scholarly journals Prenatal maternal stress is associated with increased sensitivity to neuropathic pain and sex-specific changes in supraspinal mRNA expression of epigenetic- and stress-related genes in adulthood

2020 ◽  
Vol 380 ◽  
pp. 112396
Author(s):  
Stéphanie Grégoire ◽  
Seon Ho Jang ◽  
Moshe Szyf ◽  
Laura S. Stone
2012 ◽  
Vol 41 (5) ◽  
pp. 609-626 ◽  
Author(s):  
Dawn Kingston ◽  
Wendy Sword ◽  
Paul Krueger ◽  
Steve Hanna ◽  
Maureen Markle‐Reid

2014 ◽  
Vol 2014 ◽  
pp. 1-10 ◽  
Author(s):  
Anne-Marie Turcotte-Tremblay ◽  
Robert Lim ◽  
David P. Laplante ◽  
Lester Kobzik ◽  
Alain Brunet ◽  
...  

Little is known about how prenatal maternal stress (PNMS) influences risks of asthma in humans. In this small study, we sought to determine whether disaster-related PNMS would predict asthma risk in children. In June 1998, we assessed severity of objective hardship and subjective distress in women pregnant during the January 1998 Quebec Ice Storm. Lifetime asthma symptoms, diagnoses, and corticosteroid utilization were assessed when the children were 12 years old (N=68). No effects of objective hardship or timing of the exposure were found. However, we found that, in girls only, higher levels of prenatal maternal subjective distress predicted greater lifetime risk of wheezing (OR=1.11; 90% CI = 1.01–1.23), doctor-diagnosed asthma (OR=1.09; 90% CI = 1.00–1.19), and lifetime utilization of corticosteroids (OR=1.12; 90% CI = 1.01–1.25). Other perinatal and current maternal life events were also associated with asthma outcomes. Findings suggest that stress during pregnancy opens a window for fetal programming of immune functioning. A sex-based approach may be useful to examine how prenatal and postnatal environments combine to program the immune system. This small study needs to be replicated with a larger, more representative sample.


Birth ◽  
2021 ◽  
Author(s):  
Brittain L Mahaffey ◽  
Jacqueline L Tilley ◽  
Lucero K Molina ◽  
Adam Gonzalez ◽  
Elyse Park ◽  
...  

2019 ◽  
Author(s):  
Wenwu Zhang ◽  
Jiguo Xu ◽  
Hongmei Li ◽  
Lianghui Zhou ◽  
Qinghua Nie ◽  
...  

Abstract Background As a major stressor, high temperatures negatively affect the poultry industry, through impairments to chicken immunity and production performance. The purpose of this study is to clarify how chicken immune systems responded to heat stress with and without immunization. In the present study, spleen and bursa of Fabricius of experimental chickens were subjected to RNA-seq. Key genes influencing immune response in heat-stressed chickens were identified and their functions validated. Results Immunized and heat-stressed chickens experienced a significant reduction in immune function. The expression of immune-related genes and heat stress-related genes in the spleen increased after immunization and decreased after heat stress, but in the bursa of Fabricius, few of these genes were differentially expressed after immunization and heat stress, indicating insensitivity to high temperature and the lack of vaccine processing. In the non-heat-stressed groups, spleen expression of DUSP1 and HSPA5 decreased significantly, suggesting their relationship to immunity. Upon DUSP1 or HSPA5 overexpression, the mRNA expression of MHC-I, MHC-II, CD80, CD86, CD1C, IL1B, IL6, and TLR4 was earlier than that under LPS stimulation only, indicating that DUSP1 or HSPA5 overexpression enhances HD11 recognition LPS. Inhibiting DUSP1 or HSPA5 expression, the mRNA expression levels of MHC-I, MHC-II, CD80, CD86, IL6 and TLR4 did not change significantly from LPS-stimulation-only levels but CD1C significantly decreased, suggesting that HD11 recognition of LPS is affected by DUSP1 or HSPA5 expression levels. Conclusions The inhibition of immune response due to lowly expressed DUSP1 and HSPA5 may be the cause of decreased immunity in chickens.


2015 ◽  
Vol 61 ◽  
pp. 16 ◽  
Author(s):  
Elise Beau Vangeel ◽  
Benedetta Izzi ◽  
Titia Hompes ◽  
Kristof Vansteelandt ◽  
Diether Lambrechts ◽  
...  

2003 ◽  
Vol 285 (4) ◽  
pp. F688-F693 ◽  
Author(s):  
Zheng Zhang ◽  
Joan D. Ferraris ◽  
Heddwen L. Brooks ◽  
Ioana Brisc ◽  
Maurice B. Burg

TonEBP is a transcription factor that, when activated by hypertonicity, increases transcription of genes, including those involved in organic osmolyte accumulation. Surprisingly, it is expressed in virtually all tissues, including many never normally exposed to hypertonicity. We measured TonEBP mRNA (real-time PCR) and protein (Western blot analysis) in tissues of control (plasma osmolality 294 ± 1 mosmol/kgH2O) and hyposmotic (dDAVP infusion plus water loading for 3 days, 241 ± 2 mosmol/kgH2O) rats to test whether the ubiquitous expression of TonEBP mRNA is osmotically regulated around the normal plasma osmolality. TonEBP protein is reduced by hyposmolality in thymus and liver, but not in brain, and is not detected in heart and skeletal muscle. TonEBP mRNA decreases in brain and liver but is unchanged in other tissues. There are no general changes in mRNA of TonEBP-mediated genes: aldose reductase (AR) does not change in any tissue, betaine transporter (BGT1) decreases only in liver, taurine transporter (TauT) only in brain and thymus, and inositol transporter (SMIT) only in skeletal muscle and liver. Heat shock protein (Hsp)70–1 and Hsp70–2 mRNA increase greatly in most tissues, which cannot be attributed to decreased TonEBP activity. The conclusions are as follows: 1) TonEBP protein or mRNA expression is reduced by hyposmolality in thymus, liver, and brain. 2) TonEBP protein and mRNA expression are differentially regulated in some tissues. 3) Although AR, SMIT, BGT1, and TauT are regulated by TonEBP in renal medullary cells, other sources of regulation may predominate in other tissues. 4) TonEBP abundance and activity are regulated by factors other than tonicity in some tissues.


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