Abstract
BackgroundThe rising incidence of multidrug resistant (MDR) Gram-negative bacteria including Pseudomonas aeruginosa has become a serious issue in prevention of its spread particularly among hospitalized patients. It is, however, unclear whether distinct conditions such as acute intestinal inflammation facilitate P. aeruginosa infection of vertebrate hosts.Methods and resultsTo address this, we analysed P. aeruginosa infection in human microbiota-associated (hma) mice with acute ileitis induced by peroral Toxoplasma gondii challenge. When perorally infected with P. aeruginosa at day 3 post ileitis induction, hma mice displayed higher intestinal P. aeruginosa loads as compared to hma mice without ileitis. However, the overall intestinal microbiota composition was not disturbed by P. aeruginosa (except for lowered bifidobacterial populations), and the infection did not further enhance ileal immune cell responses. Pro-inflammatory cytokines including IFN-γ and IL-12p70 were similarly increased in ileum and mesenteric lymph nodes of P. aeruginosa infected and uninfected hma mice with ileitis. The anti-inflammatory cytokine IL-10 increased multifold upon ileitis induction, but interestingly more distinctly in P. aeruginosa infected as compared to uninfected controls. Immune responses were not restricted to the intestines as indicated by elevated pro-inflammatory cytokine levels in liver and kidney upon ileitis induction. However, except for hepatic TNF-α levels, P. aeruginosa infection did not result in more distinct pro-inflammatory cytokine secretion in liver and kidney of hma mice with ileitis. Whereas viable intestinal bacteria were more frequently detected in systemic compartments such as spleen and cardiac blood of P. aeruginosa infected than uninfected mice at day 7 following ileitis induction, P. aeruginosa infection did not exacerbate systemic pro-inflammatory sequelae, but resulted in lower IL-10 serum levels.ConclusionAcute intestinal inflammation facilitates infection of the vertebrate host with MDR bacteria including P. aeruginosa and might also pose particularly hospitalized patients at risk for acquisition. Since acute T. gondii induced inflammation might mask immunopathology caused by P. aeruginosa, a subacute or chronic inflammation model might be better suited to investigate the potential role of P. aeruginosa infection in the aggravation of intestinal disease.
Highlights
The rising incidence of multidrug resistant (MDR) Gram-negative bacteria including Pseudomonas aeruginosa has become a serious issue in prevention of its spread among hospitalized patients
Since acute T. gondii induced inflammation might mask immunopathology caused by P. aeruginosa, a subacute or chronic inflammation model might be better suited to investigate the potential role of P. aeruginosa infection in the aggravation of intestinal disease
Acute ileitis induction facilitates multidrug resistant P. aeruginosa infection of human microbiota‐associated mice The primary goal of our present study was to investigate the influence of acute intestinal inflammation on intestinal infection with MDR P. aeruginosa and its Intestinal microbiota composition in multidrug resistant P. aeruginosa infected human microbiota‐associated mice suffering from acute ileitis We assessed whether MDR P. aeruginosa infection of hma mice with induced acute ileitis was accompanied by distinct changes in intestinal microbiota composition
Summary
The rising incidence of multidrug resistant (MDR) Gram-negative bacteria including Pseudomonas aeruginosa has become a serious issue in prevention of its spread among hospitalized patients. It is, unclear whether distinct conditions such as acute intestinal inflammation facilitate P. aeruginosa infection of vertebrate hosts. Pseudomonas aeruginosa, a non-fermenting Gramnegative rod, is one of the most important bacterial pathogens responsible for a multitude of opportunistic infections in humans, especially in hospitalized patients [1]. Recent clinical surveys revealed that P. aeruginosa detection rates were significantly higher in fecal and mucosal samples derived from patients suffering from irritable bowel syndrome [8] or in the colonic mucosa of a pediatric patient with ulcerative colitis [9] as compared to a healthy individual. There is currently a large gap in knowledge regarding the interplay of P. aeruginosa, the host microbiota and immune system, under conditions of intestinal inflammation
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