Valid publication of the names Caecibacterium and Caecibacterium sporoformans

Descriptions of the genus Caecibacterium and its proposed type species Caecibacterium sporoformans were published in the IJSEM by Onrust et al. (Int J Syst Evol Microbiol 2017;67:4589-4594). The type strain was deposited as LMG 27730 and DSM 26959. DSM 26959 is a patent strain, and therefore the names were effectively, but not validly, published based on Rule 30 (4) of the International Code of Nomenclature of Prokaryotes. The type strain of C. sporoformans is now available from the Deutsche Sammlung von Mikroorganismen und Zellkulturen as DSM 103070 and no restrictions have been placed on its distribution. We here present new descriptions of the genus and its type species so that the names can be validly published

Infection of Differentiated Porcine Airway Epithelial Cells by Influenza Virus: Differential Susceptibility to Infection by Porcine and Avian Viruses

BACKGROUND: Swine are important hosts for influenza A viruses playing a crucial role in the epidemiology and interspecies transmission of these viruses. Respiratory epithelial cells are the primary target cells for influenza viruses. METHODOLOGY/PRINCIPAL FINDINGS: To analyze the infection of porcine airway epithelial cells by influenza viruses, we established precision-cut lung slices as a culture system for differentiated respiratory epithelial cells. Both ciliated and mucus-producing cells were found to be susceptible to infection by swine influenza A virus (H3N2 subtype) with high titers of infectious virus released into the supernatant already one day after infection. By comparison, growth of two avian influenza viruses (subtypes H9N2 and H7N7) was delayed by about 24 h. The two avian viruses differed both in the spectrum of susceptible cells and in the efficiency of replication. As the H9N2 virus grew to titers that were only tenfold lower than that of a porcine H3N2 virus this avian virus is an interesting candidate for interspecies transmission. Lectin staining indicated the presence of both α-2,3- and α-2,6-linked sialic acids on airway epithelial cells. However, their distribution did not correlate with pattern of virus infection indicating that staining by plant lectins is not a reliable indicator for the presence of cellular receptors for influenza viruses. CONCLUSIONS/SIGNIFICANCE: Differentiated respiratory epithelial cells significantly differ in their susceptibility to infection by avian influenza viruses. We expect that the newly described precision-cut lung slices from the swine lung are an interesting culture system to analyze the infection of differentiated respiratory epithelial cells by different pathogens (viral, bacterial and parasitic ones) of swine

Multi-Platform Next-Generation Sequencing of the Domestic Turkey (Meleagris gallopavo): Genome Assembly and Analysis

The combined application of next-generation sequencing platforms has provided an economical approach to unlocking the potential of the turkey genome

Differential modulation of immune response and cytokine profiles in the bursae and spleen of chickens infected with very virulent infectious bursal disease virus

Background: Very virulent infectious bursal disease virus (vvIBDV) induces immunosuppression and inflammation in young birds, which subsequently leads to high mortality. In addition, infectious bursal disease (IBD) is one of the leading causes of vaccine failure on farms. Therefore, understanding the immunopathogenesis of IBDV in both the spleen and the bursae could help effective vaccine development. However, previous studies only profiled the differential expression of a limited number of cytokines, in either the spleen or the bursae of Fabricius of IBDV-infected chickens. Thus, this study aims to evaluate the in vitro and in vivo immunoregulatory effects of vvIBDV infection on macrophage-like cells, spleen and bursae of Fabricius. Results: The viral load was increased during the progression of the in vitro infection in the HD11 macrophage cell line and in vivo, but no significant difference was observed between the spleen and the bursae tissue. vvIBDV infection induced the expression of pro-inflammatory and Th1 cytokines, and chemokines from HD11 cells in a time- and dosage-dependent manner. Furthermore, alterations in the lymphocyte populations, cytokine and chemokine expression, were observed in the vvIBDV-infected spleens and bursae. A drastic rise was detected in numbers of macrophages and pro-inflammatory cytokine expression in the spleen, as early as 2 days post-infection (dpi). On 4 dpi, macrophage and T lymphocyte infiltration, associated with the peak expression of pro-inflammatory cytokines in the bursae tissues of infected chickens were observed. The majority of the significantly regulated pro-inflammatory cytokines and chemokines, in vvIBDV-infected spleens and bursae, were also detected in vvIBDV-infected HD11 cells. This cellular infiltration subsequently resulted in a sharp rise in nitric oxide (NO) and lipid peroxidation levels. Conclusion: This study suggests that macrophage may play an important role in regulating the early expression of pro-inflammatory cytokines, first in the spleen and then in the bursae, the latter tissue undergoing macrophage infiltration at 4 dpi

Bioactivities of a tumour necrosis like factor released by chicken rnacrophages

To test for tumour necrosis-like factor (TNF) of chickens, supernatants of a lipopolysaccharide (LPS)-stimulated chicken macrophage cell line MQ-NCSU were analysed. A sequence of ion-exchange and gel-permeation chromatography was utilised to isolate TNF-like activity from the culture supernatant. The peak of TNF-like cytotoxic activity corresponded to the fractions with a nlolecular weight of 81 kDa or higher. Polyclonal anti-human TNF-a antiserum cross-reacted by Western blotting with a 17 kDa protein in the TNF-containing fraction ~ ~ n d e denaturing conditions. This result indicated that chicken TNF-like factor in the biologically active form may be a protein multimer of monomers of about 17 kDa. The molecular weight of these monomers is similar to the molecular weight of mammalian TNF-CLC. hicken TNF-like factor stimulated macrophages by inducing morphological changes, enhancing Ia-expression, nitric oxide (NO) production and by synergising with interferon (1FN)-y in the induction of NO release from macrophages. The biological activities were not neutralised by anti-human TNF antiserum. These data suggest that LPS-stimulated chicken macrophages produced a functional homologue to mammalian TNF-CL. This may be structurally quite different from the mammalian TNF molecule. Other factors may have been co-purified with the chicken TNF-like factor having overlapping functions and molecular weight. However, CO-purification of chemokines and interleukin-l, major macrophage derived factors, with the chicken TNF-like factor can be excluded based on the purification strategies

Bioactivities of a tumour necrosis like factor released by chicken macrophages

To test for tumour necrosis-like factor (TNF) of chickens, supernatants of a lipopolysaccharide (LPS)-stimulated chicken macrophage cell line MQ-NCSU were analysed. A sequence of ion-exchange and gel-permeation chromatography was utilised to isolate TNF-like activity from the culture supernatant. The peak of TNF-like cytotoxic activity corresponded to the fractions with a nlolecular weight of 81 kDa or higher. Polyclonal anti-human TNF-a antiserum cross-reacted by Western blotting with a 17 kDa protein in the TNF-containing fraction ~ ~ n d e denaturing conditions. This result indicated that chicken TNF-like factor in the biologically active form may be a protein multimer of monomers of about 17 kDa. The molecular weight of these monomers is similar to the molecular weight of mammalian TNF-CLC. hicken TNF-like factor stimulated macrophages by inducing morphological changes, enhancing Ia-expression, nitric oxide (NO) production and by synergising with interferon (1FN)-y in the induction of NO release from macrophages. The biological activities were not neutralised by anti-human TNF antiserum. These data suggest that LPS-stimulated chicken macrophages produced a functional homologue to mammalian TNF-CL. This may be structurally quite different from the mammalian TNF molecule. Other factors may have been co-purified with the chicken TNF-like factor having overlapping functions and molecular weight. However, CO-purification of chemokines and interleukin-l, major macrophage derived factors, with the chicken TNF-like factor can be excluded based on the purification strategies