Genetic Variation in Trophic Avoidance Behaviour Shows Fruit Flies are Generally Attracted to Bacterial Substrates.

Pathogen avoidance behaviours are often assumed to be an adaptive host defence. However, there is limited experimental data on heritable, intrapopulation phenotypic variation for avoidance, a strong prerequisite for adaptive responses to selection. We investigated trophic pathogen avoidance in 122 inbred lines, and in a derived outbred population.

A naturally occurring mitochondrial genome variant confers broad protection from infection in Drosophila.

The role of mitochondria in immunity is increasingly recognized, but it is unclear how variation in mitochondrial DNA (mtDNA) contributes to variable infection outcomes. To quantify the effect of mtDNA variation on humoral and cell-mediated innate immune responses, we utilized a panel of fruit fly Drosophila melanogaster cytoplasmic hybrids (cybrids), where unique mtDNAs (mitotypes) were introgressed into a controlled isogenic nuclear background. We observed substantial heterogeneity in infection outcomes within the cybrid panel upon bacterial, viral and parasitoid infections, driven by the mitotype.

Mitochondrial background can explain variable costs of immune deployment.

Organismal health and survival depend on the ability to mount an effective immune response against infection. Yet immune defence may be energy-demanding, resulting in fitness costs if investment in immune function deprives other physiological processes of resources. While evidence of costly immunity resulting in reduced longevity and reproduction is common, the role of energy-producing mitochondria on the magnitude of these costs is unknown.

IMD-mediated innate immune priming increases Drosophila survival and reduces pathogen transmission.

Invertebrates lack the immune machinery underlying vertebrate-like acquired immunity. However, in many insects past infection by the same pathogen can 'prime' the immune response, resulting in improved survival upon reinfection. Here, we investigated the mechanistic basis and epidemiological consequences of innate immune priming in the fruit fly Drosophila melanogaster when infected with the gram-negative bacterial pathogen Providencia rettgeri.

Mitochondrial perturbation in immune cells enhances cell-mediated innate immunity in Drosophila.

Background: Mitochondria participate in various cellular processes including energy metabolism, apoptosis, autophagy, production of reactive oxygen species, stress responses, inflammation and immunity. However, the role of mitochondrial metabolism in immune cells and tissues shaping the innate immune responses are not yet fully understood. We investigated the effects of tissue-specific mitochondrial perturbation on the immune responses at the organismal level.

Mitochondrial background can explain variable costs of immune deployment.

Organismal health and survival depend on the ability to mount an effective immune response against infection. Yet immune defence may be energy-demanding, resulting in fitness costs if investment in immune function deprives other physiological processes of resources. While evidence of costly immunity resulting in reduced longevity and reproduction is common, the role of energy-producing mitochondria on the magnitude of these costs is unknown.

Duox and Jak/Stat signalling influence disease tolerance in Drosophila during Pseudomonas entomophila infection.

Disease tolerance describes an infected host's ability to maintain health independently of the ability to clear microbe loads. The Jak/Stat pathway plays a pivotal role in humoral innate immunity by detecting tissue damage and triggering cellular renewal, making it a candidate tolerance mechanism. Here, we find that in Drosophila melanogaster infected with Pseudomonas entomophila disrupting ROS-producing dual oxidase (duox) or the negative regulator of Jak/Stat Socs36E, render male flies less tolerant.

Intraspecific genetic variation in host vigour, viral load and disease tolerance during Drosophila C virus infection.

Genetic variation for resistance and disease tolerance has been described in a range of species. In , genetic variation in mortality following systemic Drosophila C virus (DCV) infection is driven by large-effect polymorphisms in the restriction factor . However, it is unclear if contributes to disease tolerance.

Ageing leads to reduced specificity of antimicrobial peptide responses in .

Evolutionary theory predicts a late-life decline in the force of natural selection, possibly leading to late-life deregulations of the immune system. A potential outcome of such deregulations is the inability to produce specific immunity against target pathogens. We tested this possibility by infecting multiple lines (with bacterial pathogens) across age groups, where either individual or different combinations of Imd- and Toll-inducible antimicrobial peptides (AMPs) were deleted using CRISPR gene editing.

The value of surgeon's perception during transurethral resection of bladder tumors: can we trust in our eyes and experience to predict grade and staging?

Unlabelled: Transurethral resection of newly diagnosed bladder tumors (TURBT) is a hallmark ¡n the treatment of bladder cancer. We evaluated the surgeon capacity to predict bladder tumor stage (T), grade, and presence of muscular layer based upon cystoscopic characteristics during primary TURBT.

Methods: Prospective study enrolling 100 consecutive patients undergoing primary TURBT for newly diagnosed bladder cancers.

Mechanisms of damage prevention, signalling and repair impact disease tolerance.

The insect gut is frequently exposed to pathogenic threats and must not only clear these potential infections, but also tolerate relatively high microbe loads. In contrast to the mechanisms that eliminate pathogens, we currently know less about the mechanisms of disease tolerance. We investigated how well-described mechanisms that prevent, signal, control or repair damage during infection contribute to the phenotype of disease tolerance.

Larval diet affects adult reproduction, but not survival, independent of the effect of injury and infection in Drosophila melanogaster.

Early-life conditions have profound effects on many life-history traits, where early-life diet affects both juvenile development, and adult survival and reproduction. Early-life diet also has consequences for the ability of adults to withstand environmental challenges such as starvation, temperature and desiccation. However, it is less well known how early-life diet influences the consequences of infection in adults.

Variation in mitochondrial DNA affects locomotor activity and sleep in Drosophila melanogaster.

Mitochondria are organelles that produce cellular energy in the form of ATP through oxidative phosphorylation, and this primary function is conserved among many taxa. Locomotion is a trait that is highly reliant on metabolic function and expected to be greatly affected by disruptions to mitochondrial performance. To this end, we aimed to examine how activity and sleep vary between Drosophila melanogaster strains with different geographic origins, how these patterns are affected by mitochondrial DNA (mtDNA) variation, and how breaking up co-evolved mito-nuclear gene combinations affect the studied activity traits.

Carry on caring: infected females maintain their parental care despite high mortality.

Parental care is a key component of an organism's reproductive strategy that is thought to trade-off with allocation toward immunity. Yet, it is unclear how caring parents respond to pathogens: do infected parents reduce care as a sickness behavior or simply from being ill or do they prioritize their offspring by maintaining high levels of care? To address this issue, we investigated the consequences of infection by the pathogen on mortality, time spent providing care, reproductive output, and expression of immune genes of female parents in the burying beetle . We compared untreated control females with infected females that were inoculated with live bacteria, immune-challenged females that were inoculated with heat-killed bacteria, and injured females that were injected with buffer.

Dissecting genetic and sex-specific sources of host heterogeneity in pathogen shedding and spread.

Host heterogeneity in disease transmission is widespread but precisely how different host traits drive this heterogeneity remains poorly understood. Part of the difficulty in linking individual variation to population-scale outcomes is that individual hosts can differ on multiple behavioral, physiological and immunological axes, which will together impact their transmission potential. Moreover, we lack well-characterized, empirical systems that enable the quantification of individual variation in key host traits, while also characterizing genetic or sex-based sources of such variation.

Testing evolutionary explanations for the lifespan benefit of dietary restriction in fruit flies (Drosophila melanogaster).

Dietary restriction (DR), limiting calories or specific nutrients without malnutrition, extends lifespan across diverse taxa. Traditionally, this lifespan extension has been explained as a result of diet-mediated changes in the trade-off between lifespan and reproduction, with survival favored when resources are scarce. However, a recently proposed alternative suggests that the selective benefit of the response to DR is the maintenance of reproduction.

Non-lupus full-house nephropathy: a case series.

Systemic lupus erythematosus (SLE) is a chronic multisystem autoimmune inflammatory disease. However, some patients may exhibit a histological pattern of kidney injury, with characteristics indistinguishable from lupus nephritis, but without presenting any extrarenal symptoms or serologies suggestive of SLE. Such involvement has recently been called non-lupus full-house nephropathy.

Genotype and sex-based host variation in behaviour and susceptibility drives population disease dynamics.

Host heterogeneity in pathogen transmission is widespread and presents a major hurdle to predicting and minimizing disease outbreaks. Using infected with C virus as a model system, we integrated experimental measurements of social aggregation, virus shedding, and disease-induced mortality from different genetic lines and sexes into a disease modelling framework. The experimentally measured host heterogeneity produced substantial differences in simulated disease outbreaks, providing evidence for genetic and sex-specific effects on disease dynamics at a population level.

Renal involvement in systemic lupus erythematosus: additional histopathological lesions.

A common criticism of the classification of lupus nephritis is the relative scarcity of information regarding tubular, interstitial, and vascular changes compared to the available information regarding glomerular changes, even though their potential for independent progression is known. This study reviewed the importance of less explored lesions by the current and widely used 2003 classification of lupus nephritis of the International Society of Nephrology/Renal Pathology Society (ISN/RPS), with emphasis on the tubulointerstitial, podocyte, and vascular lesions, increasingly recognised as being important in the pathogenesis and prognosis of the disease. Recognition of these lesions can help with therapeutic decision-making, thereby allowing better results for patients with systemic lupus erythematosus.

as a Model System to Investigate the Effects of Mitochondrial Variation on Innate Immunity.

Understanding why the response to infection varies between individuals remains one of the major challenges in immunology and infection biology. A substantial proportion of this heterogeneity can be explained by individual genetic differences which result in variable immune responses, and there are many examples of polymorphisms in nuclear-encoded genes that alter immunocompetence. However, how immunity is affected by genetic polymorphism in an additional genome, inherited maternally inside mitochondria (mtDNA), has been relatively understudied.

Terminal investment strategies following infection are dependent on diet.

When future reproductive potential is threatened, for example following infection, the terminal investment hypothesis predicts that individuals will respond by investing preferentially in current reproduction. Terminal investment involves reallocating resources to current reproductive effort, so it is likely to be influenced by the quantity and quality of resources acquired through diet. Dietary protein specifically has been shown to impact both immunity and reproduction in a range of organisms, but its impact on terminal investment is unclear.

How are arbovirus vectors able to tolerate infection?

One of the defining features of mosquito vectors of arboviruses such as Dengue and Zika is their ability to tolerate high levels of virus proliferation without suffering significant pathology. This adaptation is central to vector competence and disease spread. The molecular mechanisms, pathways, cellular and metabolic adaptations responsible for mosquito disease tolerance are still largely unknown and may represent effective ways to control mosquito populations and prevent arboviral diseases.

Viral infection causes sex-specific changes in fruit fly social aggregation behaviour.

Host behavioural changes following infection are common and could be important determinants of host behavioural competence to transmit pathogens. Identifying potential sources of variation in sickness behaviours is therefore central to our understanding of disease transmission. Here, we test how group social aggregation and individual locomotor activity vary between different genotypes of male and female fruit flies () following septic infection with C virus (DCV).

Post-transplant Lupus Nephritis Recurrence: A Case Report and Review of the Literature.

Despite progress in treating lupus nephritis, the incidence of end-stage chronic kidney disease has increased. Renal transplantation is the treatment of choice for these patients and has been successfully performed on systemic lupus erythematosus (SLE) since 1959. The main concern in these patients is post-transplant lupus nephritis recurrence.