Normal mesenteric lymph ameliorates lipopolysaccharide challenge-induced spleen injury

Abstract

PURPOSE:This study was conducted to investigate the effect of normal mesenteric lymph (NML) from mice on the spleen injury induced by lipopolysaccharide (LPS) challenge. METHODS:Mice in the LPS and LPS+NML groups received an intraperitoneal injection of LPS (35 mg/kg) and kept for 6 h.. The mice in the LPS+NML group received NML treatment at 1 h after LPS injection. Afterward, the splenic morphology, the levels of lipopolysaccharide-binding protein (LBP), cluster of differentiation 14 (CD14), phosphorylation mitogen-activated protein kinases (MAPKs), and inflammatory mediators in splenic tissue were investigated. RESULTS: LPS injection induced spleen injury, increased the levels of LBP, CD14, tumor necrosis factor-α (TNF-α), interleukin 6(IL-6), and interferon γ (IFN-γ), and decreased the IL-4 content in the spleen. By contrast, NML treatment reversed these changes.Meanwhile, the LPS challenge decreased the phosphorylation levels of p38 MAPK, extracellular regulated protein kinases 1/2, and c-Jun N-terminal kinase (JNK). Moreover, the phosphorylation levels of p38 MAPK and JNK were further decreased by the NML administration.CONCLUSION: rRdThe normal mesenteric lymph treatment alleviated lipopolysaccharide induced spleen injury by attenuating LPS sensitization and production of TNF-α, IL-6, and IFN-γ.

Raman Spectroscopy Follows Time-Dependent Changes in T Lymphocytes Isolated from Spleen of Endotoxemic Mice

“…7B, 7D). These observed morphological changes in the spleen have been reported as a result of LPS insult (64), and it is also known that cleaved caspase-3-positive cells significantly increase in numbers after the LPS exposure causing widespread leukocyte apoptosis in the spleen tissue (65). The tissue injury hypothesis can be further confirmed with the presence of Raman vibrations arising from the cytochrome-c/heme moiety and is in accordance with reported studies in literature where presence of cytochrome and heme during tissue injury in organs such as brain has been observed (38,66,67).…”

Effects of Solid-State Fermented Wheat Bran on Growth Performance, Immune Function, Intestinal Morphology and Microflora in Lipopolysaccharide-Challenged Broiler Chickens

“…Wu et al [40] found that treatment with 0.5 mg/kg body weight LPS induced acute inflammation and resulted in increased contents of pro-inflammatory cytokines in the serum, indicating that a successful inflammation model was established, which was similar to our results. The current results showed that LPS-challenged treatment significantly increased the TNF-α concentration, but had no significant effect on other cytokines, indicating that immune stress was mainly caused by the induction of large amounts of TNF-α [41]. Furthermore, the results showed that the concentrations of serum IL-4 and IL-10 were significantly increased in broilers fed with FWB-IV, and the levels of pro-inflammatory cytokines TNF-α, IL-1β, IL-6, IL-8 and CRP were significantly decreased, which was consistent with the results of Kang et al [30], and the mechanism may be that bioactive compounds in FWB, such as crude polysaccharides and total polyphenols inhibit the transcriptional expression of pro-inflammatory cytokines by downregulating the TLRs-NF-κB signal pathway and increase the levels of anti-inflammatory cytokines, further alleviate the inflammatory response caused by LPSchallenge [8,32].…”

Falcarinol Is a Potent Inducer of Heme Oxygenase‐1 and Was More Effective than Sulforaphane in Attenuating Intestinal Inflammation at Diet‐Achievable Doses

“…The rapid manifestation of epithelial shedding, preceded by the crypt appearance of LPS, suggests transmigration of intraperitoneal LPS across the visceral peritoneum and not only derived from circulation. The amelioration of splenic injury from the introduction of normal mesenteric lymph into LPS-treated mice indicates a role for mesenteric fluids in systemic inflammation [ 33 ]. Intestinal clearance of LPS causes intestinal permeability, oxidative stress, and intestinal mitochondrial damage and increases lipid peroxidation [ 34 ].…”