scholarly journals Development of the Immune System - Early Nutrition and Consequences for Later Life

Author(s):  
JoAnn Kerperien ◽  
Bastiaan Schouten ◽  
Gnther Boehm ◽  
Linette E.M. ◽  
Johan Garssen ◽  
...  
2021 ◽  
Vol 117 ◽  
pp. 103954
Author(s):  
M.S. Hollemans ◽  
G. de Vries Reilingh ◽  
S. de Vries ◽  
H.K. Parmentier ◽  
A. Lammers

Author(s):  
Simon Beggs

The central nervous system (CNS) and immune system are inextricably linked. The complexity of their interactions is still being unraveled, but the list of processes mediated wholly or in part by neuroimmune interactions continues to grow. The influence of the immune system is crucial for normal nervous system development both pre- and postnatally, for maintaining neuronal homeostasis in the mature CNS and modulating synaptic plasticity. Aberrations in this crosstalk have been implicated in many neurodevelopmental and psychiatric disorders. It is not feasible to explore neuronal function at any point in the lifespan, in health or disease, without considering the influence of the immune system. In the adult animal it is now well established that pain chronicity is maintained by immune influence upon the neuronal nociceptive system, although, fascinatingly, there is now evidence for a marked sexual dimorphism in how the immune and nervous systems interact. This holds true for pain in early life, where the two still-developing systems provide a very different environment to mediate nociception and pain. Of particular interest is how the immune system and sex interact to early life painful events to prime pain responses in later life.


2020 ◽  
Vol 7 (4) ◽  
pp. 148 ◽  
Author(s):  
Maarten S. Hollemans ◽  
Ger de Vries Reilingh ◽  
Sonja de Vries ◽  
Henk K. Parmentier ◽  
Aart Lammers

Greater antigenic exposure might accelerate activation and maturation of the humoral immune system. After hatch, commercial broiler chickens can have early (EN) or delayed (DN) access to nutrition, up to 72 h after hatch. The immune system of EN versus DN broilers is likely more exposed to antigens after hatch. This might contribute to activation and maturation of the immune system, but might also influence the development of oral tolerance, thereby altering later life antibody responses. We studied antibody (IgM, IgY, IgA) responses between 21 and 42 d of age in fast-growing EN and DN broilers, kept under low (LSC) or high sanitary conditions (HSC). In a first experiment (n = 51 broilers), we tested whether early oral exposure to bovine serum albumin (BSA) affected later life antibody responses towards BSA and a novel antigen—rabbit γ-globulin (RGG), under HSC. In a second experiment, a total of 480 EN and DN broilers were housed under either LSC or HSC, and we studied antibody responses against both BSA and RGG (n = 48 broilers per treatment) and growth performance. Broilers kept under LSC versus HSC, had higher antibody levels and their growth performance was severely depressed. Interactions between feeding strategy (EN versus DN) and sanitary conditions, or main effects of feeding strategy, on natural and specific antibody levels, and growth performance were not observed. Levels of IgA were elevated in EN versus DN broilers, in experiment I and in batch 2 of experiment II, but not in the other batches of experiment II. We concluded that EN versus DN contributes minimally to the regulation of antibody responses, irrespective of antigenic pressure in the rearing environment.


2002 ◽  
Vol 75 (6) ◽  
pp. 993-999 ◽  
Author(s):  
Atul Singhal ◽  
I Sadaf Farooqi ◽  
Stephen O'Rahilly ◽  
Tim J Cole ◽  
Mary Fewtrell ◽  
...  
Keyword(s):  

2019 ◽  
Vol 32 (1) ◽  
pp. 128-145 ◽  
Author(s):  
Sabrina Campisano ◽  
Anabela La Colla ◽  
Stella M. Echarte ◽  
Andrea N. Chisari

AbstractEarly-life nutrition plays a critical role in fetal growth and development. Food intake absence and excess are the two main types of energy malnutrition that predispose to the appearance of diseases in adulthood, according to the hypothesis of ‘developmental origins of health and disease’. Epidemiological data have shown an association between early-life malnutrition and the metabolic syndrome in later life. Evidence has also demonstrated that nutrition during this period of life can affect the development of the immune system through epigenetic mechanisms. Thus, epigenetics has an essential role in the complex interplay between environmental factors and genetics. Altogether, this leads to the inflammatory response that is commonly seen in non-alcoholic fatty liver disease (NAFLD), the hepatic manifestation of the metabolic syndrome. In conjunction, DNA methylation, covalent modification of histones and the expression of non-coding RNA are the epigenetic phenomena that affect inflammatory processes in the context of NAFLD. Here, we highlight current understanding of the mechanisms underlying developmental programming of NAFLD linked to epigenetic modulation of the immune system and environmental factors, such as malnutrition.


Parasitology ◽  
2011 ◽  
Vol 138 (12) ◽  
pp. 1508-1518 ◽  
Author(s):  
YENNY DJUARDI ◽  
LINDA J. WAMMES ◽  
TANIAWATI SUPALI ◽  
ERLIYANI SARTONO ◽  
MARIA YAZDANBAKHSH

SUMMARYThe shaping of a child's immune system starts in utero, with possible long-term consequences in later life. This review highlights the studies conducted on the development of the immune system in early childhood up to school-age, discussing the impact that environmental factors may have. Emphasis has been put on studies conducted in geographical regions where exposure to micro-organisms and parasites are particularly high, and the effect that maternal exposures to these may have on an infant's immune responses to third-party antigens. In this respect we discuss the effect on responses to vaccines, co-infections and on the development of allergic disorders. In addition, studies of the impact that such environmental factors may have on slightly older (school) children are highlighted emphasizing the need for large studies in low to middle income countries, that are sufficiently powered and have longitudinal follow-up components to understand the immunological footprint of a child and the consequences throughout life.


2008 ◽  
Vol 27 (2) ◽  
pp. 129-134 ◽  
Author(s):  
Rodney R Dietert ◽  
Michael S Piepenbrink

The developing immune system serves as a novel target for disruption by environmental chemicals and drugs, and one that can significantly influence later-life health risks. Specific immune maturational events occur during critical windows of pre- and early postnatal development that are not effectively modeled using adult exposure-assessment or general developmental toxicity screens. The range of postnatal health risks linked to developmental immunotoxicity (DIT) is influenced, in part, by the natural progression of prenatal-neonatal development. In this progression, the pregnancy itself imposes a Th2-bias in utero, and this produces a delay in the acquisition of Th1 functional capacity in the newborn. The status of Th1 regulatory and Th17 populations may also be important in immune function/dysfunction considerations. The necessary shift from a Th2 preferred capacity in late gestation to a more balance functional capacity in the neonate can be disrupted by xenobiotics leaving the child with increased vulnerability to a range of potential diseases. Knowledge of environmental factors that facilitate effective immune functional maturation as well as those xenobiotics capable of disrupting the process is important in strategies to reduce the incidence of diseases such as childhood asthma. Because hormesis has been shown to be an important factor in modulation of the adult immune system, it becomes even more important to understand potentially opposing dose-response effects for the immune system of the fetus, neonate, and juvenile. The direct linkage between immune dysfunction and chronic disease has become abundantly apparent in recent years. Therefore, a more comprehensive and effective approach for the protection of the developing immune system can help to reduce the incidence of later-life chronic diseases.


2019 ◽  
Vol 41 (1) ◽  
pp. 36-41 ◽  
Author(s):  
Simon Spichak ◽  
Timothy G. Dinan ◽  
John F. Cryan

How does the immune system impact brain development? The exciting and somewhat unexpected relationship between the immune system and the brain has become one of the most fascinating topics in neuroscience. Even though the immune system was initially implicated in resolving viral and bacterial threats, it is now becoming more evident that it also plays a role in processes in the brain, both under healthy and pathological conditions. This novel role of the immune system in brain health has been implicated in various psychopathologies where neurodevelopment, stress and mood are central. In particular, its role in healthy brain development is becoming more evident, and understanding neuroimmune communication is becoming crucial in treating neurodevelopmental and mood disorders in later life. In the brain, glia function as part of the innate immune system and are programmed to respond to pathogens and physical injury. They also play an important role in neuronal development and pruning. These cells communicate with and respond to chemical signals, such as cytokines and chemokines, which can then initiate or downregulate inflammatory responses. Finally, the trillions of microbes residing in the gut can also stimulate cytokine and chemokine responses in the periphery and play an important role in both immunity and brain development.


Author(s):  
Lorella Paparo ◽  
Rosita Aitoro ◽  
Rita Nocerino ◽  
Carmen di Scala ◽  
Margherita Di Costanzo ◽  
...  

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