“…Their function is to “alert” the immune system by activating the “inflammasome” through the interaction with the pattern recognition receptors (PRRs) situated on the plasma membrane, inside endosomes after endocytosis and in the cytosol (i.e. toll-like receptors), advanced glycosylation end product-specific receptor RAGE (receptor for advanced glycation end products), RIG-I-like receptors, NOD1-like receptors, and AIM2-like receptors [9, 10]. HMGB-1 in the nucleus play different roles such as DNA replication, repair, recombination, transcription, apoptosis and it have also genomic stability.…”
Section: Discussionmentioning
confidence: 99%
“…HMGB1 (also known as HMG1, HMG-1, HMG 1, amphoterin, p30) is the most frequently expressed of the entire HMG family proteins [5]. Recently, some studies demonstrated that HMGB1, as proinflammatory mediator belonging to the alarmin family, has a key role in different acute and chronic immune disorders [6–10]. …”
BackgroundRecently, some studies demonstrated that HMGB1, as proinflammatory mediator belonging to the alarmin family, has a key role in different acute and chronic immune disorders. Asthma is a complex disease characterised by recurrent and reversible airflow obstruction associated to airway hyper-responsiveness and airway inflammation.ObjectiveThis literature review aims to analyse advances on HMGB1 role, employment and potential diagnostic application in asthma.MethodsWe reviewed experimental studies that investigated the pathogenetic role of HMGB in bronchial airway hyper-responsiveness, inflammation and the correlation between HMGB1 level and asthma.ResultsA total of 19 studies assessing the association between HMGB1 and asthma were identified.ConclusionsWhat emerged from this literature review was the confirmation of HMGB-1 involvement in diseases characterised by chronic inflammation, especially in pulmonary pathologies. Findings reported suggest a potential role of the alarmin in being a stadiation method and a marker of therapeutic efficacy; finally, inhibiting HMGB1 in humans in order to contrast inflammation should be the aim for future further studies.
“…Their function is to “alert” the immune system by activating the “inflammasome” through the interaction with the pattern recognition receptors (PRRs) situated on the plasma membrane, inside endosomes after endocytosis and in the cytosol (i.e. toll-like receptors), advanced glycosylation end product-specific receptor RAGE (receptor for advanced glycation end products), RIG-I-like receptors, NOD1-like receptors, and AIM2-like receptors [9, 10]. HMGB-1 in the nucleus play different roles such as DNA replication, repair, recombination, transcription, apoptosis and it have also genomic stability.…”
Section: Discussionmentioning
confidence: 99%
“…HMGB1 (also known as HMG1, HMG-1, HMG 1, amphoterin, p30) is the most frequently expressed of the entire HMG family proteins [5]. Recently, some studies demonstrated that HMGB1, as proinflammatory mediator belonging to the alarmin family, has a key role in different acute and chronic immune disorders [6–10]. …”
BackgroundRecently, some studies demonstrated that HMGB1, as proinflammatory mediator belonging to the alarmin family, has a key role in different acute and chronic immune disorders. Asthma is a complex disease characterised by recurrent and reversible airflow obstruction associated to airway hyper-responsiveness and airway inflammation.ObjectiveThis literature review aims to analyse advances on HMGB1 role, employment and potential diagnostic application in asthma.MethodsWe reviewed experimental studies that investigated the pathogenetic role of HMGB in bronchial airway hyper-responsiveness, inflammation and the correlation between HMGB1 level and asthma.ResultsA total of 19 studies assessing the association between HMGB1 and asthma were identified.ConclusionsWhat emerged from this literature review was the confirmation of HMGB-1 involvement in diseases characterised by chronic inflammation, especially in pulmonary pathologies. Findings reported suggest a potential role of the alarmin in being a stadiation method and a marker of therapeutic efficacy; finally, inhibiting HMGB1 in humans in order to contrast inflammation should be the aim for future further studies.
“…Additional complexity is added by their role in pathogen-induced inflammation, generally believed to be exclusively caused by PAMPs. Evidence accumulates for DAMPs to represent essential triggers during immunity against invading microbes, not limited to bacteria, but also including viruses (104,225,279,406,559,637). Recent data support this hypothesis.…”
When cells undergo necrotic cell death in either physiological or pathophysiological settings in vivo, they release highly immunogenic intracellular molecules and organelles into the interstitium and thereby represent the strongest known trigger of the immune system. With our increasing understanding of necrosis as a regulated and genetically determined process (RN, regulated necrosis), necrosis and necroinflammation can be pharmacologically prevented. This review discusses our current knowledge about signaling pathways of necrotic cell death as the origin of necroinflammation. Multiple pathways of RN such as necroptosis, ferroptosis, and pyroptosis have been evolutionary conserved most likely because of their differences in immunogenicity. As the consequence of necrosis, however, all necrotic cells release damage associated molecular patterns (DAMPs) that have been extensively investigated over the last two decades. Analysis of necroinflammation allows characterizing specific signatures for each particular pathway of cell death. While all RN-pathways share the release of DAMPs in general, most of them actively regulate the immune system by the additional expression and/or maturation of either pro- or anti-inflammatory cytokines/chemokines. In addition, DAMPs have been demonstrated to modulate the process of regeneration. For the purpose of better understanding of necroinflammation, we introduce a novel classification of DAMPs in this review to help detect the relative contribution of each RN-pathway to certain physiological and pathophysiological conditions.
“…In addition, the infection caused an increase of the high mobility group box 1 (HMGB1) protein level as seen in lung tissue. TLRs signaling pathway can be activated by HMGB1 which belongs to the damage associated molecular patterns (DAMPs) [28] . We found an increase of TLR4 expression in lung of the infected mice.…”
Houttuynia cordata polysaccharide (HCP) is extracted from Houttuynia cordata, a key traditional Chinese medicine. The study was to investigate the effects of HCP on intestinal barrier and microbiota in H1N1 virus infected mice. Mice were infected with H1N1 virus and orally administrated HCP at a dosage of 40 mgkg -1 d -1 . H1N1 infection caused pulmonary and intestinal injury and gut microbiota imbalance. HCP significantly suppressed the expression of hypoxia inducible factor-1α and decreased mucosubstances in goblet cells, but restored the level of zonula occludens-1 in intestine. HCP also reversed the composition change of intestinal microbiota caused by H1N1 infection, with significantly reduced relative abundances of Vibrio and Bacillus, the pathogenic bacterial genera. Furthermore, HCP rebalanced the gut microbiota and restored the intestinal homeostasis to some degree. The inhibition of inflammation was associated with the reduced level of Toll-like receptors and interleukin-1β in intestine, as well as the increased production of interleukin-10. Oral administration of HCP alleviated lung injury and intestinal dysfunction caused by H1N1 infection. HCP may gain systemic treatment by local acting on intestine and microbiota. This study proved the high-value application of HCP.[KEY WORDS] H1N1 influenza virus; Houttuynia cordata; Inflammation; Intestinal Barrier; Microbiota; Polysaccharide [CLC Number] R965 [Document code] A [Article ID] 2095-6975(2019)03-0187-11 Δ These authors contributed to the work equally. These authors have no conflict of interest to declare. Published by Elsevier B.V. All rights reserved
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