Chlamydia psittaci infection increases mortality of avian influenza virus H9N2 by suppressing host immune response

Chen, Jun; Qiang, Zhang; Zhang, Tianyuan; Han, Er; Zhao, Peng; Khan, Ahrar; He, Cheng; Wu, Yongzheng

doi:10.1038/srep29421

Cited by 38 publications

(36 citation statements)

References 32 publications

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“…In our previous study, we established a SPF chicken animal model with co-infection of C. psittaci and H9N2, and found that C. psittaci infection increased the mortality of H9N2 by inhibiting humoral immunity and cellular immunity as well as altering Th1/Th2 balance ultimately weakens the immune system of the body [14]. In conclusion, we first reported that a primary C. psittaci infection may lead to immune suppression in vivo which will increase susceptibility to H9N2.…”

Section: Discussionmentioning

confidence: 87%

“…More importantly, C. psittaci and H9N2 often cause mixed infection in clinic. Our previous study found that C. psittaci infection increases the mortality of avian influenza virus H9N2 by suppressing host immune response [14]. In addition, co-infection of C. psittaci with H9N2, ORT and Aspergillus fumigatus commonly induces severe pneumonia and high mortality in SPF chickens, explaining why severe avian airsacculitis is prevalent in winter season in northern China [15].…”

Section: Introductionmentioning

confidence: 97%

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Primary Infection of Chlamydia psittaci Triggers Invasion of H9N2 Avian Influenza Virus by Impairing Functions of Chicken Macrophages

Chu¹,

Guo²,

Zhang³

et al. 2020

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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

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Section: Discussionmentioning

confidence: 87%

Section: Introductionmentioning

confidence: 97%

Primary Infection of Chlamydia psittaci Triggers Invasion of H9N2 Avian Influenza Virus by Impairing Functions of Chicken Macrophages

Chu¹,

Guo²,

Zhang³

et al. 2020

Preprint

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“…The total RNA was extracted from HD11 cells by applying Trizol (TransGen Biotech, Beijing, China), and was subsequently treated with a DNA-free kit to filter DNA contamination. Relative quantification of interleukin (IL)-1β, IL-2, IL-6, IL-10, Interferon gamma (IFN-γ) and tumor necrosis factor-α (TNF-α) was performed using an SYBR Green PCR Master Mix kit (Takara, Dalian, China), as previously described [15]. As for cytokine determination, roughly 200 µL aliquots of each sample were used to measure the cytokines IL-1β, IL-2, IL-6, IL-10, IFN-γ, and TNF-α with commercial ELISA kits (Kingfisher Biotech Inc., Saint Paul, MN, United States).…”

Section: Mrna Expression Of Cytokines By Rt-pcr and Quantitative Secrmentioning

confidence: 99%

“…More recently, it was reported that C. psittaci and H9N2 often cause mixed infections in clinic. Our previous study found that C. psittaci infection increases the mortality of avian influenza virus H9N2 by suppressing the host immune response [15]. In addition, coinfection of C. psittaci with H9N2, Ornithobacterium rhinotracheale (ORT), and Aspergillus fumigatus (A. fumigatus) contributes to severe pneumonia and a high mortality in specific pathogen-free (SPF) chickens, explaining why severe avian airsacculitis is prevalent in the winter season in northern China [16].…”

mentioning

confidence: 99%

Chlamydia psittaci Triggers the Invasion of H9N2 Avian Influenza Virus by Impairing the Functions of Chicken Macrophages

Chen

Guo

et al. 2020

Animals

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Simple Summary: Chlamydia psittaci, an obligate, intracellular, Gram-negative bacterium and economically relevant pathogen in poultry and pet bird, 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 coinfection with other pathogens. These two pathogens are easily mixed with other pathogens to aggravate the disease, and often cause mixed infection in clinics. Co-infection of C. psittaci with H9N2 commonly induces severe pneumonia and high mortality in specific pathogen-free (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: In a pilot study, simultaneous infection with Chlamydia psittaci (C. psittaci) and H9N2 virus induced 20% mortality and severe avian airsacculitis, shedding light on animal models of poultry respiratory diseases. However, the pathogenesis is still unclear. In the current study, we hypothesized that C. psittaci infection execrates macrophage function and facilitates H9N2 infection. To explore the potential mechanism, we studied the effect of C. psittaci and H9N2 on the functions of HD11 cells in vitro by simultaneous infection of C. psittaci and H9N2. At the same time, we used infection with C. psittaci or H9N2 alone as the control groups. The results showed that coinfection with C. psittaci and H9N2 could significantly aggravate the mortality of HD11 cells compared to C. psittaci or H9N2 infection alone. In addition, coinfection with C. psittaci and H9N2 did not induce high C. psittaci loads compared to C. psittaci infection alone at 12-and 24-hours post-inoculation (hpi), but coinfection with C. psittaci and H9N2 could increase the loads of H9N2 compared to H9N2 alone in HD11 cells at 12 hpi. More importantly, inducible nitric oxide synthase (iNOS) expression levels, enzyme activity, nitric oxide (NO) production, and phagocytosis were reduced significantly in the group with C. psittaci and H9N2 coinfection compared to those of H9N2 or C. psittaci alone at 24 hpi. Finally, C. psittaci infection induced robust expressions of type Th2 cytokines interleukin (IL)-4 and IL-10, while interferon gamma (IFN-γ) and tumor necrosis factor-α (TNF-α) displayed a significant decrease compared to H9N2 infection alone at 24 hpi. All the above data indicate that C. psittaci infection can facilitate H9N2 invasion and to aggravate severe avian airsacculitis by impairing macrophage functions.

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“…Avian influenza virus (AIV) is an important pathogen causing respiratory diseases (1,2) and severe economic loss to poultry farming (3), and is a serious menace to human health (4). The H9N2 subtype of the low pathogenic avian influenza virus (LPAIV) was first discovered in the United States in 1966.…”

Section: Introductionmentioning

confidence: 99%

Recombinant Lactococcus Lactis Expressing M1-HA2 Fusion Protein Provides Protective Mucosal Immunity Against H9N2 Avian Influenza Virus in Chickens

et al. 2020

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H9N2 subtype low pathogenicity avian influenza virus (LPAIV) is distributed worldwide and causes enormous economic losses in the poultry industry. Despite immunization of almost all chickens with inactivated vaccines, the disease still remains widespread. We speculated that improving mucosal or cellular immune responses could contribute to improved control of H9N2 viruses. In this study, we constructed a novel Lactococcus lactis (L. lactis) strain expressing a recombinant fusion protein consisting of the M1 and HA2 proteins derived from an antigenically conserved endemic H9N2 virus strain. The M1-HA2 fusion protein was cloned downstream of a gene encoding a secretory peptide, and we subsequently confirmed that the fusion protein was secreted from L. lactis by Western blotting. We assessed the immunogenicity and protective effects of this recombinant L. lactis strain. Eighty 1-day-old chickens were divided into four groups, and the experimental groups were orally vaccinated twice with the recombinant L. lactis strain. Fecal and intestinal samples, sera, and bronchoalveolar lavage fluid were collected at 7, 14, and 21 days post-vaccination (dpv). Chickens vaccinated with the recombinant L. lactis strain showed significantly increased levels of serum antibodies, T cell-mediated immune responses, and mucosal secretory IgA (SIgA). Following challenge with H9N2 virus at 21 dpv, chickens vaccinated with the recombinant L. lactis strain showed decreased weight loss, lower viral titers in the lung, and reduced lung pathological damage. In summary, our results demonstrated that a recombinant L. lactis strain expressing an H9N2 M1-HA2 fusion protein could induce protective mucosal and systemic immunity. This oral vaccine is H9N2 virus-specific and represents a significant design improvement compared with previous studies. Our study provides a theoretical basis for improving mucosal immune responses to prevent and control H9N2 virus infection.

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Chlamydia psittaci infection increases mortality of avian influenza virus H9N2 by suppressing host immune response

Cited by 38 publications

References 32 publications

Primary Infection of Chlamydia psittaci Triggers Invasion of H9N2 Avian Influenza Virus by Impairing Functions of Chicken Macrophages

Primary Infection of Chlamydia psittaci Triggers Invasion of H9N2 Avian Influenza Virus by Impairing Functions of Chicken Macrophages

Chlamydia psittaci Triggers the Invasion of H9N2 Avian Influenza Virus by Impairing the Functions of Chicken Macrophages

Recombinant Lactococcus Lactis Expressing M1-HA2 Fusion Protein Provides Protective Mucosal Immunity Against H9N2 Avian Influenza Virus in Chickens

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