of mice and the terminal ileum in humans, using three different sample types: mucosal washes, scraping, and intestinal content in mice and biopsies and mucosal washes in humans. We employed DNA quantification and 16S rRNA sequencing to assess how comparable the information yielded from different sample types, evaluating findings relative to expectations from state-of-the-art and under controlled benchmarks. Mucosal washes in mice exhibited higher bacterial DNA and lower host DNA contamination than scraping samples. Similarly, in humans, washes surpassed biopsies in bacterial yield. Despite variations in read counts, microbiota diversity and composition remained remarkably similar between methods in both species, faithfully reflecting expected genotypic and phenotypic differences. We conclude that washes reduce host contamination without inducing substantial compositional bias when sampling mucosal microbiota. Our findings emphasize mucosal washes as alternatives to biopsies in humans and scrapings in mice, providing insights for improving result transferability across hosts. Our research underscores the importance of considering the mucus-associated microbiota to track host-microbiome interactions closer to their actual interface surface.

systems biology↗

Subspecies divergence, hybridisation and the spatial environment shape phylosymbiosis in the microbiome of house mice

Closely related host species share similar symbionts, yet how host genetics and the environment affect symbiont communities at different stages of host genetic divergence remains largely unknown. Similarly, it is unclear whether host-symbiont associations result from or contribute to host divergence. We examined the intestinal community of 619 wild-caught mice from Germanys European house mouse hybrid zone. Here, hybridisation upon secondary contact reflects divergence and could be traced gradually. Temporal and spatial factors were strong predictors of microbiome composition. Subspecies divergence predicted the composition similarity of the overall microbiome, specifically in the bacteria, parasite and fungal components. The effect of hybridisation was generally weak but significant for the fungal component. We confirmed our results in experiments with wild-derived inbred mice: subspecies genetic distances and hybridisation predicted the overall microbiome composition, and hybridisation further predicted fungal similarities among individuals. Fungi seemed more stable to the community perturbation of infection than other components of the microbiome. Differences between subspecies were more substantial across different microbiome components than those associated with hybridisation. Diverged microbiomes are a product of host divergence and are maintained by host genetics upon large environmental effects. These results provide a unique perspective into the ecoevolutionary processes shaping phylosymbiosis.

evolutionary biology↗

Decoupling of resistance and tolerance against one of two related parasites (Eimeria) in mice

Resistance (host capacity to reduce parasite burden) and tolerance (host capacity to reduce impact on its health for a given parasite burden) manifest two different lines of defence. Tolerance can be independent from resistance, traded-off against it, or the two can be positively correlated because of redundancy in underlying (immune) processes. We here tested whether this coupling between tolerance and resistance could differ upon infection with closely related parasite species. We tested this in experimental infections with two parasite species of the genus Eimeria. We measured proxies for resistance (the (inverse of) number of parasite transmission stages (oocysts) per gram of feces at the day of maximal shedding) and tolerance (the slope of maximum relative weight loss compared to day of infection on number of oocysts per gram of feces at the day of maximal shedding for each host strain) in four inbred mouse strains and four groups of F1 hybrids belonging to two mouse subspecies, Mus musculus domesticus and M. m. musculus. We found a negative correlation between resistance and tolerance against E. falciformis, while the two are uncoupled against E. ferrisi. We conclude that resistance and tolerance against the first parasite species might be traded off, but evolve more independently in different mouse genotypes against the latter. We argue that evolution of the host immune defences can be studied largely irrespective of parasite isolates if resistance-tolerance coupling is absent or weak (E. ferrisi) but host-parasite coevolution is more likely observable and best studied in a system with negatively correlated tolerance and resistance (E. falciformis).

evolutionary biology↗

Generalist Eimeria species in rodents: multilocus analyses indicate inadequate resolution of established markers

Intracellular parasites of the genus Eimeria are described as tissue/host specific. Phylogenetic classification of rodent Eimeria suggested that some species have a broader host range than previously assumed. We explore if Eimeria spp. infecting house mice are misclassified by the most widely used molecular markers due to a lack of resolution, or if, instead, these parasite species are indeed infecting multiple host species.\n\nWith the commonly used markers (18S/COI), we recovered monophyletic clades of E. falciformis and E. vermiformis from Mus that included E. apionodes identified in other rodent host species (Apodemus spp., Myodes glareolus, and Microtus arvalis). A lack of internal resolution in these clades could suggest the existence of a species complex with a wide host range infecting murid and cricetid rodents. We question, however, the power of COI and 18S markers to provide adequate resolution for assessing host specificity. In addition to the rarely used marker ORF470 from the apicoplast genome, we present multilocus genotyping as an alternative approach. Phylogenetic analysis of 35 nuclear markers differentiated E. falciformis from house mice from isolates from Apodemus hosts. Isolates of E. vermiformis from Mus are still found in clusters interleaved with non-Mus isolates, even with this high resolution data.\n\nIn conclusion, we show that species-level resolution should not be assumed for COI and 18S markers in Coccidia. Host-parasite co-speciation at shallow phylogenetic nodes, as well as contemporary coccidian host ranges more generally, are still open questions that need to be addressed using novel genetic markers with higher resolution.

microbiology↗

Intensity of infection with intracellular Eimeria spp. and pinworms is reduced in hybrid mice compared to parental subspecies

The longstanding impression that hybrid mice are more highly parasitized and therefore less fit than parentals persists despite the findings of recent studies. Working across a novel transect of the European House Mouse hybrid zone we assessed intracellular infections by Eimeria, a parasite of high pathogenicity, and infections by pinworms, assumed to be less pathogenic. For Eimeria we found lower intensities in hybrid hosts than in parental mice but no evidence of lowered probability of infection in the centre of the hybrid zone. This means ecological and epidemiological factors are very unlikely to be responsible for the reduced load of infected hybrids. Focussing on parasite intensity (load in infected hosts) we also corroborated reduced pinworm loads reported for hybrid mice in previous studies. In addition we questioned whether differences in body condition during infection would indicate different impacts on hybrid vs. parental hosts health. We couldnt show such an effect. We conclude that intensity of diverse parasites, including the previously unstudied Eimeria, is reduced in hybrid mice compared to parental subspecies. We suggest caution in extrapolating this to differences in hybrid host fitness in the absence of, for example, evidence for a link between parasitemia and health.

evolutionary biology↗

Detection and quantification of house mouse Eimeria at the species level - challenges and solutions for the assessment of Coccidia in wildlife

Detection and quantification of coccidia in studies of wildlife can be challenging. Therefore, the prevalence of coccidia is often not assessed at the parasite species level in non-livestock animals. Parasite species-specific prevalences are especially important when studying evolutionary questions in wild populations. We tested whether increased host population density increases the prevalence of individual Eimeria species at the farm level, as predicted by epidemiological theory. We studied free-living commensal populations of the house mouse (Mus musculus) in Germany and established a strategy to detect and quantify Eimeria infections. We show that a novel diagnostic primer targeting the apicoplast genome (Ap5) and coprological assessment after flotation provide complementary detection results increasing sensitivity. Genotyping PCRs confirm detection in a subset of samples and cross-validation of different PCR markers does not indicate a bias towards a particular parasite species in genotyping. We were able to detect double infections and to determine the preferred niche of each parasite species along the distal-proximal axis of the intestine. Parasite genotyping from tissue samples provides an additional indication for the absence of species bias in genotyping amplifications. Three Eimeria species were found infecting house mice at different prevalences: Eimeria ferrisi (16.7%; 95% CI 13.2 - 20.7), E. falciformis (4.2%; 95% CI 2.6 - 6.8) and E. vermiformis (1.9%; 95% CI 0.9 - 3.8). We also find that mice in dense populations are more likely to be infected with E. falciformis and E. ferrisi.\n\nWe provide methods for the assessment of prevalences of coccidia at the species level in rodent systems. We show and discuss how such data can help to test hypotheses in ecology, evolution and epidemiology on a species level.

microbiology↗

Eimeria falciformis BayerHaberkorn1970 and novel wild derived isolates from house mice: differences in parasite lifecycle, pathogenicity and host immune reactions

Species of Eimeria (Apicomplexa:Coccidia) differ in the timing of lifecycle progression and resulting infections vary in host immune reactions and pathology they induce. Eimeria infections in house mice are used as models for basic immunology and the most commonly used isolates have been passaged in laboratory mice for over 50 years. We questioned in how far such isolates are still representative for infections in natural systems.\n\nIn the current study, we address this question by comparing the \"laboratory isolate\" E. falciformis BayerHaberkorn1970 with a novel, wild derived isolate E. falciformis Brandenburg88, and contrast this with another novel wild derived isolate, E. ferrisi Brandenburg64. We compare parasite lifecycle progression. We relate this to immune cell infiltration at the site of infection (in the caecum) and cytokine gene expression in the spleen as a measure of host immune response. We assess host weight loss as a measure of pathogenicity.\n\nA species-specific slower parasite lifecyle progression and higher pathogenicity are observed for E. falciformis vs. E. ferrisi. Host cytokines, in contrast, are expressed at significantly higher level in the spleen of mice infected with the E. falciformis laboratory isolate than in both wild derived isolates, irrespective of the species. Differences in histopathology are observable between all three isolates: The E. falciformis BayerHaberkorn1970 laboratory isolate induces the strongest inflammation and cellular infiltration (with lymphocytes, plasma cells and eosinophilic granulocytes) followed by the wild derived E. falciformis Brandenburg88 isolate. E. ferrisi Brandenburg64 is inducing milder histological changes than both E. falciformis isolates.\n\nIt can be speculated that the serial passaging of E. falciformis BayerHaberkorn1970 has resulted in evolutionary divergence rendering this isolate more virulent in NMRI mice. Caution is needed when findings from experimental infection with laboratory strains should be integrated with observations in natural systems.\n\nHighlightsO_LIE. ferrisi has a shorter pre-patency than wild-derived and laboratory isolates of E. falciformis.\nC_LIO_LIE. ferrisi is less virulent than both E. falciformis isolates and the timing of maximal oocyst shedding relative to host weight loss differs.\nC_LIO_LIThe laboratory strain of E. falciformis induces stronger cytokine expression in the spleen than both wild derived strains of E. falciformis and E. ferrisi.\nC_LIO_LIThe laboratory strain of E. falciformis induces stronger tissue infiltration of immune cells than the wild-derived strain. E. ferrisi infections are associated with the lowest infiltration.\nC_LI

microbiology↗