Abstract
Nicotine and acetylcholine cause immunosuppresion by signaling to the α7 nicotinic acetylcholine receptor (α7 nAChR) on immune cells. Neonicotinoids are nAChR agonists and widly used insecticides. We aimed to define the immunosuppressive potential of dietary exposure to the neonicotinoid imidacloprid (IMI) on the generation of innate and adaptive immune responses to porcine reproductive and respiratory syndrome virus (PRRSV). Piglets were randomized into groups based on diet and infection. Behavioral signs of illness were recorded. Urine IMI levels were measured by high performance liquid chromatography-mass spectrometry. Flow cytometry was used to determine the expression pattern of the α7 nAChR on porcine leukocytes as well as the effects of infection and treatment on circulating leukocyte populations. Serum cytokines and PRRSV-specific antibody levels were determined by ELISA. Viral RNA in lung, spleen and plasma was determined by RT-qPCR. Pigs in the treatment group had elevated urine levels of IMI. Treatment with IMI reduced body weight, caused bouts of hypothermia, increased serum IL-10 and elevated levels of virus-specific antibodies. Viral RNA levels in the spleen showed a trend toward being increased in pigs fed IMI. Our data indicates that IMI injection may modulate virus specific immune function during PRRSV infection.
Highlights
Neonicotinoids are a relatively new class of insecticides that were initially developed during the late 1980’s1
Mean fluorescent intensity analysis of α-BT stained cells isolated from blood indicated that both cytotoxic (CD3+CD8+) and helper (CD3+CD4+) T-cell populations exhibit a low level of receptor expression (Fig. 1A)
These data indicate that the expression profile for the α7 nicotinic acetylcholine receptor (nAChR) on immune cells is relatively conserved across species and that the receptor expression pattern in piglets is more similar to that of humans[34]
Summary
Neonicotinoids are a relatively new class of insecticides that were initially developed during the late 1980’s1. Almost all corn seeds in the U.S are preemptively coated with neonicotinoids prior to planting This particular practice has raised some concerns for the following reasons: First, because of their environmental stability, residual neonicotinoids become elevated in agricultural fields during cultivation and remain elevated following harvest[5]. The cholinergic anti-inflammatory pathway (CAP) is partially responsible for fulfilling this function Activation of this pathway is initiated when efferent neuron depolarization causes post-synaptic secretion of acetylcholine in the liver and intestine or depolarizes the splenic nerve. The latter results in norepinephrine release within the spleen which signals to β2-andrenergic receptors (β2AR) on a subset of T-cells[20]. Nicotine can suppress proinflammatory responses that occur during viral infection or in models of autoimmunity and does so in a manner that is thought to be contingent on the activation of α7 nAChRs on immune cells[25,26]
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