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Data from: Maternal immunization increases nestling energy expenditure, immune function, and fledging success in a passerine bird

Female birds transfer maternally-derived antibodies (matAb) to their nestlings, via the egg yolk. These antibodies are thought to provide passive protection, and allow nestlings to avoid the costs associated with mounting an innate immune response. To test whether there is an energetic benefit to nestlings of receiving matAb, we challenged adult female tree swallows (Tachycineta bicolor) prior to clutch initiation with either lipopolysaccharide (LPS) or saline (Control). Following hatching, one half of each females nestlings were immunized on day 8 post-hatch with LPS or saline, and for 4-hrs post immunization nestling metabolic rate (MR) was measured. There was no difference in either LPS-reactive antibodies or total Ig levels between offspring of immunized and non-immunized mothers on day 6 or 14 post-hatch, possibly reflecting a relatively short half-life of matAbs in altricial birds. Additionally, we found no evidence that nestlings from LPS-immunized mothers could avoid the growth-suppression that may result from activation of an inflammatory response. Unexpectedly, we found that control-nestlings from LPS-mothers had higher resting MR than control-nestlings of control-mothers. We attribute the increased MR to the costs associated with a general nonspecific enhancement of immune function in nestlings from LPS-immunized mothers. Consistent with enhanced immune function, nestlings of immunized mothers had a more robust inflammatory response to phytohaemagglutinin, and higher fledging success. Our results suggest maternal antigen exposure pre-laying can result in increased fitness for both mothers and offspring, depending on food availability.

Data from: Immune-challenged fish up-regulate their metabolic scope to support locomotion

Energy-based trade-offs occur when investment in one fitness-related trait diverts energy away from other traits. The extent to which such trade-offs are shaped by limits on the rate of conversion of energy ingested in food (e.g. carbohydrates) into chemical energy (ATP) by oxidative metabolism rather than by the amount of food ingested in the first place is, however, unclear. Here we tested whether the ATP required for mounting an immune response will lead to a trade-off with ATP available for physical activity in mosquitofish (Gambusia holbrooki). To this end, we challenged fish either with lipopolysaccharide (LPS) from E. coli or with Sheep Red Blood Cells (SRBC), and measured oxygen consumption at rest and during swimming at maximum speed 24h, 48h and 7 days post-challenge in order to estimate metabolic rates. Relative to saline-injected controls, only LPS-injected fish showed a significantly greater resting metabolic rate two days post-challenge and significantly higher maximal metabolic rates two and seven days post-challenge. This resulted in a significantly greater metabolic scope two days post-challenge, with LPS-fish transiently overcompensating by increasing maximal ATP production more than would be required for swimming in the absence of an immune challenge. LPS-challenged fish therefore increased their production of ATP to compensate physiologically for the energetic requirements of immune functioning. This response would avoid ATP shortages and allow fish to engage in an aerobically-challenging activity (swimming) even when simultaneously mounting an immune response. Nevertheless, relative to controls, both LPS- and SRBC-fish displayed reduced body mass gain one week post-injection, and LPS-fish actually lost mass. The concomitant increase in metabolic scope and reduced body mass gain of LPS-challenged fish indicates that immune-associated trade-offs are not likely to be shaped by limited oxidative metabolic capacities, but may instead result from limitations in the acquisition, assimilation or efficient use of resources.

opencc-zeroAug 2019View details →

Data from: Humoral immune responses against gut bacteria In dogs with inflammatory bowel disease

Inflammatory bowel disease (IBD) in dogs is associated with clinical signs of intestinal dysfunction, as well as abnormal lymphocytic and myeloid cell infiltrates in the small and/or large intestine. Thus, in many respects IBD in dogs resembles IBD in humans. However, the factors that trigger intestinal inflammation in dogs with IBD are not well understood and have been variously attributed to immune responses against dietary antigens or intestinal antigens. Previous studies in humans with IBD have documented increased production of IgG and IgA antibodies specific to intestinal bacteria, and this abnormal immune response has been linked to disease pathogenesis. Therefore, we investigated the humoral immune response against gut bacteria in dogs with IBD, using flow cytometry to quantitate IgG and IgA binding. Studies were also done to investigate the source of these antibodies (locally produced versus systemic production) and whether greater antibody binding to bacteria is associated with increased inflammatory responses. We found that dogs with IBD had significantly higher percentages and overall amounts of IgG bound to their intestinal bacteria compared to healthy dogs. Similarly, significantly higher percentages of bacteria were IgA+ bacteria were also found in dogs with IBD. Serum antibody recognition of gut bacteria was not different between healthy dogs and dogs with IBD, suggesting that anti-bacterial antibodies were primarily produced locally in the gut rather than systemically. Importantly, bacteria in the Actinobacteria phylum and in particular the genus Collinsella had significantly greater levels of antibody binding in dogs with IBD. Based on these findings, we concluded that antibody binding to commensal gut bacteria was significantly increased in dogs with IBD, that particular phyla were preferential targets for gut antibodies, and that anti-bacterial antibody responses may play an important role in regulating gut inflammation.

Data from: Independent and interactive effects of immune activation and larval diet on adult immune function, growth and development in the greater wax moth (Galleria mellonella)

Organisms in the wild are likely to face multiple immune challenges as well as additional ecological stressors, yet their interactive effects on immune function are poorly understood. Insects are found to respond to cues of increased infection risk by enhancing their immune capacity. However, such adaptive plasticity in immune function may be limited by physiological and environmental constraints. Here, we investigated the effects of two environmental stressors – poor larval diet and an artificial parasite-like immune challenge at the pupal stage – on adult immune function, growth and development in the greater wax moth (Galleria mellonella). Males whose immune system was activated with an artificial parasite-like immune challenge had weaker immune response – measured as strength of encapsulation response – as adults compared to the control groups, but only when raised in highnutrition larval diet. Immune activation did not negatively affect adult immune response in males reared in low-nutrition larval diet, indicating that poor larval diet improved the capacity of the insects to respond to repeated immune challenges. Low-nutrition larval diet also had a positive independent effect on immune capacity in females, yet it negatively affected development time and adult body mass in both sexes. As in the nature immune challenges are rarely isolated, and adverse nutritional environment may indicate an elevated risk of infection, resilience to repeated immune challenges as a response to poor nutritional environment could provide a significant fitness advantage. This study highlights the importance of considering environmental context when investigating the effects of immune activation in insects.

Data from: No apparent cost of evolved immune response in Drosophila melanogaster

Maintenance and deployment of the immune system are costly and are hence predicted to trade-off with other resource demanding traits, such as reproduction. We subjected this long standing idea to test using laboratory experimental evolution approach. In the present study, replicate populations of Drosophila melanogaster were subjected to three selection regimes – I (Infection with Pseudomonas entomophila), S (Sham-infection with MgSO4) and U (Unhandled Control). After 30 generations of selection flies from the I-regime had evolved better survivorship upon infection with P. entomophila compared to flies from U and S regimes. However, contrary to expectations and previous reports, we did not find any evidence of trade-offs between immunity and other life-history related traits, such as longevity, fecundity, egg hatchability or development time. After 45 generations of selection, the selection was relaxed for a set of populations. Even after 15 generations, the post-infection survivorship of populations under relaxed selection regime did not decline. We speculate that either there is a negligible cost to the evolved immune response or that trade-offs occur on traits like reproductive behaviour or other immune mechanisms that we have not investigated in this study. Our research suggests that at least under certain conditions, life-history trade-offs might play little role in maintaining variation in immunity.

Data from: Down syndrome cell adhesion molecule 1: testing for a role in insect immunity, behaviour and reproduction

Down syndrome cell adhesion molecule 1 (Dscam1) has wide-reaching and vital neuronal functions although the role it plays in insect and crustacean immunity is less well understood. In this study, we combine different approaches to understand the roles that Dscam1 plays in fitness-related contexts in two model insect species. Contrary to our expectations, we found no short-term modulation of Dscam1 gene expression after haemocoelic or oral bacterial exposure in Tribolium castaneum, or after haemocoelic bacterial exposure in Drosophila melanogaster. Furthermore, RNAi-mediated Dscam1 knockdown and subsequent bacterial exposure did not reduce T. castaneum survival. However, Dscam1 knockdown in larvae resulted in adult locomotion defects, as well as dramatically reduced fecundity in males and females. We suggest that Dscam1 does not always play a straightforward role in immunity, but strongly influences behaviour and fecundity. This study takes a step towards understanding more about the role of this intriguing gene from different phenotypic perspectives.

Data from: Females gain survival benefits from immune-boosting ejaculates

Females in many animal taxa incur significant costs from mating in the form of injury or infection, which can drastically reduce survival. Therefore, immune function during reproduction can be important in determining lifetime fitness. Trade-offs between reproduction and immunity have been extensively studied, yet a growing number of studies demonstrate that mated females have a stronger immune response than virgins. Here, we use the Texas field cricket, Gryllus texensis, to test multiple hypotheses proposed to explain this post-mating increase in immune function. Using host-resistance tests, we found that courtship, copulation, and accessory fluids alone do not affect female immunity; rather, only females that acquire intact ejaculates containing testes-derived components exhibit significant increases in survival after exposure to bacterial pathogens. Our data suggest that male-derived components originating from an intact ejaculate and transferred to females during sex are required for the increased immune function characteristic of mated female crickets to occur.

Data from: Using viromes to predict novel immune proteins in non-model organisms

Immunity is mostly studied in a few model organisms, leaving the majority of immune systems on the planet unexplored. To characterize the immune systems of non-model organisms alternative approaches are required. Viruses manipulate host cell biology through the expression of proteins that modulate the immune response. We hypothesized that metagenomic sequencing of viral communities would be useful to identify both known and unknown host immune proteins. To test this hypothesis, a mock human virome was generated and compared to the human proteome using tBLASTn, resulting in 36 proteins known to be involved in immunity. This same pipeline was then applied to reef-building coral, a non-model organism that currently lacks traditional molecular tools like transgenic animals, gene-editing capabilities, and in vitro cell cultures. Viromes isolated from corals and compared with the predicted coral proteome resulted in 2503 coral proteins, including many proteins involved with pathogen sensing and apoptosis. There were also 159 coral proteins predicted to be involved with coral immunity but currently lacking any functional annotation. The pipeline described here provides a novel method to rapidly predict host immune components that can be applied to virtually any system with the potential to discover novel immune proteins.

Data from: Comparison of the immune response during acute and chronic Staphylococcus aureus infection

Staphylococcus aureus bacteria are able to grow in a planktonic state that is associated with acute infections and in biofilms that are associated with chronic infections. Acute infections, such as skin infections, are often self-limiting. However, chronic infections, such as implant infections, can be difficult to clear and may require surgical intervention. The host immune response may contribute to the different outcomes often associated with these two disease types. We used proteomic arrays and two murine models for an initial, descriptive characterization of the contribution of the host immune response to outcomes of acute versus chronic S. aureus disease. We compared the immune responses between a model of self-limiting skin and soft tissue infection caused by the planktonic form of S. aureus versus a model of surgical mesh implant infection, which we show to be caused by a bacterial biofilm. The significantly altered host cytokines and chemokines were largely different in the two models, with responses diminished by 21 days post-implantation in surgical mesh infection. Because bacterial levels remained constant during the 21 days that the surgical mesh infection was followed, those cytokines that are significantly increased during chronic infection are not likely effective in eradicating biofilm. Comparison of the levels of cytokines and chemokines in acute versus chronic S. aureus infection can provide a starting point for evaluation of the role of specific immune factors that are present in one disease manifestation but not the other.

opencc-zeroJun 2021View details →

Fecal calprotectin as a predictor of gastrointestinal immune-related adverse events (CF-19): A prospective study - Excel data and supplementary tables

Background: Colitis is a frequent immune-related toxicity, without any biomarker that may predict its onset. It is endoscopically similar to intestinal inflammatory diseases, where fecal calprotectin (FC) is used as a biomarker to early-detect a relapse. We found contradictory evidence about FC and immunotherapy and no prospective study was already published. Methods: We present an analytical, observational and prospective study of one year's duration. We analyzed FCbasal, and then prior to each cycle until the sixth, ending with quarterly follow-up. For evaluating the predictive value of FC we estimated the area under the ROC curve for basal absolute values and for each cycle, and calculated its relative percentage change with respect to basal. We also planned to estimate sensitivity, specificity and predictive values indexes for different cut-off points. Because of lack of recruitment we did a preliminary analysis at the end of the initially estimated period before suggesting its prolongation. Results: 24 patients were included (19 male), diagnosed from lung cancer (n=15), head and neck, renal, bladder and colorectal cancer (n=2, each), melanoma (n=1). They were treated with Anti PD-1/PDL-1 mono therapy (n=18), combo with chemo (n=2), or combo with anti-CTLA4 (n=2). Three patients had G1 colitis and two, >=G2, all treated with anti-PD1 and before 6th cycle, as described on literature. ROC curve presents AUC 0,559 (CI95%:0,32-0,798) and RR for colitis taking FC value is 1,001 for each 10 units (p=0,493). Conclusion: Even though we must take into account the limitations of the study we cannot conclude that FC could be used as a predictor for detecting immune-mediated colitis.

opencc-zeroDec 2016View details →

Data from: Early-life inflammation, immune response and ageing

Age-related diseases are often attributed to immunopathology, which results in self-damage caused by an inappropriate inflammatory response. Immunopathology associated with early-life inflammation also appears to cause faster ageing, although we lack direct experimental evidence for this association. To understand the interactions between ageing, inflammation and immunopathology, we used the mealworm beetle Tenebrio molitor as a study organism. We hypothesized that phenoloxidase, an important immune effector in insect defence, may impose substantial immunopathological costs by causing tissue damage to Malpighian tubules (MTs; functionally equivalent to the human kidney), in turn accelerating ageing. In support of this hypothesis, we found that RNAi knockdown of phenoloxidase (PO) transcripts in young adults possibly reduced inflammation-induced autoreactive tissue damage to MTs, and increased adult lifespan. Our work thus suggests a causative link between immunopathological costs of early-life inflammation and faster ageing. We also reasoned that if natural selection weakens with age, older individuals should display increased immunopathological costs associated with an immune response. Indeed, we found that while old infected individuals cleared infection faster than young individuals, possibly they also displayed exacerbated immunopathological costs (larger decline in MT function) and higher post-infection mortality. RNAi-mediated knockdown of PO response partially rescued MTs function in older beetles and resulted in increased lifespan after infection. Taken together, our data are consistent with a direct role of immunopathological consequences of immune response during ageing in insects. Our work is also the first report that highlights the pervasive role of tissue damage under diverse contexts of ageing and immune response.

Data from: Dietary protein and carbohydrates affect immune function and performance in a specialist herbivore insect (Manduca sexta)

Nutrition structures ecology and evolution across all scales of biological organization. It is well known that nutrition can have direct effects on performance and fitness, but indirect effects on physiological systems that mediate biotic interactions have been studied less frequently. Here, we focus on the interaction between nutrition, performance, and the immune system in a specialist herbivorous insect, Manduca sexta. We used a conceptual framework in nutritional ecology (the geometric framework) to examine how changes in diet quality affect aspects of the immune system used for defense against parasitoids. We raised caterpillars throughout their entire larval development on five different experimental diets that varied in protein and carbohydrate content and measured five aspects of the immune system: encapsulation, phenoloxidase activity, prophenoloxidase activity, total hemolymph protein, and hemocyte density. Overall, different parts of the immune function varied in response to interactions between carbohydrates, protein, and intake, but protein reductions had the largest impacts—mostly detrimental. In addition, our data suggest that diet quality mediates the relationship between performance (growth and survival) and immune function, as well as trade-offs among different components of immune function. Our work is the first to examine the interplay between nutrition, performance, and immune function with the geometric framework in a specialist insect herbivore.

Data from: Fitness consequences of altered feeding behavior in immune-challenged mosquitoes

Background: Malaria-infected mosquitoes have been reported to be more likely to take a blood meal when parasites are infectious than when non-infectious. This change in feeding behavior increases the likelihood of malaria transmission, and has been considered an example of parasite manipulation of host behavior. However, immune challenge with heat-killed Escherichia coli induces the same behavior, suggesting that altered feeding behavior may be driven by adaptive responses of hosts to cope with an immune response, rather than by parasite-specific factors. Here we tested the alternative hypothesis that down-regulated feeding behavior prior to infectiousness is a mosquito adaptation that increases fitness during infection. Methods: We measured the impact of immune challenge and blood feeding on the fitness of individual mosquitoes. After an initial blood meal, Anopheles stephensi Liston mosquitoes were experimentally challenged with heat-killed E. coli at a dose known to mimic the same temporal changes in mosquito feeding behavior as active malaria infection. We then tracked daily egg production and survivorship of females maintained on blood-feeding regimes that either mimicked down-regulated feeding behaviors observed during early malaria infection, or were fed on a four-day feeding cycle typically associated with uninfected mosquitoes. Results: Restricting access to blood meals enhanced mosquito survival but lowered lifetime reproduction. Immune- challenge did not impact either fitness component. Combining fecundity and survival to estimate the population- scale intrinsic rate of increase (r), we found that, contrary to the mosquito adaptation hypothesis, mosquito fitness decreased if blood feeding was delayed following an immune challenge. Conclusions: Our data provide no support for the idea that malaria-induced suppression of blood feeding is an adaptation by mosquitoes to reduce the impact of immune challenge. Alternatively, the behavioral alterations may be neither host nor parasite adaptations, but rather a consequence of constraints imposed on feeding by activation of the mosquito immune response, i.e. non-adaptive illness-induced anorexia. Future work incorporating field conditions and different immune challenges could further clarify the effect of altered feeding on mosquito and parasite fitness.

opencc-zeroDec 2010View details →

Data from: Disentangling the roles of natural selection and genetic drift in shaping variation at MHC immunity genes

The major histocompatibility complex (MHC) forms an integral component of the vertebrate immune response, and, due to strong selection pressures, is one of the most polymorphic regions of the entire genome. Despite over 15 years of research, empirical studies offer highly contradictory explanations of the relative roles of opposing evolutionary forces, selection and genetic drift, acting on MHC genes during population bottlenecks. Here, we take a meta-analytical approach to quantify the results of studies into the effects of bottlenecks on MHC polymorphism. We show that the consequences of selection acting on MHC loci prior to a bottleneck event, combined with drift during the bottleneck, will result in overall loss of MHC polymorphism that is approximately 15% greater than loss of neutral genetic diversity. These results are counter to general expectations that selection should maintain MHC polymorphism, but do agree with the results of recent simulation models and at least two empirical studies. Notably, our results suggest that negative frequency-dependent selection could be more important than overdominance for maintaining high MHC polymorphism in pre-bottlenecked populations.

opencc-zeroDec 2016View details →

Data from: Optimal nutrient exchange and immune responses operate in partner specificity in the cnidarian-dinoflagellate symbiosis

The relationship between reef-building corals and phototrophic dinoflagellates of the genus Symbiodinium is fundamental to the functioning of coral reef ecosystems. It has been suggested that reef corals may adapt to climate change by changing their dominant symbiont type to a more thermally tolerant one, although the capacity for such a community shift is potentially hindered by the compatibility of different host-symbiont pairings. Here we combined transcriptomic and metabolomic analyses to characterize the molecular, cellular, and physiological processes that underlie this compatibility, with a particular focus on Symbiodinium trenchii, an opportunistic, thermally tolerant symbiont that flourishes in coral tissues after bleaching events. Symbiont-free individuals of the sea anemone Exaiptasia pallida (commonly referred to as Aiptasia), an established model system for the study of the cnidarian-dinoflagellate symbiosis, were colonized with the "normal" (homologous) symbiont Symbiodinium minutum and the heterologous S. trenchii. Analysis of the host gene and metabolite expression profiles revealed that heterologous symbionts induced an expression pattern intermediate between the typical symbiotic state and the aposymbiotic state. Furthermore, integrated pathway analysis revealed that increased catabolism of fixed carbon stores, metabolic signaling, and immune processes occurred in response to the heterologous symbiont type. Our data suggest that both nutritional provisioning and the immune response induced by the foreign "invader" are important factors in determining the capacity of corals to adapt to climate change through the establishment of novel symbioses.

opencc-by-4.0Oct 2024View details →

Supplementary data for the manuscript, "Comprehensive Assessment of Physiochemical Metrics for the Clustering of Adaptive Immune Repertoires"

This repository contains data and code used in the manuscript "Comparative Assessment of Physiochemical Metrics for the Clustering of Adaptive Immune Receptor Repertoires" by Girgis et al. For additional information regarding how these data were used, please refer to our manuscript. Code is organized per figure in the main text. Each figure folder contains a 'script-inputs' folder and 'script-outputs' folder. The outputs folder is empty and may be populated with graphs and results tables by executing code within the directory. The inputs folder contains some pre-formatted data which may be used in executing code. Most of these inputs may be generated from scratch using raw data (ie the results of Homolig clustering on simulated repertoires) but may require substantial time and/or computational resources. Raw patient data used in Figure 6 (Pancreatic cancer anti-mKRAS TCRB repertoire clustering) and Figure 7 (Rheumatoid arthritis TCRB and IGH repertoires) are not included here. However, several graphs may be reproduced stripped of sequence-specific data. Pancreatic cancer patient repertoire data will be made available on dbGaP,study accession number phs003425.v1.p1. Rheumatoid arthritis patient data will be made available on ImmuneAccess, accession pending. To browse repo, first unzip all subdirectories:  <blockquote> <code>for f in *.zip; do</code> <code>    unzip "$f"</code> <code>done</code> </blockquote> All non-code files have been compressed to .gz format. To decompress, use: <code>gzip -dr *</code>, or <code>pigz -dr ./raw-data/* </code>for parallel decompression (recommended).  Alexander Girgis  agirgis3@jhmi.edu  July 2025

opencc-by-4.0Nov 2023View details →

Machine Learning-assisted immunophenotyping of peripheral blood identifies innate immune cells as best predictor of response to induction chemo-immunotherapy in head and neck squamous cell carcinoma – knowledge obtained from the CheckRad-CD8 trial

Raw cell counts from peripheral blood immune phenotyping across individual patients.

opencc-by-4.0Nov 2023View details →

PATHOGENESIS AND IMMUNE RESPONSE IN CARDIAC ECHINOCOCOSIS

Open the record for dataset details and reuse information.

embargoedcc-by-4.0Nov 2023View details →

Single cell RNA-seq transcriptomic profile of circulating immune and progenitor cells in a mouse model of neonatal hypoxic/ischemic (HI) brain damage.

Hematopoietic cells play a pivotal role in regulating the inflammatory and reparative immune responses triggered after ischemic tissue damage. The response initiated within the injured tissue leads to compositional and transcriptional changes in circulating hematopoietic and progenitor cells, which have been utilized as biomarkers. While the importance of different immune and progenitor cell subtypes in the development of ischemic damage has been extensively researched in adult tissue injuries, there has been limited investigation in neonates. This is a critical developmental stage where ischemic damage can result in severe and irreversible health consequences if not promptly treated. To determine how ischemic damage could affect circulating cells in neonates, we have induced hypoxic-ischemic (HI) brain damage in seven-day-old mice, characterized by focal white and gray-matter injury (Rice-Vannucci model). Brain damage and circulating cells were analyzed at 48h post-HI, the intermediate reparative/inflammatory response phase post-injury.  We applied scRNAseq to dissect the transcriptional and cellular composition changes in the peripheral blood of HI-treated and SHAM control neonates. This study provides the first scRNAseq dataset for immune and progenitor circulating cells in newborns with cerebral HI damage. It may help to identify biomarkers and selective therapeutic approaches aimed at modulating inflammatory and reparative pathways. CD1 postnatal day 7 (P7) mice were subjected to   hypoxic/ischemic (HI) brain injury by permanent ligation of the left common carotid artery followed, after 2h recover, by relocation to  a hypoxia chamber for 90 minutes. Sham control mice (SHAM) underwent a skin incision and wound closure followed by hypoxia exposure.  Circulating blood cells were collected from SHAM and HI mice at P9. After red blood cells (RBC) lysis, 7AAD-Ter119- cells were FACS sorted and analysed using sc RNAseq. Other samples were FACS sorted for CD45+CD11+ and CD45-CD31+ cells and mixed.