interleukin-8 and Dysentery

Newly emerging and re-emerging viral infectious diseases cause significant economic losses in swine production. Efficacious vaccines have not yet been developed for several major swine infectious diseases, including porcine epidemic diarrhea virus (PEDV). We used the PEDV-infected Vero cell model to screen lactic acid bacteria (LAB) strains with antiviral activity. Sixty LAB strains were isolated from the feces of nursing piglets. After the elimination of LAB strains with high cytotoxicity to Vero cells, the protective effects of the remaining 6 strains against PEDV infection were determined. Vero cells pretreated with the intracellular extracts or cell wall fractions of YM22 and YM33 strains for 24 h before infection with PEDV showed significantly higher cell viabilities and lower mRNA expression of PEDV nucleocapsid (PEDV-N) than the unpretreated cells, indicating that the intracellular extracts and cell wall fractions of YM22 and YM33 possessed prophylactic effects on Vero cells against PEDV infection. PEDV-infection significantly increased the mRNA expression of proinflammatory cytokines, including tumor necrosis factor-α (TNF-α) and interleukin-8 (IL-8) in Vero cells. However, pretreatment of Vero cells with the cell wall fractions of YM22 and YM33 decreased the mRNA expression of TNF-α and IL-8, which could be a mechanism associated with the protective effects of YM22 and YM33 against PEDV. Based on the biochemical characteristics and phylogenetic analyses, YM22 and YM33 were identified as Ligilactobacillus agilis (basonym: Lactobacillus agilis) and Ligilactobacillus salivarius (basonym: Lactobacillus salivarius), respectively. These findings suggest that L. agilis YM22 and L. salivarius YM33 could provide some levels of protective effects against PEDV infections.

Topics: Animals; Antiviral Agents; Chlorocebus aethiops; Coronavirus Infections; Diarrhea; Dysentery; Interleukin-8; Lactic Acid; Lactobacillales; Phylogeny; Plant Extracts; Porcine epidemic diarrhea virus; RNA, Messenger; Swine; Swine Diseases; Tumor Necrosis Factor-alpha; Vero Cells

Dysentery caused by Shigella species is characterized by infiltration of polymorphonuclear leucocytes (PMNs) into the colonic mucosa. Shigella spp. evolved into pathogens by the acquisition of virulence genes and by the deletion of 'antivirulence' genes detrimental to its pathogenic lifestyle. An example is cadA (encoding lysine decarboxylase), which is uniformly absent in Shigella spp., whereas it is present in nearly all isolates of the closely related non-pathogen Escherichia coli. Here, using monolayers of T84 cells to model the human intestinal epithelium, we determined that the introduction of cadA into S. flexneri and the expression of lysine decarboxylase attenuated the bacteria's ability to induce PMN influx across model intestinal epithelium. Such inhibition was caused by cadaverine generated from the decarboxylation of lysine. Cadaverine treatment of model intestinal epithelia specifically inhibited S. flexneri induction of PMN transepithelial migration, while having no effect on the ability of Salmonella or enteropathogenic E. coli (EPEC) to induce PMN migration. These observations not only provide insight into mechanisms of S. flexneri pathogen evolution and pathogenesis, but also suggest a potential for the use of cadaverine in the treatment of dysentery.

Topics: Actins; Cadaverine; Carboxy-Lyases; Cell Culture Techniques; Cell Line; Cell Movement; Cell Polarity; Cell Size; Dose-Response Relationship, Drug; Dysentery; Enzyme-Linked Immunosorbent Assay; Escherichia coli O157; Humans; Interleukin-8; Intestinal Mucosa; Lysine; Membrane Proteins; Microscopy, Fluorescence; N-Formylmethionine Leucyl-Phenylalanine; Neutrophils; Phosphoproteins; Salmonella typhimurium; Shigella flexneri; Signal Transduction; Zonula Occludens-1 Protein