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Biology subjects

Oyesola, O. O.

Publications and source records attributed to Oyesola, O. O..

4 recordsLinked to original sources

Genetic and Environmental interactions contribute to immune variation in rewilded mice

The relative and synergistic contributions of genetics and environment to inter-individual immune response variation remain unclear, despite its implications for understanding both evolutionary biology and medicine. Here, we quantify interactive effects of genotype and environment on immune traits by investigating three inbred mouse strains rewilded in an outdoor enclosure and infected with the parasite, Trichuris muris. Whereas cytokine response heterogeneity was primarily driven by genotype, cellular composition heterogeneity was shaped by interactions between genotype and environment. Notably, genetic differences under laboratory conditions can be decreased following rewilding, and variation in T cell markers are more driven by genetics, whereas B cell markers are driven more by environment. Importantly, variation in worm burden is associated with measures of immune variation, as well as genetics and environment. These results indicate that nonheritable influences interact with genetic factors to shape immune variation, with synergistic impacts on the deployment and evolution of defense mechanisms.

immunology↗

Helminth exposure protects against murine SARS-CoV-2 infection through macrophage dependent T cell activation

Helminth endemic regions report lower COVID-19 morbidity and mortality. Here, we show that lung remodeling from a prior infection with a lung migrating helminth, Nippostrongylus brasiliensis, enhances viral clearance and survival of human-ACE2 transgenic mice challenged with SARS-CoV-2 (SCV2). This protection is associated with a lymphocytic infiltrate including an increased accumulation of pulmonary SCV2-specific CD8+ T cells and anti-CD8 antibody depletion abrogated the N. brasiliensis-mediated reduction in viral loads. Pulmonary macrophages with a type-2 transcriptional signature persist in the lungs of N. brasiliensis exposed mice after clearance of the parasite and establish a primed environment for increased antigen presentation. Accordingly, depletion of macrophages ablated the augmented viral clearance and accumulation of CD8+ T cells driven by prior N. brasiliensis infection. Together, these findings support the concept that lung migrating helminths can limit disease severity during SCV2 infection through macrophage-dependent enhancement of anti-viral CD8+ T cell responses. O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=139 SRC="FIGDIR/small/515832v1_ufig1.gif" ALT="Figure 1"> View larger version (55K): org.highwire.dtl.DTLVardef@1c17a22org.highwire.dtl.DTLVardef@13967b3org.highwire.dtl.DTLVardef@1c723a7org.highwire.dtl.DTLVardef@f5e038_HPS_FORMAT_FIGEXP M_FIG C_FIG

immunology↗

Single Cell Analysis Reveals Multi-faceted miR-375 Regulation of the Intestinal Crypt

The role of individual miRNAs in small intestinal (SI) epithelial homeostasis is under-explored. In this study, we discovered that miR-375 is among the most enriched miRNAs in intestinal crypts and stem cells (ISCs), especially facultative ISCs. We then showed by multiple manipulations, including CRISPR/Cas9 editing, that miR-375 is strongly suppressed by Wnt-signaling. Single-cell RNA-seq analysis of SI crypt-enriched cells from miR-375 knockout (375-KO) mice revealed elevated numbers of tuft cells and increased expression of pro-proliferative genes in ISCs. Accordingly, the genetic loss of miR-375 promoted resistance to helminth infection and enhanced the regenerative response to irradiation. The conserved effects of miR-375 were confirmed by gain-of-function studies in Drosophila midgut stem cells in vivo. Moreover, functional experiments in enteroids uncovered a regulatory relationship between miR-375 and Yap1 that controls cell survival. Finally, analysis of mouse model and clinical data revealed an inverse association between miR-375 levels and intestinal tumor development. HighlightsO_LImiR-375 is one of the most enriched miRNAs in ISCs, especially facultative ISCs. C_LIO_LImiR-375 modifies tuft cell abundance and pro-proliferative gene expression in ISCs. C_LIO_LILoss of miR-375 in mice enhances the host response to helminth infection and crypt regeneration. C_LIO_LIMouse and human intestinal cancer are associated with reduced miR-375 expression. C_LI eTOC BlurbSethupathy and colleagues show that miR-375 is a Wnt-responsive, ISC-enriched miRNA that serves as a break on intestinal crypt proliferation. They also show that miR-375 modulates tuft cell abundance and pro-proliferative gene expression in ISCs, that miR-375 loss enhances the host response to helminth infection as well as crypt regeneration post-irradiation, and its reduced expression is associated with intestinal cancer.

molecular biology↗

Limited intra-host diversity and background evolution accompany 40 years of canine parvovirus host adaptation and spread

Canine parvovirus (CPV) is a highly successful pathogen that has sustained pandemic circulation in dogs for more than 40 years. Here, integrating full-genome and deep sequencing analyses, structural information, and in vitro experimentation, we describe the macro- and micro-scale features that have accompanied CPVs evolutionary success. Despite 40 years of viral evolution, all CPV variants are >[~]99% identical in nucleotide sequence, with only a limited number (<40) of mutations becoming fixed or widespread during this time. Notably, most changes in the major capsid protein (VP2) are nonsynonymous and fall within, or adjacent to, the overlapping receptor footprint or antigenic regions, suggesting competitive selective pressures have played a key role in CPV evolution and likely constrained its evolutionary trajectory. Moreover, among the limited number of variable sites, CPV genomes exhibit complex patterns of variation that likely include parallel evolution, reversion, and recombination, making phylogenetic inference difficult. Additionally, deep sequencing of viral DNA in original clinical samples collected from dogs and other host species sampled between 1978 and 2018 revealed few sub-consensus single nucleotide variants (SNVs) above [~]0.5%, and experimental passages demonstrate that substantial pre-existing genetic variation is not necessarily required for rapid host receptor driven adaptation. Together, these findings suggest that although CPV is capable of rapid host adaptation, relatively low mutation rate, pleiotropy, and/or a lack of selective challenges since its initial emergence have reduced the long-term genetic diversity accumulation and evolutionary rate. Hence, continuously high levels of inter- and intra-host diversity are not intrinsic to highly adaptable viruses.\n\nIMPORTANCERapid mutation rates and correspondingly high levels of standing intra-host diversity and accumulated inter-host diversity over epidemic scales are often cited as key features of viruses with the capacity for emergence and sustained transmission in a new host species. However, most of this information comes from studies of RNA viruses, with relatively little being known about that evolutionary processes that occur for viruses with DNA genomes. Here we provide a unique model of virus evolution, integrating both long-term global-scale and short-term intra-host evolutionary processes of a virus in a new host animal. Our analysis reveals that successful host jumping and sustained onward transmission does not necessarily depend on a high level of intra-host diversity or result in the continued accumulation of high levels of long-term evolution change. These findings indicate that all aspects of a viruss biology and ecology are relevant when considering their adaptability.

evolutionary biology↗