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Biology of and host cell response to high and low virulent Chlamydophila psittaci strains

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Abstract
Within a few days post infection of SPF turkeys, highly pathogenic Chlamydophila (Cp.) psittaci genotype A and D strains can be found in blood monocytes/macrophages, while this effect is less pronounced for infection with a milder genotype B strain. To elucidate on the observed difference, we studied the developmental cycle of avian Cp. psittaci strains of varying virulence in a matched avian monocyte/macrophage cell line (HD11) by electron microscopy and immunofluorescence and determined the gene transcription of 26 Type III secretion related genes and six control genes upon infection of HD11 cells. Cp. psittaci strains used were 84/55 and 92/1293 (highly virulent), CP3 (low virulent) and 84/2334 (phylogenetically intermediate between Cp. psittaci and Cp. abortus). The genotype A (84/55) and D (92/1293) strains 1) clearly induced actin recruitment to the site of entry, 2) initiated host cell degeneration at earlier time points, and 3) survived and proliferated better when compared to the milder CP3 strain. Strain 84/2334, genetically intermediate between Cp. psittaci and Cp. abortus, did not induce actin recruitment. Limited mRNA transcripts for the cell division genes ftsW and ftsK were in agreement with the observed low replication of Cp. psittaci in these host cells. The results also indicated that genes coding for the structural components of the Type III secretion system were transcribed earlier compared to an infection in epithelial cells. We postulate that upon infection of blood monocytes/macrophages, Cp. psittaci deliberately limits its replication and immediately arms itself to infect other cells elsewhere in the host, whilst using the monocytes/macrophages as a quick transport vehicle. Chlamydophila psittaci and avian pathogenic Escherichia (E.) coli infections contribute to the respiratory disease complex observed in turkeys. Secondary infection with E. coli exacerbates Cp. psittaci pathogenicity and augments E. coli excretion. The innate immune response initiated by both pathogens in their avian host is unknown. We therefore determined the cytokine responses following Cp. psittaci infection and E. coli superinfection of avian monocytes/macrophages by examining gene transcripts of IL-1β, IL-6, CXCLi2 (IL-8), CXCLi1 (K60), IL-10, IL-12α/β, IL-18, TGF-β4 and CCLi2 at 4 h post inoculation with different Cp. psittaci strains or 4 h post treatment with avian E. coli LPS of Cp. psittaci pre-infected HD11 cells. The same Cp. psittaci strains as mentioned above were included in the study. At 4 h post chlamydial infection, an increased expression of IL-1β and IL-6 as well as CXCLi2, CXCLi1 and CCLi2 was observed compared to levels in uninfected HD11 controls. This effect was less pronounced for the milder CP3 strain. The pro-inflammatory response of Cp. psittaci infected cells to E. coli LPS was significantly lowered compared to uninfected controls, especially when the cells were pre-infected with highly virulent Cp. psittaci strains. In both experiments, exceptionally high IL-10 and no TGF-β4 responses were observed, and we propose that this could induce macrophage deactivation and NF-κB suppression. Consequently, pro-inflammatory and Th1-promoting responses to both the primary Cp. psittaci infection and E. coli would be inhibited, thus explaining the observed aggravated in vivo pathology.

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Chicago
Beeckman, Delphine Sylvie Anne, Lisa Rothwell, Pete Kaiser, and Daisy Vanrompay. 2010. “Biology of and Host Cell Response to High and Low Virulent Chlamydophila Psittaci Strains.” In Deutscher Chlamydien-Workshop, 8, Abstracts.
APA
Beeckman, D. S. A., Rothwell, L., Kaiser, P., & Vanrompay, D. (2010). Biology of and host cell response to high and low virulent Chlamydophila psittaci strains. Deutscher Chlamydien-Workshop, 8, Abstracts. Presented at the 8 Deutscher Chlamydien-Workshop.
Vancouver
1.
Beeckman DSA, Rothwell L, Kaiser P, Vanrompay D. Biology of and host cell response to high and low virulent Chlamydophila psittaci strains. Deutscher Chlamydien-Workshop, 8, Abstracts. 2010.
MLA
Beeckman, Delphine Sylvie Anne, Lisa Rothwell, Pete Kaiser, et al. “Biology of and Host Cell Response to High and Low Virulent Chlamydophila Psittaci Strains.” Deutscher Chlamydien-Workshop, 8, Abstracts. 2010. Print.
@inproceedings{974854,
  abstract     = {Within a few days post infection of SPF turkeys, highly pathogenic Chlamydophila (Cp.) psittaci genotype A and D strains can be found in blood monocytes/macrophages, while this effect is less pronounced for infection with a milder genotype B strain. To elucidate on the observed difference, we studied the developmental cycle of avian Cp. psittaci strains of varying virulence in a matched avian monocyte/macrophage cell line (HD11) by electron microscopy and immunofluorescence and determined the gene transcription of 26 Type III secretion related genes and six control genes upon infection of HD11 cells. 
Cp. psittaci strains used were 84/55 and 92/1293 (highly virulent), CP3 (low virulent) and 84/2334 (phylogenetically intermediate between Cp. psittaci and Cp. abortus). The genotype A (84/55) and D (92/1293) strains 1) clearly induced actin recruitment to the site of entry, 2) initiated host cell degeneration at earlier time points, and 3) survived and proliferated better when compared to the milder CP3 strain. Strain 84/2334, genetically intermediate between Cp. psittaci and Cp. abortus, did not induce actin recruitment. Limited mRNA transcripts for the cell division genes ftsW and ftsK were in agreement with the observed low replication of Cp. psittaci in these host cells. The results also indicated that genes coding for the structural components of the Type III secretion system were transcribed earlier compared to an infection in epithelial cells. We postulate that upon infection of blood monocytes/macrophages, Cp. psittaci deliberately limits its replication and immediately arms itself to infect other cells elsewhere in the host, whilst using the monocytes/macrophages as a quick transport vehicle.
Chlamydophila psittaci and avian pathogenic Escherichia (E.) coli infections contribute to the respiratory disease complex observed in turkeys. Secondary infection with E. coli exacerbates Cp. psittaci pathogenicity and augments E. coli excretion. The innate immune response initiated by both pathogens in their avian host is unknown. We therefore determined the cytokine responses following Cp. psittaci infection and E. coli superinfection of avian monocytes/macrophages by examining gene transcripts of IL-1β, IL-6, CXCLi2 (IL-8), CXCLi1 (K60), IL-10, IL-12α/β, IL-18, TGF-β4 and CCLi2 at 4 h post inoculation with different Cp. psittaci strains or 4 h post treatment with avian E. coli LPS of Cp. psittaci pre-infected HD11 cells. The same Cp. psittaci strains as mentioned above were included in the study. At 4 h post chlamydial infection, an increased expression of IL-1β and IL-6 as well as CXCLi2, CXCLi1 and CCLi2 was observed compared to levels in uninfected HD11 controls. This effect was less pronounced for the milder CP3 strain. The pro-inflammatory response of Cp. psittaci infected cells to E. coli LPS was significantly lowered compared to uninfected controls, especially when the cells were pre-infected with highly virulent Cp. psittaci strains. In both experiments, exceptionally high IL-10 and no TGF-β4 responses were observed, and we propose that this could induce macrophage deactivation and NF-κB suppression. Consequently, pro-inflammatory and Th1-promoting responses to both the primary Cp. psittaci infection and E. coli would be inhibited, thus explaining the observed aggravated in vivo pathology.},
  author       = {Beeckman, Delphine Sylvie Anne and Rothwell, Lisa and Kaiser, Pete and Vanrompay, Daisy},
  booktitle    = {Deutscher Chlamydien-Workshop, 8, Abstracts},
  language     = {eng},
  location     = {Herrsching, Germany},
  title        = {Biology of and host cell response to high and low virulent Chlamydophila psittaci strains},
  year         = {2010},
}