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Salmonella Typhimurium exploits inflammation to its own advantage in piglets.

Chirullo B, Pesciaroli M, Drumo R, Ruggeri J, Razzuoli E, Pistoia C, Petrucci P, Martinelli N, Cucco L, Moscati L, Amadori M, Magistrali CF, Alborali GL, Pasquali P - Front Microbiol (2015)

Bottom Line: This study showed that STM14028 is able to efficiently colonize in vitro porcine mono-macrophages and intestinal columnar epithelial (IPEC-J2) cells, and that the colonization significantly increases with LPS pre-treatment.This increase was then reversed by inhibiting the LPS stimulation through LPS antagonist, confirming an active role of LPS stimulation in STM14028-intracellular colonization.Typhimurium exploits inflammation for its benefit in piglets.

View Article: PubMed Central - PubMed

Affiliation: Unit of Prophyilaxis and Control of Bacterial Zoonoses, Department of Food Safety and Veterinary Public Health, Istituto Superiore di Sanità Rome, Italy.

ABSTRACT
Salmonella Typhimurium (S. Typhimurium) is responsible for foodborne zoonotic infections that, in humans, induce self-limiting gastroenteritis. The aim of this study was to evaluate whether the wild-type strain S. Typhimurium (STM14028) is able to exploit inflammation fostering an active infection. Due to the similarity between human and porcine diseases induced by S. Typhimurium, we used piglets as a model for salmonellosis and gastrointestinal research. This study showed that STM14028 is able to efficiently colonize in vitro porcine mono-macrophages and intestinal columnar epithelial (IPEC-J2) cells, and that the colonization significantly increases with LPS pre-treatment. This increase was then reversed by inhibiting the LPS stimulation through LPS antagonist, confirming an active role of LPS stimulation in STM14028-intracellular colonization. Moreover, LPS in vivo treatment increased cytokines blood level and body temperature at 4 h post infection, which is consistent with an acute inflammatory stimulus, capable to influence the colonization of STM14028 in different organs and tissues. The present study proves for the first time that in acute enteric salmonellosis, S. Typhimurium exploits inflammation for its benefit in piglets.

No MeSH data available.


Related in: MedlinePlus

LPS-treated piglets show an increased inflammation 4 h post STM14028 infection. IL-1beta and TNF-alpha production was measured at different time points on blood samples from three different groups of piglets: treated with LPS and infected with STM14028 (group A); only STM14028 infected (group B); naïve control group (group C). At 4 h post infection, group A showed a significant increase in production of both cytokines compared to the B and C groups. The differences between the groups were statistically significant (*P ≤ 0.1; **P ≤ 0.01, multiple comparisons-Fisher's Least Significant Difference test).
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Figure 4: LPS-treated piglets show an increased inflammation 4 h post STM14028 infection. IL-1beta and TNF-alpha production was measured at different time points on blood samples from three different groups of piglets: treated with LPS and infected with STM14028 (group A); only STM14028 infected (group B); naïve control group (group C). At 4 h post infection, group A showed a significant increase in production of both cytokines compared to the B and C groups. The differences between the groups were statistically significant (*P ≤ 0.1; **P ≤ 0.01, multiple comparisons-Fisher's Least Significant Difference test).

Mentions: Moreover, a remarkable increase of circulating pro-inflammatory cytokines has been found (Figure 4). TNF-alpha was in fact detected in the blood of all animals but it was produced in a higher amount in group A compared to the groups B and C, at 4 h post STM14028-infection, without significant differences within groups at 24 and 48 h post infection.


Salmonella Typhimurium exploits inflammation to its own advantage in piglets.

Chirullo B, Pesciaroli M, Drumo R, Ruggeri J, Razzuoli E, Pistoia C, Petrucci P, Martinelli N, Cucco L, Moscati L, Amadori M, Magistrali CF, Alborali GL, Pasquali P - Front Microbiol (2015)

LPS-treated piglets show an increased inflammation 4 h post STM14028 infection. IL-1beta and TNF-alpha production was measured at different time points on blood samples from three different groups of piglets: treated with LPS and infected with STM14028 (group A); only STM14028 infected (group B); naïve control group (group C). At 4 h post infection, group A showed a significant increase in production of both cytokines compared to the B and C groups. The differences between the groups were statistically significant (*P ≤ 0.1; **P ≤ 0.01, multiple comparisons-Fisher's Least Significant Difference test).
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Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4585093&req=5

Figure 4: LPS-treated piglets show an increased inflammation 4 h post STM14028 infection. IL-1beta and TNF-alpha production was measured at different time points on blood samples from three different groups of piglets: treated with LPS and infected with STM14028 (group A); only STM14028 infected (group B); naïve control group (group C). At 4 h post infection, group A showed a significant increase in production of both cytokines compared to the B and C groups. The differences between the groups were statistically significant (*P ≤ 0.1; **P ≤ 0.01, multiple comparisons-Fisher's Least Significant Difference test).
Mentions: Moreover, a remarkable increase of circulating pro-inflammatory cytokines has been found (Figure 4). TNF-alpha was in fact detected in the blood of all animals but it was produced in a higher amount in group A compared to the groups B and C, at 4 h post STM14028-infection, without significant differences within groups at 24 and 48 h post infection.

Bottom Line: This study showed that STM14028 is able to efficiently colonize in vitro porcine mono-macrophages and intestinal columnar epithelial (IPEC-J2) cells, and that the colonization significantly increases with LPS pre-treatment.This increase was then reversed by inhibiting the LPS stimulation through LPS antagonist, confirming an active role of LPS stimulation in STM14028-intracellular colonization.Typhimurium exploits inflammation for its benefit in piglets.

View Article: PubMed Central - PubMed

Affiliation: Unit of Prophyilaxis and Control of Bacterial Zoonoses, Department of Food Safety and Veterinary Public Health, Istituto Superiore di Sanità Rome, Italy.

ABSTRACT
Salmonella Typhimurium (S. Typhimurium) is responsible for foodborne zoonotic infections that, in humans, induce self-limiting gastroenteritis. The aim of this study was to evaluate whether the wild-type strain S. Typhimurium (STM14028) is able to exploit inflammation fostering an active infection. Due to the similarity between human and porcine diseases induced by S. Typhimurium, we used piglets as a model for salmonellosis and gastrointestinal research. This study showed that STM14028 is able to efficiently colonize in vitro porcine mono-macrophages and intestinal columnar epithelial (IPEC-J2) cells, and that the colonization significantly increases with LPS pre-treatment. This increase was then reversed by inhibiting the LPS stimulation through LPS antagonist, confirming an active role of LPS stimulation in STM14028-intracellular colonization. Moreover, LPS in vivo treatment increased cytokines blood level and body temperature at 4 h post infection, which is consistent with an acute inflammatory stimulus, capable to influence the colonization of STM14028 in different organs and tissues. The present study proves for the first time that in acute enteric salmonellosis, S. Typhimurium exploits inflammation for its benefit in piglets.

No MeSH data available.


Related in: MedlinePlus