Biology subjects

Talbott, K. M.

Publications and source records attributed to Talbott, K. M..

4 recordsLinked to original sources

bioRxiv2026

Mycoplasma gallisepticum uses itaconate-associated mitochondrial inhibition to suppress host immunometabolism

Many pathogens actively suppress early host immune responses to enhance their fitness. Mitochondria function as key regulators of immune activation, yet whether pathogens suppress host immunity by manipulating mitochondrial metabolism in vivo remains largely unknown. During an innate immune response, the metabolite itaconate increases in abundance and acts as an immunomodulator, due to its inhibition of succinate dehydrogenase (SDH), a key mitochondrial regulator of cellular immunity. We hypothesized that Mycoplasma gallisepticum (MG), a recently emerged pathogen of wild songbirds, most notably house finches (Haemorhous mexicanus), suppresses early host immune responses by limiting SDH-dependent immune activation via itaconate. We tested these hypotheses using experimental 3-day infection of finches with heat-killed MG, live MG or pharmacological elevation of the SDH inhibitor itaconate. Following inoculation, we quantified intracellular itaconate and mitochondrial respiratory function in peripheral blood mononuclear cells (PBMCs) and pro-inflammatory cytokine gene expression in erythrocytes, in addition to infected tissues (trachea and conjunctiva). Heat-killed MG increased SDH-dependent mitochondrial respiration in PBMCs and cytokine gene expression in erythrocytes, but live MG did not show these increases, but revealed increased itaconate accumulation in PBMCs. Dimethyl itaconate administration reproduced the suppressed metabolic and immune phenotype in blood cells observed with live MG, suggesting an itaconate-associated mechanism. In contrast, live MG increased mitochondrial respiration and gene expression levels of cytokines in eyelid conjunctiva, whereas other treatments did not. These findings indicate that MG suppresses host metabolic and cytokine signaling in systemically circulating immune cells through a mechanism consistent with itaconate-mediated inhibition of SDH-dependent mitochondrial respiration, while still inducing an inflammatory response at the site of infection. Our data suggest that MG, like other pathogens, can commandeer host immunometabolic pathways during infection to their benefit and that mitochondria are a key site of competition between host and pathogen.

immunology↗

bioRxiv2023

Determinants of spring migration departure dates in a New World sparrow: weather variables reign supreme

Numerous factors influence the timing of spring migration in birds, yet the relative importance of intrinsic and extrinsic variables on migration initiation remains unclear. To test for interactions among weather, migration distance, parasitism, and physiology in determining spring departure date, we used Dark-eyed Juncos (Junco hyemalis hyemalis) as a model migratory species known to harbor diverse and common haemosporidian parasites. Prior to spring migration departure from their wintering grounds in Indiana, USA, we quantified the intrinsic variables of fat, body condition (i.e., mass[~]tarsus residuals), physiological stress (i.e., ratio of heterophils to lymphocytes), cellular immunity (i.e., leukocyte composition and total count), migration distance (i.e., distance to the breeding grounds) using stable isotopes of hydrogen from feathers, and haemosporidian parasite intensity. We then attached nanotags to determine the timing of spring migration departure date using the Motus Wildlife Tracking System. We used additive Cox proportional hazard mixed models to test how risk of spring migratory departure was predicted by the combined intrinsic measures, along with meteorological predictors on the evening of departure (i.e., average wind speed and direction, relative humidity, and temperature). Model comparisons found that the best predictor of spring departure date was average nightly wind direction and a principal component combining relative humidity and temperature. Juncos were more likely to depart for spring migration on nights with largely southwestern winds and on warmer and drier evenings (relative to cooler and more humid evenings). Our results indicate that weather conditions at take-off are more critical to departure decisions than the measured physiological and parasitism variables.

ecology↗

bioRxiv2022

Novel Rickettsia spp. in two common overwintering North American passerines

American robins and dark-eyed juncos migrate across North America, but their contributions to arthropod-borne disease remain poorly characterized. We identified novel Rickettsia spp. in one wintering migrant per bird species related to bellii, transitional, and spotted fever group rickettsiae and suggest spring migration could disperse these pathogens hundreds-to-thousands of kilometers.

ecology↗

bioRxiv2020

Artificial light at night amplifies seasonal relapse of haemosporidian parasites in a widespread songbird

Urban habitats can shape interactions between hosts and parasites by altering not only exposure rates but also within-host processes. Artificial light at night is common in urban environments, and chronic exposure can impair host immunity in ways that may increase infection. However, studies of causal links between this stressor, immunity, and infection dynamics are rare, particularly in migratory animals. Here, we experimentally tested how artificial light at night affects cellular immunity and haemosporidian parasite intensity across the annual cycle of migrant and resident subspecies of the dark-eyed junco (Junco hyemalis). We monitored an experimental group exposed to light at night and a control group under natural light/dark cycles as they passed through short days simulating early spring to longer days simulating the breeding season, followed by fall migration. Using generalized additive models, we show that artificial light at night increased inflammation, and leukocyte counts were greatest in early spring and fall. At the start of the experiment, few birds had active infections based on microscopy, but PCR revealed many birds had chronic infections. Artificial light at night increased parasitemia across the annual cycle, with strong peaks in spring and fall that were largely absent in control birds. As birds were kept in indoor aviaries to prevent vector exposure, this increased parasitemia indicates relapse of chronic infection during costly life history stages (i.e., reproduction). Although the immunological and parasitological time series were in phase for control birds, cross-correlation analyses also revealed artificial light at night desynchronized leukocyte profiles and parasitemia, which could suggest a general exaggerated inflammatory response. Our study shows how a common anthropogenic influence can shape within-host processes to affect infection dynamics.

ecology↗