%0 Journal Article
%T Induction of cytokines in different organs after intranasal inoculation of Campylobacter jejuni in mice
%A Nadia A Al-Banna
%A Raj Raghupathy
%A M John Albert
%J Gut Pathogens
%D 2012
%I BioMed Central
%R 10.1186/1757-4749-4-23
%X Adult BALB/c mice were intranasally inoculated with C. jejuni 81¨C176 (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-¦Á, 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.Dissemination 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 extraintestinal manifestations of Campylobacter jejuni, an enteropathogenic bacterium [1], are reported in some patients [2]. C. jejuni invades epithelial cells in vitro [3], and can be isolated from the spleen and liver in infected animals [4,5]. In vitro studies demonstrated the production of proinflammatory cytokines in C. jejuni-infected monocytic [6], dendritic [7] and intestinal epithelial cell lines [8], peripheral blood mononuclear cells [9] and splenocytes [10]. The association between cytokine production and disease protection/resolution, suggested in patients [9], was shown by the increased susceptibility of mice deficient in MyD88 or NF-¦ÊB to C. jejuni[11,12]. However, cytokine responses after C. jejuni dissemination were not characterised in vivo.In the current study, we used the mouse lun
%K Campylobacter jejuni
%K Cytokines
%K Systemic
%K Mouse lung model
%U http://www.gutpathogens.com/content/4/1/23