Listeria monocytogenes has been recognized as a significant pathogen, occurring worldwide, capable of causing animal and human infections. In its most severe form, listeriosis is an invasive disease that affects immunocompromised patients. Additionally, pregnant women represent a high-risk group for L. monocytogenes infection. Abortion, stillbirth or severe neonatal infection can be the serious outcome of such an infection. In an experimental murine model of pregnancy-associated listeriosis we studied the impact of L. monocytogenes on the maternal immune response and pregnancy outcome. In comparison to virgin animals, pregnant mice mounted lower levels of protective cytokines and were unable to eliminate the pathogen. The impaired maternal immune response that has been found both on the systemic and local level, facilitated bacterial multiplication in the liver, placenta and ultimately in the fetal tissues. This resulted in severe necrotizing hemorrhagic hepatitis and Listeria-induced placental necrosis, increasing the incidence of postimplantation loss and poor pregnancy outcome.

Background: Exposure to microorganisms elicts the production of cytokines. These soluble factors enhance several innate immune functions and regulate the ensuing specific immune response aimed at limiting the spread of infection.Aim: This study was undertaken to quantify the plasma levels of pro‐inflammatory cytokines during the course of primary Listeria monocytogenes and Campylobacter jejuni infection. Using an in vivo infection the relationship between endogenous cytokines and the bacterial number in the liver of infected animals was examined.Methods: C57BL/6 mice were infected by the intraperitoneal route. At different time points we determined the number of colony‐forming units of bacteria in the liver of infected animals and paralled these with the plasma levels of interferon‐gamma (IFN‐γ), tumor necrosis factor‐alpha (TNF‐α) and interleukin‐6 (IL‐6) measured by enzyme immunoassays.Results: L. monocytogenes infection lasted 10–11 days. IFN‐γ production occurred in the early phase but was more pronounced after day 4, following the appearance of specific immunity. The duration of experimental campylobacteriosis was 15 days. Early IFN‐γ production was not significant but a progressive rise of this cytokine in plasma was seen during the second week post infection. Mice produced measurable amounts of plasma TNF‐α immediately after being given viable L. monocytogenes, peaking on day 2–3 when the greatest number of bacteria was present in the examined organs. During C. jejuni infection plasma TNF‐α was produced in a similar manner, but the highest concentrations were found a few days later than in listeriosis, in correlation with the different course of campylobacteriosis. The quantity of IL‐6 increased and decreased in concordance with clearance of L. monocytogenes and the clinical status of the animals. C. jejuni did not promote the induction of this cytokine. This is to some extent an unusual finding. With respect to the role of IL‐6 in Th2 responses and antibody production, the appearance of this cytokine in campylobacteriosis was more expected.Discussion: During systemic bacterial infection, a network of pro‐inflammatory cytokines is activated and blood levels of these cytokines are elevated, albeit inconsistently, with large individual variations and depending on microbial characteristics and structure.

We investigated the anti-Campylobacter activity of pinocembrin and its mechanism of action, as well as Campylobacter responses to pinocembrin treatment at the genetic and phenotypic levels, using C. jejuni NCTC 11168 and a multidrug efflux system repressor mutant (11168ΔcmeR). At its minimal inhibitory concentration, pinocembrin significantly increased cell membrane permeability of Campylobacter. Interestingly, at sub-inhibitory concentrations, pinocembrin did not significantly alter membrane functionality and it increased bacterial fitness. Treatment with pinocembrin evoked decreased expression of ribosomal proteins and down-regulation of several NADH dehydrogenase I chain subunits and proteins involved in iron uptake. This suggests altered protein production and redox cycle and iron metabolism. Interestingly, the chelation of Fe ions during the treatment with pinocembrin increased C. jejuni survival, although there was no increase in the formation of reactive oxygen species. Pre-treatment of C. jejuni with sub-inhibitory concentrations of pinocembrin for 2 h resulted in a 1 log decrease in C. jejuni colony forming units in mice liver at 8 days post-infection, compared to untreated C. jejuni. These findings suggest that pinocembrin modulates the metabolic activity of C. jejuni and that pre-treatment of C. jejuni with pinocembrin influences its virulence potential in mice. This anti-Campylobacter potential of pinocembrin warrants further investigation.

The aim of this study was to evaluate Campylobacter jejuni NTCT 11168 adhesion to abiotic and biotic surfaces when grown in co-culture with Escherichia coli ATCC 11229 and/or Listeria monocytogenes 4b. Adhesion of C. jejuni to polystyrene and to Caco-2 cells and Acanthamoeba castellanii was lower for at least 3 log CFU/mL compared to E. coli and L. monocytogenes. Electron micrographs of ultrathin sections revealed interactions of C. jejuni with host cells. In co-culture with E. coli and L. monocytogenes, adhesion of C. jejuni to all tested surfaces was significantly increased for more than 1 log CFU/mL. There was 10% higher aggregation for C. jejuni than for other pathogens, and high co-aggregation of co-cultures of C. jejuni with E. coli and L. monocytogenes. These data show that C. jejuni in co-cultures with E. coli and L. monocytogenes present significantly higher risk than C. jejuni as mono-cultures, which need to be taken into account in risk evaluation. C. jejuni adhesion is a prerequisite for their colonization, biofilm formation, and further contamination of the environment. C. jejuni survival under adverse conditions as a factor in their pathogenicity and depends on their adhesion to different surfaces, not only as individual strains, but also in co-cultures with other bacteria like E. coli and L. monocytogenes.