Abstract
Current evidence suggests thyroid hormones (THs) impact development of the immune system, but few studies have explored the connection between the thyroid and immune systems, especially in fish. This is important as some environmental contaminants disrupt TH homeostasis and may thus have negative impacts on the immune system. To determine the long-term consequences of early life stage (ELS) hypothyroidism on immune function, fathead minnows were exposed to the model thyroid hormone suppressant propylthiouracil (PTU) from < 1 to 30 days post hatch. Fish were transferred to clean water and raised to adulthood (5–7 months post hatch) at which time, several aspects of immune function were evaluated. Ex vivo assessment of immune cell function revealed significant decreases (1.2-fold) in the phagocytic cell activity of PTU-treated fish relative to the controls. Fish were also injected with Yersinia ruckeri to evaluate their in vivo immune responses across a suite of endpoints (i.e., transcriptomic analysis, leukocyte counts, spleen index, hematocrit, bacterial load and pathogen resistance). The transcriptomic response to infection was significantly different between control and PTU-treated fish, though no differences in bacterial load or pathogen resistance were noted. Overall, these results suggest that early life stage TH suppression causes long-term impacts on immune function at the molecular and cellular levels suggesting a key role for TH signaling in normal immune system development. This study lays the foundation for further exploration into thyroid-immune crosstalk in fish. This is noteworthy as disruption of the thyroid system during development, which can occur in response to chemicals present in the environment, may have lasting effects on immune function in adulthood.
Highlights
Current evidence suggests thyroid hormones (THs) impact development of the immune system, but few studies have explored the connection between the thyroid and immune systems, especially in fish
Similar observations have been made in zebrafish (Danio rerio) exposed to methimazole (MMI, a model thyroid suppressant) from 5 to 28 days post fertilization, where fish exposed to MMI experienced decreases in thymus volume as well as the downregulation of transcripts involved in lymphocyte development and maturation[9]
The results of the current study demonstrate that female fathead minnows exposed to PTU from < 1 to 30 dph experience alterations in the transcriptomic response to Y. ruckeri and decreases in ex vivo phagocytic cell activity
Summary
Current evidence suggests thyroid hormones (THs) impact development of the immune system, but few studies have explored the connection between the thyroid and immune systems, especially in fish. The transcriptomic response to infection was significantly different between control and PTU-treated fish, though no differences in bacterial load or pathogen resistance were noted Overall, these results suggest that early life stage TH suppression causes long-term impacts on immune function at the molecular and cellular levels suggesting a key role for TH signaling in normal immune system development. Adult female mice gestated under hypothyroid conditions were found to have significantly increased survival following Streptococcus pneumoniae infection[10] or increased severity of experimental autoimmune encephalomyelitis[11,12] Despite evidence demonstrating both the sensitivity of early life stage (ELS) fish to contaminant-induced thyroid disruption[13] and the crosstalk between the thyroid and immune systems in fish[4,5,9], to our knowledge, there are no studies that explore the potential long-term consequences of ELS thyroid disruption on immune function in fish. It is important to consider the developing immune system as a potential indirect target of thyroid disrupting chemicals
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