scholarly journals TLR4-Mediated Blunting of Inflammatory Responses to Eccentric Exercise in Young Women

2014 ◽  
Vol 2014 ◽  
pp. 1-11 ◽  
Author(s):  
Rodrigo Fernandez-Gonzalo ◽  
José A. De Paz ◽  
Paula Rodriguez-Miguelez ◽  
María J. Cuevas ◽  
Javier González-Gallego
Keyword(s):  
Inflammatory Response ◽  
Training Program ◽  
Signaling Pathway ◽  
Young Women ◽  
Eccentric Exercise ◽  
Inflammatory Responses ◽  
Control Group ◽  
Eccentric Training ◽  
Tlr4 Signaling ◽  
Tlr4 Signaling Pathway

This study assessed the inflammatory response mediated by the toll-like receptor 4 (TLR4) signaling pathway after acute eccentric exercise before and after an eccentric training program in women. Twenty women performed two acute eccentric bouts using a squat machine over a ~9 week interval. The training group (TG) carried out an eccentric training program during 6 weeks, while the control group (CG) did not follow any training. Protein content of markers involved in the TLR4-mediated activation of several nuclear transcription factors, such as nuclear factorκB (NF-κB), and interferon regulatory transcription factor 3 (IRF3), was analyzed. The inflammatory response after the first acute bout was similar between TG and CG, showing an upregulation of all the markers analyzed, with the exception of IRF3. After the second bout, the upregulation of TLR4 signaling pathway was blunted in TG, but not in CG, through both the myeloid differentiation factor 88- and toll/interleukin-1 receptor domain containing adapter inducing interferon-β-dependent pathways. These results highlight the role of the TLR4 in controlling the exercise-induced inflammatory response in young women. More importantly, these data suggest eccentric training may help to prevent TLR4 activation principally through NF-κB, and perhaps IRF3, downstream signaling in this population.

Effects of eccentric exercise on toll-like receptor 4 signaling pathway in peripheral blood mononuclear cells

2012 ◽  
Vol 112 (12) ◽  
pp. 2011-2018 ◽  
Author(s):  
Rodrigo Fernandez-Gonzalo ◽  
José A. De Paz ◽  
Paula Rodriguez-Miguelez ◽  
María J. Cuevas ◽  
Javier González-Gallego
Keyword(s):  
Signaling Pathway ◽  
Eccentric Exercise ◽  
Mononuclear Cells ◽  
Eccentric Training ◽  
Proinflammatory Response ◽  
Peripheral Blood Mononuclear ◽  
Tlr4 Signaling ◽  
Tnf Α ◽  
Tlr4 Signaling Pathway ◽  
Myeloid Differentiation Factor

This study aimed to investigate the response of the toll-like receptor 4 (TLR4) signaling pathway to an acute bout of eccentric exercise, and to assess whether eccentric training attenuated the effects induced by acute eccentric exercise. Twenty men (22.4 ± 0.5 yr) were divided into a control group (CG, n = 8) and a training group (TG, n = 12). Both groups performed two acute eccentric bouts on a squat machine in a 9-wk interval. During this time, TG followed a 6-wk eccentric training program (3 session/wk; 3–5 sets of 10 repetitions with loads ranging between the 40 and 50% of maximal isometric voluntary contraction). CD14, TLR4, and TNF-α mRNA levels, and CD14, TLR4, myeloid differentiation factor 88, tumor necrosis factor receptor-associated factor 6, TIR-domain-containing adapter-inducing interferon-β, phospho-IκB kinases, phospho-IκB, phospho-ERK-1/2, and TNF-α protein concentration were measured in peripheral blood mononuclear cells, before, immediately, and 2 h after each eccentric bout. The first acute eccentric bout triggered a proinflammatory response mediated by an upregulation of all of the factors measured within the TLR4 signaling pathway. Following the training period and after the second acute bout, CG showed a similar proinflammatory response than that seen after the first bout. However, the eccentric training intervention decreased significantly the protein concentration of all factors analyzed in TG compared with results obtained after the first bout. These results suggest that the TLR4-signaling pathway plays a critical role in the proinflammatory response seen after acute eccentric exercise. This response was attenuated after an eccentric training program through myeloid differentiation factor 88-dependent and -independent pathways.

scholarly journals Monocytes Undergo Functional Reprogramming to Generate Immunosuppression through HIF-1α Signaling Pathway in the Late Phase of Sepsis

2020 ◽  
Vol 2020 ◽  
pp. 1-9 ◽  
Author(s):  
Li-Li Li ◽  
Bing Dai ◽  
Yu-Han Sun ◽  
Ting-Ting Zhang
Keyword(s):  
Clinical Study ◽  
Inflammatory Response ◽  
Signaling Pathway ◽  
Animal Study ◽  
Inflammatory Responses ◽  
Late Phase ◽  
Severe Pneumonia ◽  
Control Group ◽  
L1 Protein ◽  
Control Injection

Severe pneumonia with sepsis is characterized by a dysregulated inflammatory response of endotoxin. In our study, we attempted to investigate the roles of the immune guardian cells (monocytes) in the immune-inflammatory response of severe pneumonia-induced sepsis. We performed analysis in the blood samples of human and animals with ELISA, western blot, flow cytometry (FCM) methods, etc. Results showed that the proinflammatory status shifted to hypoinflammatory phases during the sepsis process. In a clinical study, the levels of IL-1β, IL-6, TNF-α, etc., except for IL-10, were inhibited in the late phase of sepsis, while, in an animal study, the immune suppression status was attenuated with administration of the adenovirus Ade-HIF-1α. Conversely, the amount of IL-10 was lower in the adenovirus Ade-HIF-1α group compared with the sepsis model group and the Ade-control group. Moreover, in the clinical study, the programmed cell death-ligand 1 (PD-L1) was overexpressed in monocytes in the late phase of sepsis, while the expression of proteins HIF-1α and STAT3 was decreased in the late phase of sepsis. However, in the animal study, we found that the HIF-1α factor facilitated the inflammatory response. The expression of the proteins HIF-1α and STAT3 was increased, and the PD-L1 protein was decreased with the adenovirus Ade-HIF-1α administration compared with the rats without Ade-HIF-1α injection and with the Ade-control injection. Additionally, the proteins HIF-1α and STAT3 were coregulated at transcriptional levels during the inflammatory responses of sepsis. Taken together, monocytes undergo reprogramming to generate immunosuppression through the HIF-1α signaling pathway in the late phase of sepsis.

scholarly journals Dietary Silk Peptide Inhibits LPS-Induced Inflammatory Responses by Modulating Toll-Like Receptor 4 (TLR4) Signaling

Biomolecules ◽  
2020 ◽  
Vol 10 (5) ◽  
pp. 771
Author(s):  
Sungwoo Chei ◽  
Hyun-Ji Oh ◽  
Kippeum Lee ◽  
Heegu Jin ◽  
Jeong-Yong Lee ◽  
...  
Keyword(s):  
Immune Responses ◽  
Signaling Pathway ◽  
Inflammatory Responses ◽  
Innate Immune Responses ◽  
Toll Like Receptor ◽  
Serum Samples ◽  
Toll Like Receptor 4 ◽  
Tlr4 Signaling ◽  
Tlr4 Signaling Pathway ◽  
Silk Peptide

Acid-hydrolyzed silk peptide (SP) is a valuable material that has been used traditionally to treat various diseases, however, the mechanism by which it affects inflammatory responses is unknown. To examine the effects of SP on inflammatory responses, we used macrophages as a vehicle for examining signaling via toll-like receptor 4 (TLR4), which plays an important role in innate immune responses to pathogenic infections and pathogen-derived molecules such as lipopolysaccharide (LPS). We then confirmed the anti-inflammatory effects of SP by examining lymph node, spleen, and serum samples from C57BL/6 mice injected with LPS. We also used LPS-induced bone marrow-derived macrophages and RAW264.7 cells (a murine macrophage cell line) to identify the mechanism by which SP modulates immune responses via the TLR4 signaling pathway. In addition, we showed that SP prevents LPS-induced production of nitric oxide and reactive oxygen species. In summary, SP inhibits LPS-induced inflammatory responses by modulating the TLR4 signaling pathway.

Geniposide Reduces Inflammatory Responses of Oxygen-Glucose Deprived Rat Microglial Cells via Inhibition of the TLR4 Signaling Pathway

2012 ◽  
Vol 37 (10) ◽  
pp. 2235-2248 ◽  
Author(s):  
Jun Wang ◽  
Jincan Hou ◽  
Peng Zhang ◽  
Dan Li ◽  
Cuixiang Zhang ◽  
...  
Keyword(s):  
Signaling Pathway ◽  
Inflammatory Responses ◽  
Microglial Cells ◽  
Tlr4 Signaling ◽  
Tlr4 Signaling Pathway

scholarly journals The Cancer Prevention, Anti-Inflammatory and Anti-Oxidation of Bioactive Phytochemicals Targeting the TLR4 Signaling Pathway

2018 ◽  
Vol 19 (9) ◽  
pp. 2729 ◽  
Author(s):  
Chung-Yi Chen ◽  
Chiu-Li Kao ◽  
Chi-Ming Liu
Keyword(s):  
Inflammatory Response ◽  
Signaling Pathway ◽  
Cancer Progression ◽  
Epigallocatechin Gallate ◽  
Caffeic Acid Phenethyl Ester ◽  
Host Immune System ◽  
Tlr4 Signaling ◽  
Tlr4 Signaling Pathway ◽  
Bioactive Phytochemicals ◽  
Anti Inflammatory

Toll-like receptors (TLRs) are a well-known family of pattern recognition receptors that play an important role in a host immune system. TLR triggering leads to the induction of pro-inflammatory cytokines and chemokines, driving the activation of both innate and adaptive immunity. Recently, an increasing number studies have shown the link between TLRs and cancer. Among them, the toll-like receptor 4 (TLR4) signaling pathway is associated with inflammatory response and cancer progression. Dietary phytochemicals are potential modulators of immunological status with various pharmacological properties including anti-cancer, anti-oxidant and anti-inflammatory. Curcumin, 6-gingerol, 6-shogaol, 1-dehydro-10-gingerdione, epigallocatechin gallate (EGCG), luteolin, quercetin, resveratrol, caffeic acid phenethyl ester, xanthohumol, genistein, berberine, and sulforaphane can inhibit TLR4 activation. The aim of the present review is to describe the role of the TLR4 signaling pathway between inflammatory response and cancer progression. We further introduce bioactive phytochemicals with potential anti-inflammation and chemoprevention by inhibiting TLR activation.

scholarly journals Swine IRF3/IRF7 attenuates inflammatory responses through TLR4 signaling pathway

Oncotarget ◽  
2017 ◽  
Vol 8 (37) ◽  
pp. 61958-61968 ◽  
Author(s):  
Pei-Ge Chen ◽  
Yan-Jing Guan ◽  
Guang-Ming Zha ◽  
Xian-Qin Jiao ◽  
He-Shui Zhu ◽  
...  
Keyword(s):  
Signaling Pathway ◽  
Inflammatory Responses ◽  
Tlr4 Signaling ◽  
Tlr4 Signaling Pathway
Sign in / Sign up

Export Citation Format

Share Document