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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-treatment of piglets induces a rise in body temperature 4 h after infection with STM14028. The body temperature was measured at different time points on 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 rise in body temperature compared to the B and C groups. Data refer to one out of two separate experiments performed with comparable results. The differences between groups were statistically significant (****P ≤ 0.0001; *P ≤ 0.1; **P ≤ 0.01 multiple comparisons-Fisher's Least Significant Difference test).
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Figure 3: LPS-treatment of piglets induces a rise in body temperature 4 h after infection with STM14028. The body temperature was measured at different time points on 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 rise in body temperature compared to the B and C groups. Data refer to one out of two separate experiments performed with comparable results. The differences between groups were statistically significant (****P ≤ 0.0001; *P ≤ 0.1; **P ≤ 0.01 multiple comparisons-Fisher's Least Significant Difference test).

Mentions: LPS was able to induce a rise in body temperature in piglets of group A already at 4 h post STM14028-infection (Figure 3) compared to the control (C) and the STM14028-infected group (B), reaching body temperature similar to those of group A only at 24 and 48 h post infection. No significant differences in body weight were measured among the three groups throughout the 48 h of analysis (data not shown).


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-treatment of piglets induces a rise in body temperature 4 h after infection with STM14028. The body temperature was measured at different time points on 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 rise in body temperature compared to the B and C groups. Data refer to one out of two separate experiments performed with comparable results. The differences between groups were statistically significant (****P ≤ 0.0001; *P ≤ 0.1; **P ≤ 0.01 multiple comparisons-Fisher's Least Significant Difference test).
© Copyright Policy
Related In: Results  -  Collection

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

Figure 3: LPS-treatment of piglets induces a rise in body temperature 4 h after infection with STM14028. The body temperature was measured at different time points on 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 rise in body temperature compared to the B and C groups. Data refer to one out of two separate experiments performed with comparable results. The differences between groups were statistically significant (****P ≤ 0.0001; *P ≤ 0.1; **P ≤ 0.01 multiple comparisons-Fisher's Least Significant Difference test).
Mentions: LPS was able to induce a rise in body temperature in piglets of group A already at 4 h post STM14028-infection (Figure 3) compared to the control (C) and the STM14028-infected group (B), reaching body temperature similar to those of group A only at 24 and 48 h post infection. No significant differences in body weight were measured among the three groups throughout the 48 h of analysis (data not shown).

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