The effect of dietary neonicotinoid supplementation on innate and adaptive immune responses to porcine reproductive and respiratory syndrome virus

Neonicotinoids are currently the most widely used insecticides in the world to treat crops and seeds in the commercial agricultural industry. Acting as nicotine analogues neonicotinoids signal to α-bungarotoxin (α-BT) sensitive insect nicotinic acetylcholine receptors (nAChR), which are expressed throughout the insect nervous system. The predominant nAChR in the mammalian brain is the α4β2 subunit that is resistant to α-BT but the α7nAChR, which is expressed at much lower levels and has been characterized on immune cells, is α-BT sensitive. Activation of nAChRs can initiate the cholinergic anti-inflammatory pathway (CAP) that has immunosuppressive capabilities. Cultures of porcine bone marrow derived dendritic cells (BMDC) stained with α-BT indicated that CD172a+SLA DR+ dendritic cells expressed the α7nAChR. We hypothesized that exposure to a 5 mg/kg body weight/day diet of the neonicotinoid imidacloprid (IMI) would activate the α7nAChR and the CAP causing suppression of virus-specific immunity to porcine reproductive and respiratory syndrome virus (PRRSV). Over the course of 14 days blood samples were collected and analyzed by flow cytometry, qRT-PCR, and ELISA for cell populations, cytokines, humoral response, α7nAChR expression, and viral RNA. Hypothermia and reductions in body weight were observed in both PRRSV infected and uninfected groups receiving dietary supplementation with IMI. Serum cytokine production of IL-10 was increased in those groups receiving dietary IMI supplementation over the course of the experiment. Furthermore, CD172a+SLA DR+SSClo monocytes had reduced expression of major histocompatibility complex (MHC) class II (SLA DR) in infected piglets receiving IMI. Finally, elevated levels of virus-specific antibodies were measured at day 14 post infection (p.i.) in IMI treated groups. Infection with PRRSV increased production of virus-specific antibodies, circulating IL-10, and percentage of circulating monocytes and helper T-cells (CD3+CD4+). Additionally, the ability for T-cells (CD3+) to produce interferon (IFN)-γ was increased at day 7 p.i. compared to day 3 p.i. as a result of infection and regardless of dietary IMI supplementation. This is the first study, to our knowledge, to characterize the effects of neonicotinoids on the immune response to a viral pathogen in pigs. Our data indicates that IMI may adversely affect the generation of Type I immunity and increase virus-specific antibody production and promote viremia and viral dissemination.

Name thesis:degree_name

M.S.

Level thesis:degree_level

Thesis

Discipline thesis:degree_discipline

Animal Sciences

Grantor

University of Illinois at Urbana-Champaign

Year dc:date

2018

Author dc:creator

• Hernandez, Jessica

Contributors dc:contributor

• Steelman, Andrew
• Johnson, Rodney
• Dilger, Ryan

• Imidacloprid
• Neonicotinoids
• Porcine reproductive and respiratory syndrome virus
• Innate immunity
• Adaptive immunity
• α-Bungarotoxin

Statement dc:rights

• Copyright 2017 Jessica Hernandez

Language dc:language

en

Handle dc:identifier

http://hdl.handle.net/2142/99202

OAI identifier oai:identifier

oai:www.ideals.illinois.edu:2142/99202