Autoinducer-2 of quorum sensing is involved in cell damage caused by avian pathogenic Escherichia coli.

Avian pathogenic Escherichia coli (APEC) infections are responsible for great losses in the poultry industry. Quorum sensing (QS) acts as a global regulatory system that controls genes involved in bacterial pathogenesis, metabolism and protein biosynthesis. However, whether QS of APEC is related to cell damage has not been elucidated. In the present study, we explored the correlation between the damage of chicken type II pneumocytes induced by APEC and the autoinducer-2 (AI-2) activity of APEC. The results showed that when chicken type II pneumocytes were co-cultured with 108 CFU/ml of APEC-O78 for 6 h, the release of LDH reached the highest level (192.5 ± 13.4 U/L) (P < 0.01), and the percentages of dead cells followed the same trend in trypan blue exclusion assay. In addition, the AI-2 activity of cell-free culture fluid (CF) reached the maximum value after 6 h co-culture with 108 CFU/ml of APEC-O78. At the same time, the mRNA expressions of eight virulence genes (papC, fimA, fimC, hlyE, ompA, luxS, pfs, and qseA) of 108 CFU/ml APEC-O78 were significantly increased compared with those of 107 CFU/ml, and the mRNA expressions of four virulence genes (hlyE, tsh, iss, and luxS) of 108 CFU/ml APEC-O78 were higher than those of 109 CFU/ml (p < 0.05) after incubation for 6 h. These results suggested that AI-2-mediated QS is involved in the cell damage induced by APEC-O78, indicating AI-2 may be one new potential target for preventing chicken colibacillosis.

Astragaloside IV Inhibits the Inflammatory Injury of Chicken Type II Pneumocytes Induced by Avian Pathogenic Escherichia coli.

Avian pathogenic Escherichia coli (APEC) induces septicemia in chickens by invading type II pneumocytes after breaching the blood-air barrier. Type II pneumocytes play an important role in maintaining the function of the blood-air barrier. Astragaloside IV has been shown in previous studies to have an anti-inflammatory effect. To explore whether astragaloside IV can inhibit APEC-induced injury in chicken type II pneumocytes, cells were infected with APEC-O78. The results showed that astragaloside IV significantly reduced cell damage in chicken type II pneumocytes induced by APEC-O78 by downregulating the production of TNF-α and IL-1ß, upregulating the secretion of IL-4 and IL-10, suppressing the mRNA levels of TLR-4, TLR-5, ERK, and p38 of chicken type II pneumocytes as well as inhibiting bacterial adhesion and F-actin cytoskeleton polymerization. These results suggest that astragaloside IV may be useful in novel pharmaco-therapeutic approaches to the treatment of chicken colibacillosis.

Andrographolide interferes quorum sensing to reduce cell damage caused by avian pathogenic Escherichia coli.

Avian pathogenic Escherichia coli (APEC) induce septicemia in chickens by invading type II pneumocytes to breach the blood-air barrier. The virulence of APEC can be regulated by quorum sensing (QS). Andrographolide is a QS inhibitor of Pseudomonas aeruginosa (P. aeruginosa). Therefore, we investigate whether andrographolide inhibits the injury of chicken type II pneumocytes by avian pathogenic E. coli O78 (APEC-O78) by disrupting the bacterial QS system. The results showed that sub-MIC of andrographolide significantly reduced the release of lactate dehydrogenase (LDH), F-actin cytoskeleton polymerization, and the degree of the adherence to chicken type II pneumocytes induced by APEC-O78. Further, we found that andrographolide significantly decreased the autoinducer-2 (AI-2) activity and the expression of virulence factors of APEC-O78. These results suggest that andrographolide reduce the pathogenicity of APEC-O78 in chicken type II pneumocytes by interfering QS and decreasing virulence. These results provide new evidence for colibacillosis prevention methods in chickens.