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<p>The field of "perinatal programming" has increasingly implicated an adverse early-life environment in the etiology of many chronic health problems and mental disorders. The following dissertation research is based on the hypothesis that the programming of brain and behavior by an altered early-life environment is propagated by inflammatory mechanisms in the placenta and developing brain. Offspring outcomes of two different maternal environmental exposures--air pollution and a "Western diet" (both highly relevant for the modern world)--were assessed in a mouse model in order to identify mechanisms common to developmental programming more generally.</p><p>The first set of experiments characterized the long-term behavioral and metabolic consequences of prenatal air pollution exposure in adult offspring. The male offspring of diesel exhaust particle (DEP)-exposed dams were predisposed to obesity, insulin resistance, and increased anxiety following placement on a high-fat diet (HFD) in adulthood. Furthermore, DEP/HFD male offspring exhibited evidence of macrophage priming, both in microglia and peripheral macrophages. The next experiment examined whether prenatal air pollution exposure could also synergize with a simultaneous "second hit" (i.e., maternal stress) during gestation. The offspring of mothers exposed to both air pollution and stress during gestation were more anxious as adults, but only the male offspring of this group also exhibited impaired cognition, in conjunction with neuroinflammatory changes. A further experiment revealed that prenatal air pollution exposure altered microglial maturation in a TLR4- and sex-dependent manner, consistent with the previous results. However, we found limited evidence of a placental immune response to DEP, potentially due to analysis too late in gestation. </p><p>The second set of experiments characterized the enduring behavioral and metabolic consequences of maternal consumption of a "Western diet" (HFD in combination with BCAA supplementation) prior to and during gestation and lactation. The adult offspring of HFD-fed dams were more anxious in adulthood, despite being placed on a low-fat diet at weaning. Male HFD offspring were also hyperactive, whereas female HFD offspring exhibited more severe metabolic disturbances. Furthermore, there was evidence of microglial priming and peripheral macrophage priming in male HFD offspring, similar to the prenatal air pollution model. The next experiment also found evidence of altered microglial development due to maternal HFD, in conjunction with widespread, sex-specific immune gene regulation in the placenta in response to maternal diet. Moreover, maternal HFD decreased placental serotonin production, and also programmed long-term alterations in serotonergic function in the prefrontal cortex of adult HFD offspring. Taken together, these experiments define sexually dimorphic innate immune mechanisms in the placenta and developing brain that may underlie the long-term metabolic and behavioral consequences of maternal environmental exposures.</p> / Dissertation

Fatores dietéticos como o selênio (Se) são apontados como importantes moduladores do risco de desenvolvimento do câncer de mama. Essa neoplasia pode apresentar sua origem no início do desenvolvimento e, assim, a alimentação materna poderia ter importantes repercussões na programação fetal da doença. A fim de verificar se diferentes concentração de selênio na dieta materna poderiam programar o risco da progênie feminina ao câncer de mama, ratas foram alimentadas com ração contendo 0,15 (CO), 1,0 (SUP) ou 0,05 (DEF) ppm de Se durante a gestação e sua progênie feminina iniciada com DMBA. A progênie do grupo SUP apresentou menor suscetibilidade à carcinogênese, indicado pelo menor número médio e multiplicidade de adenocarcinomas mamários (p< 0,05), enquanto a do grupo DEF apresentou maior suscetibilidade à carcinogênese, indicado pela maior incidência dos mesmos (p< 0,05). Mães do grupo DEF apresentaram menor concentração de Se no sangue (p< 0,05) e sua prole apresentou menor atividade da enzima GPx1 (p< 0,05). Além disso, observou-se na glândula mamária da progênie de 50 dias menor expressão (western blot e qPCR) de ER&#945;, Her-2, EGFR e Ras no grupo SUP em comparação aos grupos CO e DEF (p< 0,05). Analisou-se, ainda, o padrão de metilação global do DNA (HPLC-DAD), expressão das enzimas DNMT1, 3a e 3b (qPCR), o padrão global de modificações pós traducionais em histonas (western blot) e o padrão de metilação da região promotora do gene Er&#945; (modificação com bissulfito e pirossequenciamento) na glândula mamária da progênie de 50 dias. Não houve diferença no padrão de metilação global do DNA e expressão das enzimas DNMTs (p>0,05). Houve aumento na expressão de H4K16 acetilada nos grupos SUP e DEF (p< 0,05). Finalmente, em comparação a progênie do grupo DEF, a do grupo SUP apresentou região promotora de Er&#945; com aumento marginal (p=0,07) na metilação de dois dinucleotídeos CpG. Conclui-se que o consumo de diferentes concentrações de Se na dieta materna tem impacto sobre a suscetibilidade da progênie ao câncer de mama na vida adulta através da modulação da expressão de receptores e oncogenes relacionados ao desenvolvimeto dessa neoplasia, além da influência em processos epigenéticos. Tais resultados apontam para a existência de uma \"janela de programação\" no início do desenvolvimento sensível a ação do Se, resultando em diminuição do risco de câncer de mama quando suplementado na dieta materna e o inverso quando de sua deficiencia. / Based on epidemiological studies and animal models, the essential micronutrient selenium has been highlighted as a promising dietary factor associated to breast cancer risk reduction. Breast cancer may have its origin in early development and thus the maternal diet could have important implications in the fetal programming of the disease. In order to ascertain whether differences in selenium concentration in maternal diet could modulate the susceptibility of female offspring to breast cancer, a biological assay was conducted in which female rats were fed a diet with 0.15 (CO), 1.0 (SUP) or 0.05 (DEF) ppm of selenium during gestational period and the female offspring subjected to a mammary carcinogenesis model induced by DMBA. SUP group offspring presented decreased susceptibility to mammary carcinogenesis, as indicated by lower (p< 0,05) average number and multiplicity od adenocarcinomas, while the DEF group offspring had a greater susceptibility, as indicated by the increase (p< 0,05) in adenocarcinomas incidency. Mothers of the DEF group pesented lower (p< 0,05) Se blood concetrations and their offspring presented lower (p<0,05).GPx1 activity. In addition, there was a decrease (p< 0,05) in ER&#945;, Her-2, EGFR and Ras expression (western blot and qPCR) in the mammary gland of 7 weeks old female SUP group offspring when compared to CO and DEF groups offspring. DNA global methylation pattern (HPLC-DAD), DNMT1, 3a e 3b expression (qPCR), global pattern of post-translational modification in histones (western blot) and methylation status of Er&#945; promoter region (bisulfite modification and pyrosequencing) were also evaluated in the mammary gland of 7 weeks old offspring. There was no diffrence (p>0,05) in DNA global methylation pattern and DNMTs expression. There was an increase in acetilated H4K16 expression in groups SUP and DEF (p< 0,05). Lastly, when compared to DEF offspring, the SUP offspring presented a marginal increase in the methylation of two CpG dinucleotides in the Er&#945; promoter region. In conclusion, the consumption of different selenium concentration in maternal diet plays a role in the progeny\'s breast cancer susceptibility through the modulation of receptors and oncogenes expression, in addition to modifications in epigenetic patterns. These results indicate the presence of a \"programming window\" in the beggining of development susceptible to selenium effects, resulting in decreased breast cancer risk when supplemented and the opposite when deficient.

Fatores dietéticos como o selênio (Se) são apontados como importantes moduladores do risco de desenvolvimento do câncer de mama. Essa neoplasia pode apresentar sua origem no início do desenvolvimento e, assim, a alimentação materna poderia ter importantes repercussões na programação fetal da doença. A fim de verificar se diferentes concentração de selênio na dieta materna poderiam programar o risco da progênie feminina ao câncer de mama, ratas foram alimentadas com ração contendo 0,15 (CO), 1,0 (SUP) ou 0,05 (DEF) ppm de Se durante a gestação e sua progênie feminina iniciada com DMBA. A progênie do grupo SUP apresentou menor suscetibilidade à carcinogênese, indicado pelo menor número médio e multiplicidade de adenocarcinomas mamários (p< 0,05), enquanto a do grupo DEF apresentou maior suscetibilidade à carcinogênese, indicado pela maior incidência dos mesmos (p< 0,05). Mães do grupo DEF apresentaram menor concentração de Se no sangue (p< 0,05) e sua prole apresentou menor atividade da enzima GPx1 (p< 0,05). Além disso, observou-se na glândula mamária da progênie de 50 dias menor expressão (western blot e qPCR) de ER&#945;, Her-2, EGFR e Ras no grupo SUP em comparação aos grupos CO e DEF (p< 0,05). Analisou-se, ainda, o padrão de metilação global do DNA (HPLC-DAD), expressão das enzimas DNMT1, 3a e 3b (qPCR), o padrão global de modificações pós traducionais em histonas (western blot) e o padrão de metilação da região promotora do gene Er&#945; (modificação com bissulfito e pirossequenciamento) na glândula mamária da progênie de 50 dias. Não houve diferença no padrão de metilação global do DNA e expressão das enzimas DNMTs (p>0,05). Houve aumento na expressão de H4K16 acetilada nos grupos SUP e DEF (p< 0,05). Finalmente, em comparação a progênie do grupo DEF, a do grupo SUP apresentou região promotora de Er&#945; com aumento marginal (p=0,07) na metilação de dois dinucleotídeos CpG. Conclui-se que o consumo de diferentes concentrações de Se na dieta materna tem impacto sobre a suscetibilidade da progênie ao câncer de mama na vida adulta através da modulação da expressão de receptores e oncogenes relacionados ao desenvolvimeto dessa neoplasia, além da influência em processos epigenéticos. Tais resultados apontam para a existência de uma \"janela de programação\" no início do desenvolvimento sensível a ação do Se, resultando em diminuição do risco de câncer de mama quando suplementado na dieta materna e o inverso quando de sua deficiencia. / Based on epidemiological studies and animal models, the essential micronutrient selenium has been highlighted as a promising dietary factor associated to breast cancer risk reduction. Breast cancer may have its origin in early development and thus the maternal diet could have important implications in the fetal programming of the disease. In order to ascertain whether differences in selenium concentration in maternal diet could modulate the susceptibility of female offspring to breast cancer, a biological assay was conducted in which female rats were fed a diet with 0.15 (CO), 1.0 (SUP) or 0.05 (DEF) ppm of selenium during gestational period and the female offspring subjected to a mammary carcinogenesis model induced by DMBA. SUP group offspring presented decreased susceptibility to mammary carcinogenesis, as indicated by lower (p< 0,05) average number and multiplicity od adenocarcinomas, while the DEF group offspring had a greater susceptibility, as indicated by the increase (p< 0,05) in adenocarcinomas incidency. Mothers of the DEF group pesented lower (p< 0,05) Se blood concetrations and their offspring presented lower (p<0,05).GPx1 activity. In addition, there was a decrease (p< 0,05) in ER&#945;, Her-2, EGFR and Ras expression (western blot and qPCR) in the mammary gland of 7 weeks old female SUP group offspring when compared to CO and DEF groups offspring. DNA global methylation pattern (HPLC-DAD), DNMT1, 3a e 3b expression (qPCR), global pattern of post-translational modification in histones (western blot) and methylation status of Er&#945; promoter region (bisulfite modification and pyrosequencing) were also evaluated in the mammary gland of 7 weeks old offspring. There was no diffrence (p>0,05) in DNA global methylation pattern and DNMTs expression. There was an increase in acetilated H4K16 expression in groups SUP and DEF (p< 0,05). Lastly, when compared to DEF offspring, the SUP offspring presented a marginal increase in the methylation of two CpG dinucleotides in the Er&#945; promoter region. In conclusion, the consumption of different selenium concentration in maternal diet plays a role in the progeny\'s breast cancer susceptibility through the modulation of receptors and oncogenes expression, in addition to modifications in epigenetic patterns. These results indicate the presence of a \"programming window\" in the beggining of development susceptible to selenium effects, resulting in decreased breast cancer risk when supplemented and the opposite when deficient.

The purpose of this systematic review was to determine the impact of plant-based diets during pregnancy on physical development of a child, beginning in utero, compared to a standard omnivore diet. Peer reviewed articles were retrieved from PubMed, Cumulative Index to Nursing and Allied Health Literature (CINAHL), Medical Literature On-line (Medline), American Psychological Association Psychological Information Database (APA PsychINFO), Health Source, and Alternative Healthwatch. Articles that were reviewed were restricted to the last 15 years. Literature reviewed included randomized control trials, observational cohorts, and case series of human subjects within the United States and the United Kingdom. The literature reviewed demonstrated that maternal nutrition has a significant role in long term fetal health and programming. Diet quality and sufficient intake of nutrients has effects on birth outcomes. The literature also made it clear that adequate nutrient intake is dependent on effective nutritional and pregnancy education. In conclusion, the literature themes of fetal programming, nutritional education, and diet quality indicate that well planned plant-based diets could be effective in pregnancy. Further observational and experimental studies need to be done on this topic so that more conclusive data can be collected.

Human milk is recognized as the main component for growth, metabolism, and immune development in infants. Furthermore, during lactation, human milk is an important source of microorganisms for the intestinal colonization of newborns. Mother-related factors have been associated with the human milk microbiota composition. Nevertheless, apparently, there has not been any study in which the maternal diet was evaluated as a modulator of the human milk microbiota. Therefore, the aim of this study was to investigate the impact of the maternal diet on the human milk microbiota composition of healthy women, and subsequently, to evaluate the effect of fructooligosaccharides supplementation on the human milk microbiota. This study consisted of two parts; the first was a cross-sectional study, including 94 lactating women recruited at the University Hospital of the University of São Paulo (HU/USP), to investigate the association between the maternal nutrient intake during pregnancy and lactation over the first month and the human milk microbiota. The second part consisted of a randomized, placebo-controlled clinical trial with 53 lactating, classified as FOS group (n = 28), which received 4.5 g of fructooligosaccharides + 2 g of maltodextrin or placebo group (n = 25), which received 2 g of maltodextrin, over a period of 20 days. The DNA was isolated and used as template for amplification and sequencing by the Illumina MiSeq&#174; System. Overall, the maternal diet during lactation (\"short-term\" food intake) influenced specific bacterial groups, including positive correlations between polyunsaturated fatty acids/linoleic fatty acids and Bifidobacterium. However, only the maternal diet during pregnancy (\"long-term\" food intake) was statistically significant (p = 0.02) for the clustering analyzes (community structure analyzes), in which higher levels of vitamin C intake during pregnancy was related to cluster 2, driven by the Staphylococcus genus. After the intervention period on the maternal diet, no differences were found for relative abundance of genera between the placebo and the FOS groups. However, the distances of the trajectories covered by the samples from the beginning to the end of the supplementation was higher for the FOS group (p = 0.0007). According to our results, the maternal age affects the response for FOS supplementation (p = 0.02), though no patterns in the differences of relative abundances were found between the groups. Our results suggest that the maternal diet may influence the human milk microbiota, and the diet during pregnancy is a stronger factor over the bacterial community structure. Minor changes were found by the maternal short-term food intake or the maternal intervention with the prebiotic, and the changes seem to be individual-dependent and influenced by the maternal age, particularly in the intervention study. / O leite humano é, reconhecidamente, o principal componente para o crescimento e o desenvolvimento metabólico e imunológico de lactentes. Adicionalmente, durante a lactação, o leite humano consiste em uma importante fonte de micro-organismos para a formação da microbiota intestinal de neonatos. Fatores relacionados à mãe têm sido associados à composição da microbiota do leite humano. Entretanto, poucos estudos avaliaram a dieta materna como componente modulador da microbiota do leite humano. Os objetivos deste estudo foram investigar o impacto da dieta materna sobre a composição da microbiota do leite humano de mães saudáveis e, posteriormente, avaliar a influência da intervenção com fruto-oligossacarídeo na microbiota do leite humano, durante 20 dias de lactação. O estudo foi dividido em duas partes; a primeira parte consistiu de um estudo transversal, com 94 lactantes atendidas no Hospital Universitário da Universidade de São Paulo (HU/USP), a fim de investigar a associação entre o consumo materno de nutrientes durante a gestação e durante o primeiro mês de lactação e a microbiota do leite humano. A segunda parte consistiu em um ensaio clínico, aleatorizado, placebo-controlado, com 53 lactantes, classificadas em grupo FOS, que recebeu 4.5 g de fruto-oligossacarídeo + 2 g de maltodextrina (n = 28) ou grupo placebo, que recebeu 2 g de maltodextrina (n = 25), suplementados por 20 dias. O DNA das amostras de leite foi isolado e utilizado como molde para amplificação e sequenciamento em Illumina MiSeq&#174; System. Em geral, a dieta materna durante a lactação (consumo a curto prazo) apresentou influência pontual sobre diversos grupos de micro-organismos, incluindo correlações positivas entre ácidos graxos poli-insaturados/linoleico e o gênero Bifidobacterium. No entanto, somente a dieta materna durante a gestação (consumo a longo prazo) foi estatisticamente significante (p = 0.02) para as análises de agrupamento das amostras (análises de estrutura de comunidade), sendo o maior teor de vitamina C consumido durante a gestação relacionado ao agrupamento 2, direcionado por maiores populações do gênero Staphylococcus. Após o período de intervenção na dieta materna, não foram encontradas diferenças entre a abundância relativa de gêneros entre os grupos placebo e FOS. No entanto, as distâncias do percurso das amostras do início até o final da suplementação foram maiores para o grupo FOS (p = 0.0007). De acordo com os resultados, a idade materna influencia essa resposta à suplementação por FOS (p = 0.02), embora, não tenham sido encontrados padrões nítidos nas diferenças de abundância relativa entre os grupos. Os resultados obtidos sugerem que a dieta materna consiste em um fator de modulação da microbiota do leite humano, sendo a dieta durante a gestação um fator mais intenso sobre a estrutura da comunidade bacteriana do leite humano. No entanto, o consumo a curto prazo ou a intervenção alimentar com prebiótico sobre a dieta materna apresentou influência pontual sobre a dinâmica da microbiota do leite, ainda que mudanças observadas sejam indivíduo-dependentes e influenciadas pela idade materna, como no caso do estudo de intervenção.

L’alimentation maternelle conditionne la santé métabolique et cardiovasculaire de la progéniture, mais l’impact sur les systèmes sensoriels reste peu étudié. L’olfaction joue un rôle comportemental crucial pour l’évitement des dangers et pour la prise alimentaire. Dès le plus jeune âge, les odeurs participent à l’établissement des préférences alimentaires, qui influencent les habitudes alimentaires de l’adulte. Le système olfactif repose sur le fonctionnement de neurones qui se développent pendant la vie embryonnaire, continuent leur maturation après la naissance et sont continuellement régénérés au cours de la vie. Ces neurones sont en permanence modulés par les facteurs métaboliques. Les patients atteints de troubles métaboliques ont plus de risques de présenter des altérations de la perception des odeurs, et l’exposition à une alimentation de type obésogène ou diabétogène induit des perturbations olfactives chez le rongeur.Le but de cette thèse était d’explorer les effets d’une exposition périnatale au gras et au sucre, à travers l’alimentation maternelle pendant les périodes de préconception, gestation et lactation, sur la physiologie olfactive de souris juvéniles.L’alimentation grasse et sucrée (high-fat high-sucrose, HFHS) a modifié la composition lipidique du lait maternel. La caractérisation métabolique des petits a révélé un surpoids, un excès de masse grasse épididymaire et une hyperleptinémie chez les petits provenant d'une mère sous alimentation HFHS. Les capacités olfactives évaluées lors d'un test de nourriture enfouie et par mesure du comportement de flairage induit par les odeurs étaient altérées chez les petits dont la mère a été exposée à l'alimentation HFHS. Cependant, nos résultats n’ont pas montré de modification de la sensibilité de l’épithélium olfactif (EO) ou de l’expression des gènes codant pour les éléments de la cascade de transduction olfactive. L’exploration du traitement central du signal olfactif a révélé un impact de l’alimentation maternelle HFHS sur le degré de ramification dendritique des interneurones du bulbe olfactif. En revanche, l’activation des neurones dans le cortex piriforme après une exposition odorante n’était pas modifiée.Ainsi, l'alimentation maternelle HFHS pendant les périodes de développement des petits induit chez les mâles des altérations de la perception olfactive, sans perturbation de la détection des odeurs par l'EO, mais associées à des modifications neuronales dans les structures olfactives centrales. La leptine, hormone métabolique connue pour son action sur l’olfaction et sur le développement neuronal, pourrait être à l’origine de ces déficits olfactifs. / The influence of maternal diet on progeny’s health has been thoroughly investigated regarding metabolic and cardiovascular diseases, but the impact on sensory systems remains unknown. Olfaction is of great behavioral importance for avoiding hazards and for feeding behavior. In childhood especially, olfaction participates in establishing food preferences, which partly determine adult eating habits. The olfactory system is made of sensory neurons that develop during the embryonic life, pursue their maturation after birth and are continuously regenerated over life. Olfactory neurons activity can be modulated by metabolic factors. Patients with metabolic disorders are at risk of impaired olfactory sensitivity. Adult mice exposed to an obesogenic or diabetogenic diet exhibit disrupted olfactory behavior.The aim of this thesis was to investigate the effect of a perinatal exposure to fat and sugar, through maternal diet during preconception, gestation and lactation, on the olfactory system of young mice.Maternal high fat high sugar (HFHS) diet modified milk lipids composition. When investigating pups’ metabolic phenotype, overweight, increased epididymal fat and hyperleptinemia were revealed in pup’s born from dams fed with the HFHS diet. Olfactory abilities were assessed in a buried food test and by measuring odor-induced sniffing behavior and were disrupted in the progeny of HFHS diet fed dams. However, olfactory epithelium sensitivity and gene expression of constituents of the olfactory transduction cascade were not affected by maternal HFHS diet. When investigating olfactory central processing, dendritic complexity of interneurons in the olfactory bulb was found to be affected by maternal HFHS diet. Meanwhile, neuronal activation in piriform cortex was not altered.These results show that maternal HFHS diet during pups’ development alters olfactory perception in male progeny, without impairing odor detection by the OE, and associated with neuronal modifications in olfactory central areas. Leptin is a metabolic hormone known to influence olfaction and neurons development which could have induced the olfactory defects.

Maternal effects are the non-genetic contributions of mothers (or fathers) towards the phenotype of their offspring. Maternal effects are now well recognised as a facilitator for evolutionary change in offspring phenotypes and life history strategies which can have effects on population dynamics, population divergence and even speciation. Furthermore, maternal effects have been shown to have a heritable genetic basis and that they are genetically variable, which suggests that they contribute to maintaining phenotypic variation. Maternal effects may impede or accelerate responses to selection which has implications for adaptive evolution and making predictions about their evolutionary potential. The importance of their contribution to phenotypic variation and life history evolution has made maternal effects an important consideration in fields such as conservation and population biology, evolutionary ecology and evolutionary genetics. The aim of this thesis is to investigate if maternal effects can influence offspring life history traits and fitness parameters through maternal resources via the egg. Main questions that are asked include: can maternal effects help facilitate transition to a novel host-diet (Chapter 2); does maternal diet influence egg composition and, if so, does this have an effect on offspring life-history parameters (Chapter 3); is there a genetic basis to egg composition and is there potential for egg composition to evolve (Chapter 4); and are defensive compounds from the diet transferred into the eggs, if so, are these uni- or biparentally transferred and does this offer protection against predation (Chapter 5)? To address these questions we used a specialist insect herbivore, the large milkweed bug Oncopeltus fasciatus (Hemiptera: Lygaeidae). In the wild, O. fasciatus feed on plants from the genus Asclepias (Apocynacea). However, O. fasciatus can be reared successfully in laboratories on sunflower seeds Helianthus annus. For our experiments we used two populations of O. fasciatus, one population has been maintained on dry seeds of A. syriaca while the other population has been reared and maintained on sunflower seeds. The results of Chapter 2 were suggestive of a maternal host-diet effect on egg mass and hatching success, but we did not find evidence that maternal host-diet was significant in influencing a transition to a novel host. In Chapter 3 we found that there was variation in the free amino acid profiles of the eggs between our treatments suggesting that amino acid profiles may be influenced by maternal diet. The results of our multivariate selection analysis to examine linear and nonlinear (quadratic) relationships between maternal diet and the free amino acid profiles of the eggs suggest that there may be population-specific responses which can influence specific amino acid profiles in relation to hatchling mass. In Chapter 4 we used only the milkweed-adapted population to determine if there was a genetic basis to amino acid profiles in the eggs. We constructed a genetic variance-covariance (G) matrix to determine the strength and direction of the relationships between amino acids and to assess the potential for amino acid profiles to evolve. While we found genetic variation for amino acids, and that there was evidence for positive moderate to strong genetic correlations between many of them, we also found evidence for constraints for the potential for amino acid profiles to evolve as evidenced by the calculation of gmax (which represents the linear combination of components that has the highest genetic variance and which is the most accessible to evolution). In Chapter 5 we found maternal, but not paternal, transmission of cardenolides into the eggs. However, this did not confer protection of all eggs against predation from larvae of the green lacewing Chrysoperla carnea. Overall, results suggest that for our populations of O. fasciatus, maternal effects are significant in influencing early life history traits such as egg mass and hatchling mass. However, we did not find any significant effects on other offspring life history or fitness parameters that we measured. This may be surprising as positive, and negative, effects of non-genetic contributions of females (and males) to their offspring has been widely reported in many taxa. The patterns and implications of maternal resource allocation and their effects on offspring life history evolution are explored and discussed, as are the limitations of our experimental designs. I hope that this research can be used to stimulate further investigations into maternal effects and the relationships between host-plant, maternal allocation strategies and life history evolution.

Maternal obesity has significant consequences on the lifelong health of the developing child and rising global incidences make it one of the most common comorbidities during pregnancy. Offspring of obese mothers are at an increased risk of hospitalization for respiratory infections throughout childhood, which predispose these children to non-communicable respiratory diseases in later life. Animal models of maternal high fat diet (mHFD) feeding have observed common inflammatory outcomes with obesogenic models, but the effect on offspring varies with timing of the nutritional challenge and diet composition across studies. These studies demonstrate significant alterations to circulating and lung specific immune cells but the sequence of events that link maternal diet to these fetal outcomes are unclear, nor have they been tested in the context of a bacterial respiratory infection. Streptococcus pneumonaie is the most common causative pathogen of bacterial pneumonia and meningitis, making it of high clinical relevance. We aimed to investigate the effect of a mHFD (45% kcal from fat) during gestation and lactation, on offspring outcome and recovery from Streptococcus pneumoniae infection. Immunophenotyping, both before and after infection, revealed a hypo-inflammatory phenotype in circulating monocytes of the mHFD offspring with a decreased capacity to both initiate and terminate inflammatory responses. These offspring had significantly higher bacterial counts in lung tissues during infection and sustained cellular inflammation in survivors. In this thesis, we present foundational work on the detrimental influence of excess maternal nutrition on offspring immune function and infection outcomes, which may be involved in susceptibility to inflammatory and chronic disease in later life. A better understanding of this deep and lasting influence of the maternal environment will allow us to target preconception health as a form of harm reduction, informing stake holders and institutions to direct efforts towards DOHaD knowledge translation. / Thesis / Master of Science (MSc)