The protective effect of nigeglanine on dextran sulfate sodium-induced experimental colitis in mice and Caco-2 cells.

Ulcerative colitis (UC) was a nonspecific inflammatory disease. The treatment of UC is imperative. The present study aimed to investigate the effect of nigeglanine on dextran sulfate sodium-induced UC in experimental mice and Caco-2 cells and define the underlying mechanism. The nigeglanine was shown a significant protective effect on the colon, significantly reduced the weight and colon length loss and inhibited intestinal epithelial cell damage. Nigeglanine also reduced proinflammatory factors and increased anti-inflammatory factor production. The results indicate that nigeglanine suppresses the nuclear factor kappa B and mitogen-activated protein kinases pathways in addition to NLRP3 inflammasome action, inhibiting colon epithelial cell pyroptosis. Surprisingly, ZO-1 and occludin protein levels increased with nigeglanine treatment, suggesting that nigeglanine plays a protective role in barrier integrity, reducing colitis progression. The present study suggests that dietary therapy with nigeglanine may be a useful treatment for prophylaxis and palliative UC.

Identification of a surface protective antigen, MAP of Streptococcus equi subspecies zooepidemicus.

Streptococcus equi subspecies zooepidemicus (SEZ) is a zoonotic pathogen with adhesive and invasive properties. Due to the shortcomings of antibiotics and traditional inactivated vaccine, identifying protective antigens against SEZ would be helpful to the development of novel vaccines. MAP has been identified as a membrane anchored protein with a typical LPXTG-like cell wall-anchored motif. In present study, the objective was to evaluate the effects of MAP as a subunit vaccine with mouse model. The Western blot analysis shown that the purified recombinant MAP presented good immunoreactive to convalescent porcine sera against SEZ. The protein could elicit a remarkable humoral antibody response and protect 80% of mice against lethal dose challenge of SEZ in mouse model. Moreover, the hyperimmune sera against MAP could efficiently kill the bacteria in whole blood killing assay and conferred significant protection against SEZ in passive immunization experiments. This study suggests with good reasons that MAP could be a novel and effective vaccine candidate for SEZ.

Selenium deficiency inhibits micRNA-146a to promote ROS-induced inflammation via regulation of the MAPK pathway in the head kidney of carp.

Selenium (Se) is a necessity in multiple species of fish. Se plays an important role in immunoregulation, inflammation, and antioxidant systems in fish and other animals. The head kidney is the major immune organ in adult carp, and it produces white blood cells and destroys old red blood cells. The present study aimed to explore the effects and regulatory molecular mechanisms of Se on ROS and micRNA-146a as part of the inflammatory response in fancy carp. Adult fancy carp were fed different concentrations of Se in their diets. The Se content of the head kidney changed in a pattern consistent with the dietary content of Se. Se deficiency induced a significant increase in ROS, restrained the activities of GPx, SOD and CAT and increased MDA content. qPCR analysis showed a reduction in micRNA-146a with Se deficiency. The Se content, miRNA-146a expression and ROS levels were correlated. H2O2 cell stimulation assays found that ROS could activate the MAPK pathway, and ELISA results showed p38, JNK and ERK phosphorylation significantly increased with H2O2 stimulation. TNF-α, IL-1ß, and IL-6 were appreciably increased. At same time, miRNA-146a, which should have increased to regulate the inflammatory response, was reduced with Se deficiency. Therefore, with Se deficiency, the head kidney was inflamed. All these results indicated that Se deficiency inhibits micRNA-146a to promote ROS-induced inflammation via regulating the MAPK pathway in the head kidney of carp. The present study revealed that supplementing the diet of carp with selenium is beneficial for growth and disease prevention.

Selenium deficiency induced an inflammatory response by the HSP60 - TLR2-MAPKs signalling pathway in the liver of carp.

Selenium (Se) is one of the essential trace elements for immune regulation and antioxidant systems in fish growth. The dietary Se plays an important role in immune regulation and inflammation by regulating HSPs and TLRs in liver of many animals. The liver is an important digestive organ in carp. Liver damage can seriously affect the growth and survival of carp. This study was conducted to determine whether Se regulated liver inflammation by affecting HSPs-TLR2 signalling and the potential mechanisms of action in common carp. The gene was analysed by qPCR. The proteins of inflammatory factors were detected by ELISA. The others proteins were analysed by Western blot. The results indicated the Se concentrations in blood and liver tissues were significantly influenced by dietary Se. The Se deficiency increased the expression of HSP60 and TLR2 and the secretion of the proinflammatory factor TNF-α, IL-1ß and IL-6, induced a low secretion of the anti-inflammatory TGF-ß, but the Se supplements could transform these events. Further research showed that with the dose-dependently decrease of Se, the HSP60 expressions were increased, and the MAPKs pathway were significantly activated by the phosphorylation of p38, JNK and ERK in liver tissue and cell. The results provide evidence that Se deficiency induced and exacerbated inflammatory injury to the liver through the HSP60 and TLR2-MAPKs signalling pathways in carp.

Identification and characterization of a novel protective antigen, Sec_205 of Streptococcus equi ssp. Zooepidemicus.

Streptococcus equi ssp. zooepidemicus (SEZ) is an important pathogen of swine streptococcal diseases and can infect a wide range of animals as well as human beings. The absence of effective vaccine confounds the control of SEZ infection. Sec_205, a novel protein identified in the previous study, was inducibly over-expressed in Escherichia coli in the present study. The purified recombinant protein could elicit a significant humoral antibody response and provide efficient protection against lethal challenge of SEZ C55138 in mouse model. The protection against SEZ infection was mediated by specific antibodies to Sec_205 to some extent and was identified by the passive protection assay. The Sec_205 was an in vivo-induced antigen confirmed by the real-time PCR and could adhere to the Hep-2 cells by the inhibition assay. These suggest that Sec_205 may play a vital role in pathogenicity and serve as a new vaccine candidate against SEZ infection.

miR-194b-3p partially inhibits Streptococcus equi subsp. zooepidemicus adherence to PK15 cells.

MicroRNAs are increasingly reported implicated in the host cell response to bacterial pathogens. In order to investigate whether miR-194b-3p regulates the adherence of Streptococcus equi subsp. Zooepidemicus (SeZ) to porcine kidney cell line PK15, the miR-194b-3p agomir and antagomir were transfected into PK15 cells respectively and the adherence rate of SeZ to each was determined. Adherence rate of SeZ C55138 was significantly decreased when miR-194b-3p agomir was transfected in PK15, while that of miR-194b-3p antagomir evaluated. These results confirmed that miR-194b-3p markedly inhibit the adherence of SeZ C55138 to PK15 cells. In addition, miR-194b-3p indeed regulated the expression level of CD44 in PK15 cells by targeting CD44 3' UTR, and this interaction was involved in adhesion process. This study contributes to understanding the mechanism of the crosstalk between SeZ and PK15 cells.