Biology subjects

Jiang, R. H.

Publications and source records attributed to Jiang, R. H..

4 recordsLinked to original sources

bioRxiv2023

Bacterial sepsis triggers stronger transcriptomic responses in larger primates

Empirical data relating body mass to immune defense against infections remain limited. Although the Metabolic Theory of Ecology predicts that larger organisms would have weaker immune responses, recent studies have suggested that the opposite may be true. These discoveries have led to the Safety Factor hypothesis, which proposes that larger organisms have evolved stronger immune defenses because they carry greater risks of exposure to pathogens and parasites. In this study, we simulated sepsis by exposing blood from nine primate species to a bacterial lipopolysaccharide (LPS), measured the relative expression of immune and other genes using RNAseq, and fit phylogenetic models to determine how gene expression was related to body mass. In contrast to non-immune-annotated genes, we discovered hypermetric scaling in the LPS-induced expression of innate immune genes, such that large primates had a disproportionately greater increase in gene expression of immune genes compared to small primates. Hypermetric immune gene expression appears to support the Safety Factor hypothesis, though this pattern may represent a balanced evolutionary mechanism to compensate for lower per-transcript immunological effectiveness. This study contributes to the growing body of immune allometry research, highlighting its importance in understanding the complex interplay between body size and immunity over evolutionary timescales. Author SummaryUnderstanding the relationship between an animals size and its ability to defend against disease can inform predictions about evolutionary tradeoffs and susceptibility to infection. Two major theories - the Metabolic Theory of Ecology (MTE) and the Safety Factor hypothesis - offer opposing views on how body size influences it immune defenses. In this study, we compared the immune gene expression of nine primate species to a simulated bacterial infection. We found that larger species mounted a stronger transcriptional immune response, consistent with either the Safety Factor hypothesis or an evolutionary pressure to compensate for and balance the effects expected in the context of the MTE.

evolutionary biology↗

bioRxiv2020

Extreme hyperallometry of mammalian antibacterial defenses

Terrestrial mammals span 7 orders of magnitude in body size, ranging from the < 2 g pygmy shrew (Suncus etruscus) to the > 3900 kg African elephant (Loxodonta africana). Although body size has profound effects on the behavior, physiology, ecology, and evolution of animals, how investment in immune defenses changes with body size is unknown. Here, we develop a novel 12-point dilution-curve approach to describe and compare antibacterial capacity against 3 bacterial species among >160 terrestrial species of mammals. We show that antibacterial activity in serum across mammals exhibits isometry, but the serum of large mammals is less hospitable to bacteria than would be predicted by their metabolic rates. Specifically, hypometric metabolic rates would predict that a large species should have disproportionately lower antibacterial capacity than small species, but body size is unrelated to killing capacity across species. Scaling of antibacterial immune defenses provides novel perspectives on the ecology of host-pathogen interactions, and on their co-evolutionary dynamics. These results have direct implications for effectively modeling the evolution of immune defenses and identifying potential reservoir hosts of zoonotic pathogens.

ecology↗

bioRxiv2020

Light pollution affects West Nile virus exposure risk across Florida.

Emerging infectious diseases (EIDs), including zoonotic arboviruses, present a global health threat. Multiple components of human land use change have been linked to arboviral emergence, but one pervasive factor that has received comparatively little attention is light pollution. Although often considered a component of built environments, artificial light at night (ALAN) outpaces the growth and spatial extent of urbanization, and thus affects areas where human population density and anthropogenic land changes are modest. West Nile virus (WNV) emergence has been described as peri-urban, but recent research suggests that its relative ubiquity in human-altered environments might actually be due to ALAN. Indeed, we found previously that experimental ALAN exposure enhanced avian competence to transmit WNV to mosquitoes. In the present study, we asked whether such organismal effects manifest ecologically by determining whether WNV exposure among sentinel chickens in Florida is related to local ALAN conditions. We found strong support for a nonlinear relationship between ALAN and WNV exposure in chickens with peak WNV risk occurring at low ALAN levels. Importantly, effects of ALAN on WNV exposure were stronger than other aspects of urbanization; only ambient temperature in the month prior to sampling had a comparable effect to ALAN. These results represent the first field evidence that ALAN might affect infectious disease exposure risk. We advocate for further research on how ALAN influences zoonotic risk, as well as efforts to study alternative nighttime lighting methods to reduce such risk. Significance StatementLight pollution associated with human development is a globally pervasive and rapidly expanding anthropogenic stressor; but despite documented effects on host immune functions and vector behaviors, how it affects infectious disease risk is unknown. Using data from the Florida Department of Health arbovirus surveillance program, we show that light pollution is a stronger predictor of variation in West Nile virus (WNV) exposure risk than many other previously implicated anthropogenic and natural environmental variables. Light pollution effects are nonlinear, so risk is highest in areas with dim light pollution. Our results highlight a new way that light pollution might affect human and wildlife health.

ecology↗

bioRxiv2017

Mitochondrial heteroplasmy is responsible for Atovaquone drug resistance in Plasmodium falciparum

Malaria is the most significant parasitic disease affecting humans, with 212 million cases and 429,000 deaths in 2 0151, and resistance to existing drugs endangers the global malaria elimination campaign. Atovaquone (ATO) is a safe and potent antimalarial drug that acts on cytochrome b (cyt. b) of the mitochondrial electron transport chain (mtETC) in Plasmodium falciparum, yet treatment failures result in resistance-conferring SNPs in cyt. b. Herein we report that rather than the expected de novo selection of resistance, previously unknown mitochondrial diversity is the genetic mechanism responsible for resistance to ATO, and potentially other cyt. b targeted drugs. We found that P. falciparum harbors cryptic cyt. b. Y268S alleles in the multicopy ([~]22 copies) mitochondrial genome prior to drug treatment, a phenomenon known as mitochondrial heteroplasmy. Parasites with cryptic Y268S alleles readily evolve into highly resistant parasites with >95% Y268S copies under in vitro ATO selection. Further we uncovered high mitochondrial diversity in a global collection of 1279 genomes in which heteroplasmic polymorphisms were >3-fold more prevalent than homoplasmic SNPs. Moreover, significantly higher mitochondrial genome copy number was found in Asia (e.g., Cambodia) versus Africa (e.g., Ghana). Similarly, ATO drug selections in vitro induced >3-fold mitochondrial copy number increases in ATO resistant lines. Hidden mitochondrial diversity is a previously unknown mechanism of antimalarial drug resistance and characterization of mitochondrial heteroplasmy will be of paramount importance in combatting resistance to antimalarials targeting the electron transport chain.

cell biology↗