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Does paternal immunocompetence affect offspring vulnerability to maternal androgens? A study in domestic chickens.

ABSTRACT: Exposure of yolk androgens can positively stimulate chick growth and competitive ability, but may negatively affect immunity. It has been hypothesized that only chicks from immunologically superior fathers can bear the cost of prenatal exposure to high androgen levels. To test this hypothesis, we paired roosters from two selection lines, one up- and one down-selected for natural antibodies (NAbs), with hens from a control line. We measured yolk testosterone and androstenedione levels, and we injected the treatment group of eggs of each female with testosterone suspended in sesame oil and the control group with sesame oil only. We then measured hatching success and growth, and characterized the humoral and cellular immune responses using three different challenges: a phyto-hemagglutinin, a lipopolysaccharide and a sheep red blood cell challenge. We found that the hatching success, body mass, initial levels of natural antibodies and the chicks' immunological responses to the three different challenges and development were affected neither by paternal immunocompetence nor by treatment. These results do not support the hypothesis that chicks from low-NAb line fathers are more sensitive to testosterone exposure during embryonic development than chicks from high-NAb line fathers.

SUBMITTER: Lelono A

PROVIDER: S-EPMC6899007 | biostudies-literature | 2019 Nov

REPOSITORIES: biostudies-literature

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Does paternal immunocompetence affect offspring vulnerability to maternal androgens? A study in domestic chickens.

Lelono Asmoro A Robledo-Ruiz Diana A DA Berghof Tom V L TVL Parmentier Henk K HK Riedstra Bernd B Groothuis Ton G TG

Biology open 20191120 11

Exposure of yolk androgens can positively stimulate chick growth and competitive ability, but may negatively affect immunity. It has been hypothesized that only chicks from immunologically superior fathers can bear the cost of prenatal exposure to high androgen levels. To test this hypothesis, we paired roosters from two selection lines, one up- and one down-selected for natural antibodies (NAbs), with hens from a control line. We measured yolk testosterone and androstenedione levels, and we inj ...[more]

PMID: 31748241

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Project description:BACKGROUND:In recent decades, there has been a shift to later childbearing in high-income countries. There is limited large-scale evidence of the relationship between maternal age and child outcomes beyond the perinatal period. The objective of this study is to quantify a child's risk of developmental vulnerability at age five, according to their mother's age at childbirth. METHODS AND FINDINGS:Linkage of population-level perinatal, hospital, and birth registration datasets to data from the Australian Early Development Census (AEDC) and school enrolments in Australia's most populous state, New South Wales (NSW), enabled us to follow a cohort of 99,530 children from birth to their first year of school in 2009 or 2012. The study outcome was teacher-reported child development on five domains measured by the AEDC, including physical health and well-being, emotional maturity, social competence, language and cognitive skills, and communication skills and general knowledge. Developmental vulnerability was defined as domain scores below the 2009 AEDC 10th percentile cut point. The mean maternal age at childbirth was 29.6 years (standard deviation [SD], 5.7), with 4,382 children (4.4%) born to mothers aged <20 years and 20,026 children (20.1%) born to mothers aged ?35 years. The proportion vulnerable on ?1 domains was 21% overall and followed a reverse J-shaped distribution according to maternal age: it was highest in children born to mothers aged ?15 years, at 40% (95% CI, 32-49), and was lowest in children born to mothers aged between 30 years and ?35 years, at 17%-18%. For maternal ages 36 years to ?45 years, the proportion vulnerable on ?1 domains increased to 17%-24%. Adjustment for sociodemographic characteristics significantly attenuated vulnerability risk in children born to younger mothers, while adjustment for potentially modifiable factors, such as antenatal visits, had little additional impact across all ages. Although the multi-agency linkage yielded a broad range of sociodemographic, perinatal, health, and developmental variables at the child's birth and school entry, the study was necessarily limited to variables available in the source data, which were mostly recorded for administrative purposes. CONCLUSIONS:Increasing maternal age was associated with a lesser risk of developmental vulnerability for children born to mothers aged 15 years to about 30 years. In contrast, increasing maternal age beyond 35 years was generally associated with increasing vulnerability, broadly equivalent to the risk for children born to mothers in their early twenties, which is highly relevant in the international context of later childbearing. That socioeconomic disadvantage explained approximately half of the increased risk of developmental vulnerability associated with younger motherhood suggests there may be scope to improve population-level child development through policies and programs that support disadvantaged mothers and children.

Dataset Information

Does paternal immunocompetence affect offspring vulnerability to maternal androgens? A study in domestic chickens.

Publications

Does paternal immunocompetence affect offspring vulnerability to maternal androgens? A study in domestic chickens.

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