Simple Summary: Chlamydia psittaci, an obligate intracellular gram-negative bacterium and economically relevant pathogen in poultry and pet birds, could cause psittacosis/ornithosis, and is also a human pathogen causing atypical pneumonia after zoonotic transmission. H9N2 influenza virus, a low pathogenic avian influenza viruses subtype, has become endemic in different types of domestic poultry in lots of countries, resulting in great economic loss due to reduced egg production or high mortality associated with co-infection with other pathogens. These two pathogens are easily mixed with other pathogens to aggravate the disease, and C. psittaci and H9N2 often cause mixed infection. Co-infection of C. psittaci with H9N2 commonly induces severe pneumonia and high mortality in SPF chickens. According to previous studies, we postulated that C. psittaci infection may beneficial for the replication of H9N2 in HD11. Consequently, in this study, we clarify the pathogenic mechanism of coinfection with C. psittaci and H9N2 in the chicken macrophage cell line HD11, which is the first study of the coinfection of C. psittaci and H9N2 in vitro.
Abstract:We investigated the effect regarding coinfection of C. psittaci and H9N2 on HD11 cells, expecting to find the potential pathogenesis of the coinfection induced airsacculitis. HD11 cells were infected with C. psittaci and/or H9N2 in different orders, and effects of the coinfection on iNOS expression and activity, NO synthesis, cell phagocytosis, and cytokines in HD11 cells were determined. Results showed that coinfection of C. psittaci and H9N2 significantly aggravated the mortality of HD11 cells compared to one pathogen alone. Furthermore, C. psittaci infection increased the replication of H9N2 in HD11 cells, whereas decreased the iNOS, enzyme activity, and NO of HD11 cells with H9N2 infection. Additionally, H9N2 also increased the pathogen loads of C. psittaci in HD11 cells. We also found that C. psittaci infection alone significantly decreased the phagocytosis of HD11 cells, compared to H9N2 alone. What's more, C. psittaci infection increased type Th2 cytokines IL-6 and IL-10 of HD11 cells with H9N2 infection. All the above data indicated that primary C. psittaci infection is able to aggravate H9N2 invasion by down-regulating functions of HD11 cells.Preprints (www.preprints.org) | NOT PEER-REVIEWED | Posted: 12 March 2020