Abstract
Exposure to heat stress can alter the development and immune system function in dairy calves. Serotonin is an immunomodulatory biogenic amine that functions as a neurotransmitter and as a stress-response mediator. Our objectives were to characterize the patterns of serum serotonin concentrations and the pattern of serotonin-related genes expressed by immune cells of calves exposed to chronic heat stress or heat stress abatement during early life, and to explore whether these might relate to immune system development. Dairy calves were exposed to chronic heat stress (HS; n = 6) or heat stress abatement (cooling, CL; n = 6) across the prenatal (late gestation, last 46 d) and postnatal (from birth to weaning, 56 d) developmental windows. Blood samples were collected to harvest serum (weekly, from d 1 to 49), to isolate of circulating leukocyte mRNA (at 1, 21 and 42 d of age) and characterize immune cell populations by flow cytometry (at 21 and 47 d of age). Calves exposed to chronic heat stress pre- and postnatally had lower red blood cell counts and lower circulating serotonin, immunoglobulin G, and B-lymphocytes compared to CL calves. Circulating blood leukocyte mRNA expression of serotonin receptors -1A, -1F, -4 and -5 was greater, while heat shock protein 70 and immune-related genes (i.e., TBX21, TLR4, and TGFβ) were lower in HS relative to CL calves. Peripheral blood leukocytes from all calves secreted serotonin and interleukin-6 after in-vitro lipopolysaccharide stimulation. However, the HS calves produced more serotonin and less interleukin-6 than CL calves when activated in-vitro. Together, our data suggest that providing heat stress abatement to dairy calves across prenatal and postnatal developmental windows might modulate the serotonin synthesis pathway in ways that may benefit humoral immunity against microbial pathogens.
Highlights
Dairy calves in hot regions can experience heat stress, both during pre- and postnatal developmental windows, when there is a lack of heat stress abatement infrastructure [1,2,3]
We evaluated the gene expression of heat shock factor 1 (HSF1), heat shock proteins (HSP70, HSP72 and HSP90), T-cell transcription factors (GATA3, FoxP3, TBX21 and RORγδ), toll like receptors 2 and 4 (TLR2 and toll-like receptor 4 (TLR4)), Lselectin (CD62L), co-stimulatory molecules (CD28 and CD80), interleukins (IL2, IL4, IL10 and IL12B), interleukin 2 receptor (CD25), transforming growth factor beta (TGFB1), interferon gamma (IFNG), apoptosis regulator BAX (BAX), Bcl-2-related protein A1 (BCL2A1) and serotonin machinery related genes including serotonin transporter (SERT), TPH1 and serotonin receptors (5-HT1A, -1B, -1D, -1F, -2A, -2B, -2C, -4, -5, -6, -7)
To determine whether temporal differences in humoral immunity exist between heat stress (HS) and CL calves, IgG concentrations were measured from the colostrum fed to calves and from serum samples collected from calves weekly from d 1 to d 49
Summary
Dairy calves in hot regions can experience heat stress, both during pre- and postnatal developmental windows, when there is a lack of heat stress abatement infrastructure (i.e., sprinklers, fans, or shade) [1,2,3]. The immune system in dairy calves starts developing prenatally Calves exposed to prenatal heat stress have impaired passive transfer of Ig from ingested colostrum [3]. Colostrum-acquired IgG concentrations gradually decrease during the calf’s first month of life [6], while the calf begins to produce its own T and B-lymphocytes capable of inducing active immunity to pathogens. This process may be impaired in HS calves as it has been reported that such calves have altered immune responses that could have long-lived effects on host immunity and disease resistance [3]
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