Anti-Inflammatory Properties of Plasma from Children with Short Bowel Syndrome

Abstract

Sepsis, resulting from a dysregulated host immune response to invading pathogens, is the leading cause of mortality in critically ill patients worldwide. Immunomodulatory treatment for sepsis is currently lacking. Children with short bowel syndrome (SBS) may present with less severe symptoms during gram-negative bacteremia. We, therefore, tested the hypothesis that plasma from children with SBS could confer protection against Escherichia coli sepsis. We showed that SBS plasma at 5% and 10% concentrations significantly (p < 0.05) inhibited the production of both TNF-α and IL-6 induced by either E. coli- or LPS-stimulated host cells when compared to plasma from healthy controls. Furthermore, mice treated intravenously with select plasma samples from SBS or healthy subjects had reduced proinflammatory cytokine levels in plasma and a significant survival advantage after E. coli infection. However, SBS plasma was not more protective than the plasma of healthy subjects, suggesting that children with SBS have other immunomodulatory mechanisms, in addition to neutralizing antibodies, to alleviate their symptoms during gram-negative sepsis.

Lactic Acid Bacteria Mixture Isolated From Wild Pig Alleviated the Gut Inflammation of Mice Challenged by Escherichia coli

“…On the other hand, studies indicated that inhibition of cytokines could exert beneficial effects against intestinal mucosal damage and development of inflammation in the gut ( 61 ). However, no significant difference of inflammation cytokines in serum was observed including TNF-α, IL-6, and IL-1β between four groups, indicating that the challenge of E. coli ATCC 25922 ( 18 ) might induce a local rather than a systemic inflammation in mice.…”

“…As shown in Figure S1A , mice were randomly divided into four groups of nine mice each. Four groups were treated as follows: (1) mice orally administrated with 200 μl of PBS for 3 weeks (C); (2) mice orally administrated with 200 μl of PBS for 3 weeks followed by oral challenge with E. coli ATCC 25922 ( 18 ) as gut inflammatory model (2 × 10 9 CFU) (CE); (3) mice orally administrated with mixed LAB (2 × 10 9 CFU) for 3 weeks (M); and (4) mice orally administrated with mixed LAB (2 × 10 9 CFU) for 3 weeks followed by oral challenge with E. coli ATCC 25922 (2 × 10 9 CFU) (ME), respectively. The body weight of all mice was recorded daily, and feces of all mice was collected aseptically and suspended into sterile saline to determine viable LAB counts.…”

Role of adherent invasive Escherichia coli in pathogenesis of inflammatory bowel disease

“…In contrast, the numbers of AIEC cells and proinflammatory cytokines released by macrophages were significantly reduced under pharmacologically induced autophagy. Notably, autophagy was blocked at the autophagolysosome stage, and this inhibitory effect was accompanied by AIEC infection of PLB-985 neutrophil-like cells, which enabled intracellular bacterial survival and increased the Il-8 secretion level[ 58 ]. In addition, the microRNAs miR106B and miR93 reduced the expression of ATG16L1 and prevented the elimination of intracellular bacteria by regulating autophagy[ 59 ].…”