TLR-2 and TLR-4 expression in monocytes of newborns with late-onset sepsis

Redondo, Ana Carolina Costa; Ceccon, Maria Esther Jurfest Rivero; Silveira-Lessa, Ana Lúcia; Quinello, Camila; Palmeira, Patrícia; Carvalho, Werther Brunow de; Carneiro‐Sampaio, Magda

doi:10.1016/j.jped.2013.12.012

Cited by 18 publications

(10 citation statements)

References 22 publications

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“…During the initiation of the inflammatory septic process, changes occur in the expression levels of numerous inflammatory mediators, including an increase in the expression levels of pro-inflammatory cytokines IL-8, IL-6 and IL-1β, and anti-inflammatory cytokine IL-10 (26). Sepsis and endotoxemia have been associated with increased production of IL-1β, IL-6, IL-8, and TNF-α in the plasma and colon tissue (26). The results of the present study showed that the presence of LPS resulted in increased expression of IL-1β, IL-6, IL-8, TNF-α in the plasma and colon tissue.…”

Section: Discussionsupporting

confidence: 56%

Rhein inhibits lipopolysaccharide-induced intestinal injury during sepsis by blocking the toll-like receptor 4 nuclear factor-κB pathway

Zhang

Jiao

et al. 2015

Molecular Medicine Reports

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Abstract. Sepsis is one of the leading causes of mortality in severe systemic inflammatory syndrome. The endotoxin-induced inflammatory response has been linked to the development of sepsis. Rhein is a lipophilic anthraquinone isolated from Rheum rhabarbarum (rhubarb), which has a protective effect on intestinal damage in vivo. However, the underlying mechanism responsible for the protective effects of rhein remains to be elucidated. In the present study, mice were exposed to 20 mg/kg lipopolysaccharide (LPS), prior to being treated with either 100 mg/kg rhein or 0.3 mg/kg toll-like receptor 4 (TLR4) signaling inhibitor TAK-242. In the rhein-treated mice, the colon length (cm) was extended and colon injury was attenuated. In addition, treatment with rhein significantly decreased the expression levels of the LPS-induced inflammatory cytokines interleukin (IL)-1β, IL-6, IL-8, and tumor necrosis factor-α, in both the plasma and colon tissue. However, mice treated with TAK-242 exhibited increased expression levels of IL-10, as determined by ELISA and western blot analysis. In addition, immunohistochemistry and western blot analyses demonstrated that treatment with rhein was able to reduce TLR4 expression and inhibit nuclear factor-κB (NF-κB) phosphorylation in colon tissue. Furthermore, LPS induction was blocked by TAK-242. These results demonstrate that the observed rhein-attenuated inflammatory response during sepsis may be achieved via the TLR4 NF-κB signaling pathway. In conclusion, the results of the present study provide a novel insight into the protective effects of rhein on LPS-induced intestinal inflammation, and demonstrate that rhein may act as a beneficial therapeutic agent in the treatment of sepsis-induced intestinal damage.

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Section: Discussionsupporting

confidence: 56%

Rhein inhibits lipopolysaccharide-induced intestinal injury during sepsis by blocking the toll-like receptor 4 nuclear factor-κB pathway

Zhang

Jiao

et al. 2015

Molecular Medicine Reports

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“…Two important receptors involved in recognizing pathogenic ligands and maintaining host defense are TLR2 and TLR4, which predominantly bind to constituents of gram positive and gramnegative bacteria respectively (79). However, there are several studies showing that a dysregulation in these receptors can cause excess pro-inflammatory cytokines and chemokines, leading to autoimmunity, sepsis and multi-organ dysfunction (80,81).…”

Section: Toll Like Receptorsmentioning

confidence: 99%

Immune Dysregulation in Children With Down Syndrome

Huggard

Doherty

2020

Front. Pediatr.

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“…Patients with acute coronary syndromes have an increased expression of TLR-2 and TLR-4 on circulating monocytes [26,27]. During sepsis in newborns, monocytes express higher levels of TLR-4 [28]. Monocytes from HIV-infected patients displayed enhanced expression of TLR-2 [29].…”

Section: Monocyte Surface Biomarkersmentioning

confidence: 99%

Perspectives for Monocyte/Macrophage-Based Diagnostics of Chronic Inflammation

Kzhyshkowska¹,

Gudima

Moganti

et al. 2016

Transfus Med Hemother

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Low-grade chronic inflammation underlies the development of the most dangerous cardiometabolic disorders including type 2 diabetes and its vascular complications. In contrast to acute inflammation induced by bacteria and viruses, chronic inflammation can be driven by abnormal reaction to endogenous factors, including Th2 cytokines, metabolic factors like advanced glycation end products (AGEs), modified lipoproteins, or hyperglycemia. The key innate immune cells that recognize these factors in blood circulation are monocytes. Inflammatory programming of monocytes which migrate into tissues can, in turn, result into generation of tissue macrophages with pathological functions. Therefore, determination of the molecular and functional phenotype of circulating monocytes is a very promising diagnostic tool for the identification of hidden inflammation, which can precede the development of the pathology. Here we propose a new test system for the identification of inflammatory programming of monocytes: surface biomarkers and ex vivo functional system. We summarize the current knowledge about surface biomarkers for monocyte subsets, including CD16, CCR2, CX3CR1, CD64, stabilin-1 and CD36, and their association with inflammatory human disorders. Furthermore, we present the design of an ex vivo monocyte-based test system with minimal set of parameters as a potential diagnostic tool for the identification of personalized inflammatory responses.

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TLR-2 and TLR-4 expression in monocytes of newborns with late-onset sepsis

Abstract: This study investigated the innate immune response in septic newborns. Septic newborns that relied almost exclusively on the innate immune system showed little in vivo response at monocyte activation, suggesting impaired immune response and increased susceptibility to infection.

Cited by 18 publications

References 22 publications

Rhein inhibits lipopolysaccharide-induced intestinal injury during sepsis by blocking the toll-like receptor 4 nuclear factor-κB pathway

Rhein inhibits lipopolysaccharide-induced intestinal injury during sepsis by blocking the toll-like receptor 4 nuclear factor-κB pathway

Immune Dysregulation in Children With Down Syndrome

Perspectives for Monocyte/Macrophage-Based Diagnostics of Chronic Inflammation

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