Induction of innate host responses characterized by production of interleukin (IL)-1β and recruitment of macrophages to the respiratory tract of chickens following infection with infectious bronchitis virus (IBV)

Infectious bronchitis virus (IBV) infection is a major cause of economic losses to the poultry industry. Due to limitations in current control measures, alternative approaches, based on thorough understanding of the host responses are required. As one of the key component of the avian immune system, the innate immune system has a crucial role in limiting virus replication at the initial stage of the infection. As parts of the innate host response, macrophages and cytokines, such as interleukin (IL)-1 beta, are critical components as shown in other host-virus infection models. Since information on the importance of macrophages and IL-1 beta in IBV infection in chickens is limited, our objective was to determine the association of IL-1 beta, originating from avian macrophages and IBV infection in the trachea and lung. Following experimental IBV infection in 6 days old chickens, we found increased production of IL-1 beta and increased recruitment of macrophages in the respiratory tract. Towards the end of the study (5 and 7 days following the IBV infection), the recruited macrophages appear to be a significant source IL-1 beta. However, only the recruitment of macrophages in the lung correlated with IBV genome loads in this tissue. In conclusion, the present study demonstrates that recruitment of macrophages and the production of IL-1 beta originating from macrophages, as well as other sources, occur following IBV infection in the respiratory tract suggesting potential roles of these mediators in the host responses to IBV infection. However, further studies are warranted to elucidate whether macrophages and IL-1 beta are the causes of reduced IBV genome loads in the respiratory tract and also to investigate whether immune mediators that were not measured in the current study were involved in reducing IBV genome load in the respiratory tract towards the end of the study.