Effects of Newcastle Disease Virus Infection on Chicken Intestinal Intraepithelial Natural Killer Cells.

Mostafa Abdolmaleki,Sheau Wei Tan,Aini Ideris,Muhammad Bashir Bello,Abdul Rahman Omar,Mohd Hair Bejo,Swee Keong Yeap,Mohammad Zareian Jahromi,Dilan Amila Satharasinghe

doi:10.3389/fimmu.2018.01386

Abstract

The intestinal intraepithelial natural killer cells (IEL-NK) are among the earliest effectors of antiviral immunity in chicken. Unfortunately, their role during Newcastle disease virus (NDV) infection remains obscure. Previous study has reported the development of a monoclonal antibody (mAb) known as 28-4, which is specifically directed against the CD3− IEL-NK cells. In the present study, we used this mAb to investigate the effects of velogenic and lentogenic NDV infection on avian IEL-NK cells. Our findings revealed that chickens infected with velogenic NDV strains have a reduced population of purified CD3−/28-4+ IEL-NK cells as determined by flow cytometry. Furthermore, the CD3−/28-4+ IEL-NK cells from chicken infected with velogenic NDV strains were shown to have a downregulated expression of activating receptors (CD69 and B-Lec), effector peptide (NK-LYSIN), and IFN gamma. On the contrary, the expression of the inhibitory receptor (B-NK) and bifunctional receptor (CHIR-AB1) were upregulated on these purified CD3−/28-4+ IEL-NK cells following velogenic NDV infection. Meanwhile, the lentogenic NDV demonstrated insignificant effects on both the total population of CD3−/28-4+ IEL-NK cells and the expression of their surface receptors. In addition, using real-time PCR and transmission electron microscopy, we showed that CD3−/28-4+ IEL-NK cells were susceptible to velogenic but not lentogenic NDV infection. These findings put together demonstrate the ability of different strains of NDV to manipulate the activating and inhibitory receptors of CD3−/28-4+ IEL-NK cells following infection. Further studies are, however, required to ascertain the functional importance of these findings during virulent or avirulent NDV infection.

Highlights

Newcastle disease (ND) is one of the most important viral diseases of birds that cause devastating economic losses in the global poultry industry
Our findings revealed that velogenic, but not lentogenic Newcastle disease virus (NDV), downregulates the activating receptors on chicken CD3−/28-4+ intraepithelial natural killer cells (IEL-natural killer cells (NK)) cells, and in turn increase the expression of the inhibitory receptors
To determine the effect of different NDV pathotypes on the population of Intraepithelial Lymphocyte (IEL), the cells were counted before the infection and at different time points post infection

Summary

Introduction

Newcastle disease (ND) is one of the most important viral diseases of birds that cause devastating economic losses in the global poultry industry. The disease is distributed worldwide and affects a wide range of avian species, causing high mortality and severe clinical symptoms [1]. The etiologic agent of the disease is a negative-stranded RNA virus known as Newcastle disease virus (NDV), an avian paramyxovirus type 1, which belongs to the genus Avulavirus in the family Paramyxoviridae [2]. Depending on the severity of clinical disease in chicken, NDV strains can be classified into three pathotypes: velogenic, mesogenic, and lentogenic strains. NDV Modulate Chicken IEL-NK Cells (reaching 100% mortality) with clinical signs and lesions severely affecting the respiratory, gastrointestinal, and nervous system [3]. The mesogenic strains are of intermediate virulence causing clinical illness in chickens characterized by moderate neurological and respiratory symptoms with low mortality. The lentogenic strains such as LaSota, V4, and Ulster strains do not usually cause notable clinical disease in adult chickens and are used as live vaccines [4]

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