Induction of cytokines in different organs after intranasal inoculation of Campylobacter jejuni in mice

Abstract

BackgroundCytokine production and histopathological changes occur in the lungs of mice after intranasal inoculation with Campylobacter jejuni, but the levels of cytokines in different organs to which C. jejuni disseminates have not been studied.FindingsAdult BALB/c mice were intranasally inoculated with C. jejuni 81–176 (test) or phosphate-buffered saline (control) (n=16 per group). The levels of cytokines in the organs (spleen, liver, and small and large intestines) to which C. jejuni disseminated were measured by ELISA. Two cytokine patterns were observed. First, increased proinflammatory cytokines, TNF-α, IL-1, and IL-2, were followed by anti-inflammatory cytokines, IL-4 and IL-10 in the spleen and large intestine. Second, in the liver and small intestine, there was a predominant production of anti-inflammatory cytokines, IL-4 and IL-10, with some increase in IL-2 levels. In the spleen and intestines, the levels of pro- and anti-inflammatory cytokines were concurrently increased.ConclusionDissemination of C. jejuni is associated with the production of different cytokine profiles in different tissues, with the proinflammatory response appearing in the spleen and large intestine at an earlier time point than in the liver and small intestine. The organs produce different cytokine profiles in response to C. jejuni dissemination. These preliminary findings should be confirmed with a study involving a larger group of animals.

The Effect of Co-infection of Food-Borne Pathogenic Bacteria on the Progression of Campylobacter jejuni Infection in Mice

“…This indicates that changes in the host’s immune status may have an important impact in C. jejuni infection. It has been reported that TNF-α, IL-1, IL-4, and IL-10 are all elevated in mice after C. jejuni infection ( Al-Banna et al, 2012 ). In this study, co-infection of T. gondii and C. jejuni further increased the levels of IFN-γ and IL-6 caused by T. gondii , much in the same way as the changes in cytokines induced by C. jejuni in gnotobiotic mice ( Bereswill et al, 2011 ), which suggests that T. gondii infection promotes C. jejuni infection symptoms.…”

Investigation of a mouse and a sheep model to study pathogenic mechanisms of Campylobacter jejuni fetoplacental infection

“…This is partly in agreement with cellular investigations of C. jejuni which supports a transcellular translocation. 5 Similarly, there is agreement with findings from pregnant guinea pig studies, where C. jejuni IA3902 was identified within the cytoplasm of trophoblasts, within phagocytes, in extracellular spaces surrounding trophoblasts in areas of placentitis and necrosis and occasionally surrounding uteroplacental arteries. 7 The presence of C. jejuni within murine trophoblasts and vasculature of the fetoplacental unit is also consistent with what has been described in sheep where the organism has been detected within trophoblasts and blood vessels of infected ovine placenta.…”

“…7 IL1β was found to act as a mediator of endothelial cell function and the placenta contributed to elevation in serum levels within the maternal circulation. 5 While the placenta was thought to produce small quantities of IL1β, trophoblasts can be induced to produce significant quantities of bioactive IL1β in vitro via endotoxin stimulation as evidenced by increased m RNA expression. 25 High levels of IL10 mRNA were expressed in trophoblasts with lesser quantities from the endometrial mucosa.…”

“…The oral route has been used to successfully replicate C. jejuni IA3902 induced reproductive disease in mice (Lashley, submitted for publication), guinea pigs, 5 and occasionally in sheep, 23 though usually at a lower rate than parenteral routes. The oral route of inoculation replicates the natural route of infection in sheep and represents the preferred model to study disease pathogenesis, organism virulence factors, and assess protective immunity in sheep.…”

“…61 Systemic infection of C. jejuni in BALB/c mice was associated with the initial production of pro-inflammatory cytokines, TNF, IL1 and IL2 and subsequent production of anti-inflammatory cytokines IL4 and IL10 in the spleen and large intestine. 5 In that same study, it was found that once the systemic infection had been cleared, the cytokine response was predominantly anti-inflammatory and associated with the production of IL4 and IL10 in the liver and small intestine. Interestingly, even mucin expression in reproductive tract epithelia may vary in response to cytokine influences.…”