11 research outputs found
Intestinal, extra-intestinal and systemic sequelae of Toxoplasma gondii induced acute ileitis in mice harboring a human gut microbiota
Background Within seven days following peroral high dose infection with
Toxoplasma gondii susceptible conventionally colonized mice develop acute
ileitis due to an underlying T helper cell (Th) -1 type immunopathology. We
here addressed whether mice harboring a human intestinal microbiota developed
intestinal, extra-intestinal and systemic sequelae upon ileitis induction.
Methodology/Principal findings Secondary abiotic mice were generated by broad-
spectrum antibiotic treatment and associated with a complex human intestinal
microbiota following peroral fecal microbiota transplantation. Within three
weeks the human microbiota had stably established in the murine intestinal
tract as assessed by quantitative cultural and culture-independent (i.e.
molecular 16S rRNA based) methods. At day 7 post infection (p.i.) with 50
cysts of T. gondii strain ME49 by gavage human microbiota associated (hma)
mice displayed severe clinical, macroscopic and microscopic sequelae
indicating acute ileitis. In diseased hma mice increased numbers of innate and
adaptive immune cells within the ileal mucosa and lamina propria and elevated
intestinal secretion of pro-inflammatory mediators including IFN-γ, IL-12 and
nitric oxide could be observed at day 7 p.i. Ileitis development was
accompanied by substantial shifts in intestinal microbiota composition of hma
mice characterized by elevated total bacterial loads and increased numbers of
intestinal Gram-negative commensals such as enterobacteria and Bacteroides /
Prevotella species overgrowing the small and large intestinal lumen.
Furthermore, viable bacteria translocated from the inflamed ileum to extra-
intestinal including systemic compartments. Notably, pro-inflammatory immune
responses were not restricted to the intestinal tract as indicated by
increased pro-inflammatory cytokine secretion in extra-intestinal (i.e. liver
and kidney) and systemic compartments including spleen and serum.
Conclusion/Significance With respect to the intestinal microbiota composition
“humanized” mice display acute ileitis following peroral high dose T. gondii
infection. Thus, hma mice constitute a suitable model to further dissect the
interactions between pathogens, human microbiota and vertebrate host immunity
during acute intestinal inflammation
Virulence of a T6SS Campylobacter jejuni chicken isolate from North Romania
Objectives: In this study we have investigated the in vitro and in vivo virulence characteristics of a new T6SS positive Campylobacter jejuni chicken isolate (SV12) originating from a poultry population in North Romania. A detailed phenotypic characterization was performed and compared to the T6SS negative C. jejuni 81-176 wild strain. Results: Our results indicate that the significantly higher capacity to attach and invade HCT-8 cells of C. jejuni SV12 isolate is associated with increased motility, increased resistance to bile salts and serum resistance, when compared to C. jejuni strain 81-76. Mice infected with the SV12 isolate showed statistically higher levels of colonization at both 7- and 14-days post-inoculation and in the stomach, caecum, duodenum and large intestine. Infection with the SV12 strain induced a stronger immune response as the gene transcript levels of IL-17, TNFα and IFNγ were more pronouncedly up-regulated compared to the C. jejuni strain 81-176. The present study showed that the new isolate SV12 had an enhanced virulence capacity compared to the wild strain which was evident in vivo as well. This work also provides an insight on the colonization pattern and host immune response differences between T6SS positive and T6SS negative C. jejuni