Analysis of chicken macrophage functions and gene expressions following infectious bronchitis virus M41 infection

Abstract

Infectious bronchitis virus (IBV) is a pathogenic coronavirus with high morbidity and mortality in chicken breeding. Macrophages with normal biofunctions are essential for host immune responses. In this study, the HD11 chicken macrophage cell line and chicken peripheral blood mononuclear cell-derived macrophages (PBMCs-Mφ) were infected with IBV at multiplicity of infection (MOI) of 10. The dynamic changes of their biofunctions, including cell viability, pathogen elimination function, phagocytic ability, and gene expressions of related proteins/mediators in innate and acquired immunity, inflammation, autophagy and apoptosis were analyzed. Results showed that IBV infection decreased chicken macrophage viability and phagocytic ability, and increased pathogen elimination function. Moreover, IBV augmented the gene expressions of most related proteins in macrophages involved in multiple host bioprocesses, and the dynamic changes of gene expressions had a close relationship with virus replication. Among them, MHCII, Fc receptor, TLR3, IFN-α, CCL4, MIF, IL-1β, IL-6, and iNOS showed significantly higher expressions in IBV-infected cells. However, TLR7, MyD88, MDA5, IFN-γ, MHCII, Fc receptor, MARCO, CD36, MIF, XCL1, CXCL12, TNF-α, iNOS, and IL-10 showed early decreased expressions. Overall, chicken macrophages play an important role in host innate and acquired immune responses to resist IBV infection, despite early damage or suppression. Moreover, the IBV-induced autophagy and apoptosis might participate in the virus-host cell interaction which is attributed to the biological process.

Inhibitory Effect of Ursolic Acid on Proliferation and Migration of Renal Carcinoma Cells and Its Mechanism

“…Autophagy can be both activated and inhibited in renal carcinoma, and it plays a double-edged role in the development of renal carcinoma [ 8 , 9 ]; in the early stage of cancer, autophagy can suppress tumors, while in the late stage, autophagy contributes to the survival of tumor cells in an unfavorable environment, and some autophagy-related proteins P62, LC3B, and beclin-1 have become indicators of the prognosis of patients with renal carcinoma [ 10 , 11 ]. Autophagy is a dynamically changing process [ 12 , 13 ], and this experiment was conducted to map the autophagy time point, and the results showed that the activation of autophagy was more obvious when ursolic acid acted on 786-O cells at 24 h. Therefore, the time point of the subsequent experiment was set to 24 h. It was found that ursolic acid could increase the expression level of LC3II protein in 786-O cells, which is considered as autophagy. However, the reason for this may be the increased autophagosome production and also the blocked degradation phase of autophagosomes, so the degradation phase was inhibited using the autophagic tool drug CQ in combination to observe whether the expression level of LC3II was changed [ 14 ].…”

Genetic and Immunological Characterization of Commercial Infectious Bronchitis Virus (IBV) Vaccines Used in Korea

“…Upon infection with the M41 variant, the viability and phagocytic function of macrophages are inhibited. Conversely, overall innate immunity was enhanced such as antimicrobial activity, toll like receptor (TLR) activation, and type I IFN or pro-in ammatory cytokine induction [35]. We detected a minimal number of activated macrophages that expressed MHCII molecules on their surface, probably because of the optimal inducing condition for myeloid cells was not provided.…”

Host Antiviral Responses against Avian Infectious Bronchitis Virus (IBV): Focus on Innate Immunity

“…Several genes including IFN-α, IL-1β, IL-6, etc. were significantly increased in these IBV-infected macrophages, and apoptosis was triggered by virus replication [ 28 ]. Overall, these results suggest macrophages play an important role in host innate and acquired immunity to resist IBV infection.…”

“…It can also facilitate virus spread at a later stage of infection [ 81 ]. There have been reports about IBV-induced apoptosis both in vivo [ 55 ] and in vitro [ 28 , 82 ].…”

“…In mammalian cells, the Bcl 2 family of proteins, including proapoptotic (Bax and Bak) and anti-apoptotic (Mcl 1, Bcl 2, and Bcl XL) proteins, modulated IBV-induced apoptosis at an early stage of IBV infection [ 55 ]. In IBV M41-infected HD11 and PBMCs-Mφ cells, a decreased expression of Bcl-2 accompanied by increased expression of Bcl-2-associated X (Bax) suggests viral replication provokes apoptosis at 48 hpi [ 28 ]. At a late stage of infection, apoptosis was demonstrated to facilitate IBV replication.…”