The Role of Porcine Monocyte Derived Dendritic Cells (MoDC) in the Inflammation Storm Caused by Streptococcus suis Serotype 2 Infection.

BACKGROUND: Streptococcus suis is an important swine pathogen and zoonotic agent. Infection with this highly pathogenic strain can cause streptococcal toxic shock-like syndrome (STSLS), characterized by a Th-1 inflammatory cytokine storm, and a high mortality rate. Monocyte derived dendritic cells (MoDCs) are known to stimulate Th-1 cell differentiation, but the role of MoDCs in STSLS remains to be elucidated. METHODOLOGY AND FINDINGS: Porcine CD14-positive monocytes, purified from peripheral blood mononuclear cells (PBMCs), were used to generate MoDCs using granulocyte-macrophage colony-stimulating factor (GM-CSF) and interleukin-4 (IL-4). Highly pure MoDCs were generated, as proved by their morphology, phenotype analysis, phagocytic ability, and induction of T cells proliferation. The MoDCs were further stimulated by the virulent S. suis serotype 2 (SS2) SC19 strain which triggered a strong release of several pro-inflammatory cytokines, including IL-1ß, IL-8, TNF-α, IFN-γ, and IL-12. Furthermore, the stimulated MoDCs induced CD4+ T cell differentiation towards Th-1 cells in vitro. CONCLUSIONS: The results of this study indicated that the porcine MoDCs stimulated by SS2 could release high levels of Th-1 inflammatory cytokines and induce CD4+ T cell differentiation towards Th-1 cells. Hence, it is likely that porcine MoDCs play an important role in the STSLS caused by SS2.

The relationship of resistance mechanism of two strains of Enterobacteriaceae resistant to carbapenems isolated from a single specimen / 中华微生物学和免疫学杂志

Objective To investigate the relationship of resistance mechanisms of a Klebsiella pneumoniae strain and a Morganella morganii strain resistance to carbapenems isolated from a single specimen. Methods Sensibility of antimicrobial agents was detected by agar dilution method. Specific PCR and DNA sequence analysis were performed to detect resistance genes. Plasmid feature was detected by plasmid conjugation and electrophoresis analysis. Genetic environment around blaKPC was analyzed with sequencing. The changes of outer membrane permeability were analyzed with electrophoresis of outer membrane proteins. Results blaKPC-2 was detected in 2 original isolates strains and their transconjugants. Carbapenem-resistance was successfully transfered by conjugation experiments. blaKPC-2 was located on dissimilar plasmids, but genetic environment around blaKPC-2 was the same sequence. The Morganella morganii isolate showed a loss of 38 ×103 OMPs and an additional 36 ×103 OMPs appearance, while the Klebsiella pneumoniae isolate showed a loss of OMPK36. Conclusion blaKPC-2 was detected in 2 isolates. This gene encoded by two plasmids with different sizes was located on the same composite transposon. The lack of outer membrane proteins could also play an important role causing isolates to exhibite resistance to carbapenems.

[Induction or inhibition of apoptosis by pseudorabies virus ea strain in suckling piglets].

To study induction or inhibition of apoptosis by pseudorabies virus (PrV) Ea strain in suckling piglets, Aujeszky s disease was replicated by artificially inoculating 15 day-old piglets with PrV-Ea strain. Various tissue sections, such as lymphoid tissues and nervous tissues were collected. Transmission electron microscopy, DNA fragmentation assay, and in situ terminal-deoxynucleotidyl transferase-mediated dUTP nick end-labeling (TUNEL) staining were carried to analyze apoptotic cells. It was shown that piglets infected with PrV-Ea strain took on typical clinical symptoms and apoptotic cells were found in lymphoid tissues but not in nerve tissues. The results indicated that the PrV infection caused apoptosis in a big number of lymphatic cells, thus leading to death of suckling piglets due to lowered immune function. It might play an important role in PrV s attack on immune system. A latent infection of pseudorabies virus was established in the neuronal tissue cells by inhibition of nervous cell apoptosis; this might be the way for PrV to establish latent infection, leading to sporadic recurrence of the disease.