Neonatal stress modulates sickness behavior.
Identifieur interne : 000740 ( PubMed/Curation ); précédent : 000739; suivant : 000741Neonatal stress modulates sickness behavior.
Auteurs : Ronit Avitsur [Israël] ; John F. SheridanSource :
- Brain, behavior, and immunity [ 1090-2139 ] ; 2009.
Descripteurs français
- KwdFr :
- Analyse de variance, Animaux, Animaux nouveau-nés (immunologie), Caractères sexuels, Comportement de maladie (physiologie), Consommation alimentaire (immunologie), Facteurs de l'âge, Femelle, Infections à Orthomyxoviridae (immunologie), Lipopolysaccharides (immunologie), Lipopolysaccharides (toxicité), Mâle, Poids du corps (immunologie), Souris, Souris de lignée C57BL, Stress psychologique (immunologie), Séparation d'avec la mère, Virus de la grippe A (immunologie).
- MESH :
- immunologie : Animaux nouveau-nés, Consommation alimentaire, Infections à Orthomyxoviridae, Lipopolysaccharides, Poids du corps, Stress psychologique, Virus de la grippe A.
- physiologie : Comportement de maladie.
- toxicité : Lipopolysaccharides.
- Analyse de variance, Animaux, Caractères sexuels, Facteurs de l'âge, Femelle, Mâle, Souris, Souris de lignée C57BL, Séparation d'avec la mère.
English descriptors
- KwdEn :
- Age Factors, Analysis of Variance, Animals, Animals, Newborn (immunology), Body Weight (immunology), Eating (immunology), Female, Illness Behavior (physiology), Influenza A virus (immunology), Lipopolysaccharides (immunology), Lipopolysaccharides (toxicity), Male, Maternal Deprivation, Mice, Mice, Inbred C57BL, Orthomyxoviridae Infections (immunology), Sex Characteristics, Stress, Psychological (immunology).
- MESH :
- chemical , immunology : Lipopolysaccharides.
- immunology : Animals, Newborn, Body Weight, Eating, Influenza A virus, Orthomyxoviridae Infections, Stress, Psychological.
- physiology : Illness Behavior.
- chemical , toxicity : Lipopolysaccharides.
- Age Factors, Analysis of Variance, Animals, Female, Male, Maternal Deprivation, Mice, Mice, Inbred C57BL, Sex Characteristics.
Abstract
The quality of the early environment, especially during the neonatal period, influences the development of individual differences in resistance to stress and illness in adulthood. A previous study demonstrated that neonatal stress augmented proinflammatory cytokine expression and viral replication in influenza virus-infected adult mice. The goal of the following study was to examine the lifelong effects of neonatal stress on the behavioral response to an immune challenge. Neonatal stress consisted of separating mouse pups from their dams (maternal separation, MSP) at critical points of their development. In the first study, pups were separated from the dam daily for 6h between postnatal day 1 and 14. As adults, these mice were infected with influenza A/PR8 virus. In a second study, a similar paradigm of MSP was employed, and as adults mice were injected with lipopolysaccharide (LPS) (ip). In a third study pups were separated from the dam for 24h on postnatal day 4 or 9. As adults, these mice received ip injections of LPS. In all three studies, changes in body weight, food and sweet solution consumption were examined following immune challenge. As previously described, activation of the immune system using influenza virus infection or LPS administration resulted in sickness behavior that consisted of body weight loss, anorexia and reduced consumption of a sweet solution. Furthermore, neonatal stress induced more rapid kinetics of sickness behavior and augmented several aspects of these symptoms. Together with previous studies, these findings suggest that neonatal stress disrupted the regulation of innate resistance to an immune challenge resulting in enhanced immunological and behavioral responses to immune activation. Thus, long lasting effects of early stress events may be the basis for individual differences in health and susceptibility to disease.
DOI: 10.1016/j.bbi.2009.05.056
PubMed: 19464359
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A previous study demonstrated that neonatal stress augmented proinflammatory cytokine expression and viral replication in influenza virus-infected adult mice. The goal of the following study was to examine the lifelong effects of neonatal stress on the behavioral response to an immune challenge. Neonatal stress consisted of separating mouse pups from their dams (maternal separation, MSP) at critical points of their development. In the first study, pups were separated from the dam daily for 6h between postnatal day 1 and 14. As adults, these mice were infected with influenza A/PR8 virus. In a second study, a similar paradigm of MSP was employed, and as adults mice were injected with lipopolysaccharide (LPS) (ip). In a third study pups were separated from the dam for 24h on postnatal day 4 or 9. As adults, these mice received ip injections of LPS. In all three studies, changes in body weight, food and sweet solution consumption were examined following immune challenge. As previously described, activation of the immune system using influenza virus infection or LPS administration resulted in sickness behavior that consisted of body weight loss, anorexia and reduced consumption of a sweet solution. Furthermore, neonatal stress induced more rapid kinetics of sickness behavior and augmented several aspects of these symptoms. Together with previous studies, these findings suggest that neonatal stress disrupted the regulation of innate resistance to an immune challenge resulting in enhanced immunological and behavioral responses to immune activation. Thus, long lasting effects of early stress events may be the basis for individual differences in health and susceptibility to disease.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">19464359</PMID><DateCompleted><Year>2009</Year><Month>10</Month><Day>28</Day></DateCompleted><DateRevised><Year>2018</Year><Month>11</Month><Day>13</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1090-2139</ISSN><JournalIssue CitedMedium="Internet"><Volume>23</Volume><Issue>7</Issue><PubDate><Year>2009</Year><Month>Oct</Month></PubDate></JournalIssue><Title>Brain, behavior, and immunity</Title><ISOAbbreviation>Brain Behav. Immun.</ISOAbbreviation></Journal><ArticleTitle>Neonatal stress modulates sickness behavior.</ArticleTitle><Pagination><MedlinePgn>977-85</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1016/j.bbi.2009.05.056</ELocationID><Abstract><AbstractText>The quality of the early environment, especially during the neonatal period, influences the development of individual differences in resistance to stress and illness in adulthood. A previous study demonstrated that neonatal stress augmented proinflammatory cytokine expression and viral replication in influenza virus-infected adult mice. The goal of the following study was to examine the lifelong effects of neonatal stress on the behavioral response to an immune challenge. Neonatal stress consisted of separating mouse pups from their dams (maternal separation, MSP) at critical points of their development. In the first study, pups were separated from the dam daily for 6h between postnatal day 1 and 14. As adults, these mice were infected with influenza A/PR8 virus. In a second study, a similar paradigm of MSP was employed, and as adults mice were injected with lipopolysaccharide (LPS) (ip). In a third study pups were separated from the dam for 24h on postnatal day 4 or 9. As adults, these mice received ip injections of LPS. In all three studies, changes in body weight, food and sweet solution consumption were examined following immune challenge. As previously described, activation of the immune system using influenza virus infection or LPS administration resulted in sickness behavior that consisted of body weight loss, anorexia and reduced consumption of a sweet solution. Furthermore, neonatal stress induced more rapid kinetics of sickness behavior and augmented several aspects of these symptoms. Together with previous studies, these findings suggest that neonatal stress disrupted the regulation of innate resistance to an immune challenge resulting in enhanced immunological and behavioral responses to immune activation. 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