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Haihua Li, Lei Zhang, Longbin Chen, Qi Zhu, Wenjie Wang, Jiayun Qiao
BACKGROUND: A newly isolated L. acidophilus strain has been reported to have potential anti-inflammatory activities against lipopolysaccharide (LPS) challenge in piglet, while the details of the related inflammatory responses are limited. Here we aimed to analysis the ability of L. acidophilus to regulate inflammatory responses and to elucidate the mechanisms involved in its anti-inflammatory activity. RESULTS: The ETEC (enterotoxigenic Escherichia coli) K88-induced up-regulations of IL-1β, IL-8 and TNF-α were obviously inhibited by L...
November 10, 2016: BMC Microbiology
Shuo Geng, Keqiang Chen, Ruoxi Yuan, Liang Peng, Urmila Maitra, Na Diao, Chun Chen, Yao Zhang, Yuan Hu, Chen-Feng Qi, Susan Pierce, Wenhua Ling, Huabao Xiong, Liwu Li
Sustained low-grade inflammation mediated by non-resolving inflammatory monocytes has long been suspected in the pathogenesis of atherosclerosis; however, the molecular mechanisms responsible for the sustainment of non-resolving inflammatory monocytes during atherosclerosis are poorly understood. Here we observe that subclinical endotoxemia, often seen in humans with chronic inflammation, aggravates murine atherosclerosis through programming monocytes into a non-resolving inflammatory state with elevated Ly6C, CCR5, MCP-1 and reduced SR-B1...
November 8, 2016: Nature Communications
Peipei Jin, Lulong Bo, Yongjian Liu, Wenbin Lu, Shengwei Lin, Jinjun Bian, Xiaoming Deng
Interleukin-1 receptor-associated kinase M (IRAK-M) is a well-known negative regulator for Toll-like receptor signaling, which can regulate immune homeostasis and tolerance in a number of pathological settings. However, the mechanism for IRAK-M regulation at transcriptional level remains largely unknown. In this study, a 1.4kb upstream sequence starting from the major IRAK-M transcriptional start site was cloned into luciferase reporter vector pGL3-basic to construct the full-length IRAK-M promoter. Luciferase reporter plasmids harboring the full-length and the deletion mutants of IRAK-M were transfected into 293T and A549 cells, and their relative luciferase activity was measured...
August 22, 2016: Biomedicine & Pharmacotherapy, Biomédecine & Pharmacothérapie
Jaya Talreja, Harvinder Talwar, Nisar Ahmad, Ruchi Rastogi, Lobelia Samavati
Sarcoidosis is a multisystem granulomatous disease of unknown etiology that primarily affects the lungs. Our previous work indicates that activation of p38 plays a pivotal role in sarcoidosis inflammatory response. Therefore, we investigated the upstream kinase responsible for activation of p38 in sarcoidosis alveolar macrophages (AMs) and PBMCs. We identified that sustained p38 phosphorylation in sarcoidosis AMs and PBMCs is associated with active MAPK kinase 4 but not with MAPK kinase 3/6. Additionally, we found that sarcoidosis AMs exhibit a higher expression of IRAK1, IRAK-M, and receptor interacting protein 2 (Rip2)...
August 15, 2016: Journal of Immunology: Official Journal of the American Association of Immunologists
Brendan J Jenkins
Dysregulated interactions between the host immune system and gut microbiota can underpin inflammation, leading to colorectal cancer (CRC). In this issue of Cancer Cell, Kesselring et al. reveal a bimodal role of the TLR/IL-1R-signaling negative regulator, IRAK-M, in promoting tumoral microbial colonization and STAT3 oncoprotein stabilization during CRC.
May 9, 2016: Cancer Cell
Rebecca Kesselring, Joachim Glaesner, Andreas Hiergeist, Elisabeth Naschberger, Helmut Neumann, Stefan M Brunner, Anja K Wege, Caroline Seebauer, Gudrun Köhl, Susanne Merkl, Roland S Croner, Christina Hackl, Michael Stürzl, Markus F Neurath, André Gessner, Hans-Juergen Schlitt, Edward K Geissler, Stefan Fichtner-Feigl
Colorectal cancer (CRC) is associated with loss of epithelial barrier integrity, which facilitates the interaction of the immunological microenvironment with the luminal microbiome, eliciting tumor-supportive inflammation. An important regulator of intestinal inflammatory responses is IRAK-M, a negative regulator of TLR signaling. Here we investigate the compartment-specific impact of IRAK-M on colorectal carcinogenesis using a mouse model. We demonstrate that IRAK-M is expressed in tumor cells due to combined TLR and Wnt activation...
May 9, 2016: Cancer Cell
Chen Wang, Xiao-Xi Liu, Kai-Bin Huang, Su-Bing Yin, Jing-Jing Wei, Ya-Fang Hu, Yong Gu, Guo-Qing Zheng
Preconditioning with ligands of toll-like receptors (TLRs) is a powerful neuroprotective approach whereby a low dose of stimulus confers significant protection against subsequent substantial brain damage by reprogramming the ischemia-activated TLRs signaling. Herein, we aim to explore whether preconditioning with recombinant high-mobility group box 1 (rHMGB1), one of the TLRs ligands, decreases cerebral ischemia-reperfusion injury (IRI). Rats were intracerebroventricularly pretreated with rHMGB1, 1 or 3 days before induction of middle cerebral artery occlusion...
May 2016: Journal of Neurochemistry
Ryan J Stark, Hyehun Choi, Stephen R Koch, Benjamin A Fensterheim, Fred S Lamb, Edward R Sherwood
Prior exposure to lipopolysaccharide (LPS) produces a reduced or "tolerant" inflammatory response to subsequent challenges with LPS, however the potent pro-inflammatory effects of LPS limit its clinical benefit. The adjuvant monophosphoryl lipid A (MPLA) is a weak toll-like receptor 4 (TLR4) agonist that induces negligible inflammation but retains potent immunomodulatory properties. We postulated that pre-treatment with MPLA would inhibit the inflammatory response of endothelial cells to secondary LPS challenge...
March 2016: Clinical Science (1979-)
Amit Saxena, Arti V Shinde, Zaffar Haque, Yi-Jin Wu, Wei Chen, Ya Su, Nikolaos G Frangogiannis
In the infarcted myocardium, necrotic cardiomyocytes activate innate immune pathways, stimulating pro-inflammatory signaling cascades. Although inflammation plays an important role in clearance of the infarct from dead cells and matrix debris, repair of the infarcted heart requires timely activation of signals that negatively regulate the innate immune response, limiting inflammatory injury. We have previously demonstrated that Interleukin receptor-associated kinase (IRAK)-M, a member of the IRAK family that suppresses toll-like receptor/interleukin-1 signaling, is upregulated in the infarcted heart in both macrophages and fibroblasts, and restrains pro-inflammatory activation attenuating adverse remodeling...
December 2015: Journal of Molecular and Cellular Cardiology
P Fernandes, J MacSharry, T Darby, A Fanning, F Shanahan, A Houston, E Brint
The innate immune system is currently seen as the probable initiator of events which culminate in the development of inflammatory bowel disease (IBD) with Toll-like receptors (TLRs) known to be involved in this disease process. Many regulators of TLRs have been described, and dysregulation of these may also be important in the pathogenesis of IBD. The aim of this study was to perform a co-ordinated analysis of the expression levels of both key intestinal TLRs and their inhibitory proteins in the same IBD cohorts, both ulcerative colitis (UC) and Crohn's disease (CD), in order to evaluate the potential roles of these proteins in the pathogenesis of IBD...
March 2016: Clinical and Experimental Immunology
Sanica C Sakharwade, Arunika Mukhopadhaya
Porins can act as pathogen-associated molecular patterns, can be recognized by the host immune system and modulate immune responses. Vibrio choleraeporin OmpU aids in bacterial survival in the human gut by increasing resistance against bile acids and anti-microbial peptides. V. choleraeOmpU is pro-inflammatory in nature. However, interestingly, it can also down-regulate LPS-mediated pro-inflammatory responses. In this study, we have explored how OmpU-pretreatment affects LPS-mediated responses. Our study indicates that OmpU-pretreatment followed by LPS-activation does not induce M2-polarization of macrophages/monocytes...
December 2015: Molecular Immunology
Sunhyo Ryu, Andrew Johnson, Yoonkyung Park, Beomjoon Kim, David Norris, Cheryl A Armstrong, Peter I Song
Alpha-melanocyte stimulating hormone (α-MSH) is a highly conserved 13-aa neuropeptide derived from pro-opiomelanocortin by post-translational processing, which has been reported to exhibit potent anti-inflammatory activity and a wide range of immunosuppressive activities in the skin. However, the regulatory effect of α-MSH is not completely clear in cutaneous innate immunity. In this study, we investigate the functional regulation of α-MSH in TLR2-mediated inflammatory responses in normal human keratinocytes (HKs)...
2015: PloS One
Mark W Julian, Heather R Strange, Megan N Ballinger, Richard S Hotchkiss, Tracey L Papenfuss, Elliott D Crouser
OBJECTIVE: Immune suppression during critical illness predisposes to serious infections. We sought to determine the mechanisms regulating tolerance and cross-tolerance to common pro-inflammatory danger signals in a model that recapitulates the intact in vivo immune response. MATERIALS AND METHODS: Flt3-expanded splenocytes obtained from wild-type or matching IRAK-M knockout (IRAK-M-/-), C57BL/6, male mice (8-10 weeks old) were treated repeatedly or alternately with either LPS or CpGA DNA, agonists of Toll-like receptor (TLR)-4 and -9, respectively, over successive 24-hour periods...
2015: PloS One
Supriya Srivastav, Amrita Saha, Jayita Barua, Anindita Ukil, Pijush K Das
Intramacrophage protozoan parasite Leishmania donovani, causative agent of visceral leishmaniasis, escapes Toll-like receptor (TLR) dependent early host immune response by inducing the deubiquitinating enzyme A20, which is sustained up to 6 h postinfection only. Therefore, Leishmania must apply other means to deactivate late host responses. Here, we elucidated the role of IL-1 receptor-associated kinase M (IRAK-M), a negative regulator of TLR signaling, in downregulating macrophage proinflammatory response during late hours of in vitro infection...
October 2015: European Journal of Immunology
Tomoko Hayashi, Shiyin Yao, Brian Crain, Victor J Promessi, Luke Shyu, Caroline Sheng, McNancy Kang, Howard B Cottam, Dennis A Carson, Maripat Corr
Autoimmune diabetes mellitus (DM) results from the destruction of pancreatic islet cells by activated T lymphocytes, which have been primed by activated dendritic cells (DC). Individualized therapy with ex vivo DC manipulation and reinfusion has been proposed as a treatment for DM, but this treatment is limited by cost, and requires specialized facilities. A means of in situ modulation of the DC phenotype in the host would be more accessible. Here we report a novel innate immune modulator, 1Z1, generated by conjugating a TLR7 ligand to six units of polyethylene glycol (PEG), which skews DC phenotype in vivo...
2015: PloS One
Van Hieu Dong, Pang-Yan Tu, Pei-Chun Tsai, Yi-Hsin Lin, Hsiu-Luan Chang, Tsun-Yung Kuo, Ming-Tang Chiou, Chao-Nan Lin, Wen-Bin Chung
Pigs co-infected with porcine reproductive and respiratory syndrome virus (PRRSV) and porcine circovirus type 2 (PCV2) have been shown to develop more severe diseases than pigs infected with PRRSV or PCV2 only. The underlying interaction mechanisms between the two viruses in developing the disease are unclear. The present study investigates the mRNA expression of Toll-like receptor (TLR) signaling-related molecules in peripheral blood mononuclear cells from pigs infected with PRRSV or PCV2 or both. The mRNA expression levels were determined by quantitative real-time RT-PCR...
August 2015: Research in Veterinary Science
Jacqueline Neagos, Theodore J Standiford, Michael W Newstead, Xianying Zeng, Steven K Huang, Megan N Ballinger
To protect the host against exuberant inflammation and injury responses, cells have the ability to become hyporesponsive or "tolerized" to repeated stimulation by microbial and nonmicrobial insults. The lung airspace is constantly exposed to a variety of exogenous and endogenous Toll-like receptor (TLR) ligands, yet the ability of alveolar epithelial cells (AECs) to be tolerized has yet to be examined. We hypothesize that type II AECs will develop a tolerance phenotype upon repeated TLR agonist exposure. To test this hypothesis, primary AECs isolated from the lungs of mice and a murine AEC cell line (MLE-12) were stimulated with either a vehicle control or a TLR ligand for 18 hours, washed, then restimulated with either vehicle or TLR ligand for an additional 6 hours...
December 2015: American Journal of Respiratory Cell and Molecular Biology
Jintaek Im, Jung Eun Baik, Kyoung Whun Kim, Seok-Seong Kang, Jun Ho Jeon, Ok-Jin Park, Hyun Young Kim, Kee-Yeon Kum, Cheol-Heui Yun, Seung Hyun Han
Periodontitis is caused by multi-bacterial infection and Aggregatibacter actinomycetemcomitans and Enterococcus faecalis are closely associated with inflammatory periodontal diseases. Although lipopolysaccharide (LPS) of A. actinomycetemcomitans (Aa.LPS) and lipoteichoic acid of E. faecalis (Ef.LTA) are considered to be major virulence factors evoking inflammatory responses, their combinatorial effect on the induction of chemokines has not been investigated. In this study, we investigated the interaction between Aa...
August 2015: International Immunology
Han-Fei Huang, Zhong Zeng, Kun-Hua Wang, Hai-Yan Zhang, Shuai Wang, Wen-Xiang Zhou, Zhan-Bo Wang, Wang-Gang Xu, Jian Duan
AIM: To investigate the efficacy and molecular mechanisms of induced heme oxygenase (HO)-1 in protecting liver from warm ischemia/reperfusion (I/R) injury. METHODS: Partial warm ischemia was produced in the left and middle hepatic lobes of SD rats for 75 min, followed by 6 h of reperfusion. Rats were treated with saline, cobalt protoporphyrin (CoPP) or zinc protoporphyrin (ZnPP) at 24 h prior to the ischemia insult. Blood and samples of ischemic lobes subjected to ischemia were collected at 6 h after reperfusion...
March 14, 2015: World Journal of Gastroenterology: WJG
J Shiu, M B Piazuelo, H Ding, S J Czinn, M L Drakes, A Banerjee, N Basappa, K S Kobayashi, W F Fricke, T G Blanchard
Lymphoid tissue inducer (LTi) cells are activated by accessory cell IL-23, and promote lymphoid tissue genesis and antibacterial peptide production by the mucosal epithelium. We investigated the role of LTi cells in the gastric mucosa in the context of microbial infection. Mice deficient in IRAK-M, a negative regulator of TLR signaling, were investigated for increased LTi cell activity, and antibody mediated LTi cell depletion was used to analyze LTi cell dependent antimicrobial activity. H. pylori infected IRAK-M deficient mice developed increased gastric IL-17 and lymphoid follicles compared to wild type mice...
September 2015: Mucosal Immunology
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