Association between HMGB1 and asthma: a literature review

Imbalzano, Egidio; Quartuccio, S.; Salvo, Eleonora Di; Créa, T.; Casciaro, Marco; Gangemi, Sebastiano

doi:10.1186/s12948-017-0068-1

Cited by 52 publications

(45 citation statements)

References 37 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Our cytokine/chemokine data were consistent with previous findings that periostin can be upregulated in severe asthmatics [ 45 , 46 , 47 , 48 , 49 ]. The importance of RAGE in allergic inflammation has been demonstrated in animal models [ 50 , 51 , 52 ] and single-nucleotide polymorphisms (SNPs) in RAGE were identified in patients with poor lung function [ 53 , 54 ], suggesting that higher levels of RAGE may either be a direct correlate or a proxy for asthma severity.…”

Section: Discussionsupporting

confidence: 92%

Questioning Cause and Effect: Children with Severe Asthma Exhibit High Levels of Inflammatory Biomarkers Including Beta-Hexosaminidase, but Low Levels of Vitamin A and Immunoglobulins

et al. 2020

View full text Add to dashboard Cite

Asthma affects over 8% of the pediatric population in the United States, and Memphis, Tennessee has been labeled an asthma capital. Plasma samples were analyzed for biomarker profiles from 95 children with severe asthma and 47 age-matched, hospitalized nonasthmatic controls at Le Bonheur Children’s Hospital in Memphis, where over 4000 asthmatics are cared for annually. Asthmatics exhibited significantly higher levels of periostin, surfactant protein D, receptor for advanced glycation end products and β-hexosaminidase compared to controls. Children with severe asthma had lower levels of IgG1, IgG2 and IgA, and higher levels of IgE compared to controls, and approximately half of asthmatics exhibited IgG1 levels that were below age-specific norms. Vitamin A levels, measured by the surrogate retinol-binding protein, were insufficient or deficient in most asthmatic children, and correlated positively with IgG1. Which came first, asthma status or low levels of vitamin A and immunoglobulins? It is likely that inflammatory disease and immunosuppressive drugs contributed to a reduction in vitamin A and immunoglobulin levels. However, a nonmutually exclusive hypothesis is that low dietary vitamin A caused reductions in immune function and rendered children vulnerable to respiratory disease and consequent asthma pathogenesis. Continued attention to nutrition in combination with the biomarker profile is recommended to prevent and treat asthma in vulnerable children.

show abstract

Section: Discussionsupporting

confidence: 92%

Questioning Cause and Effect: Children with Severe Asthma Exhibit High Levels of Inflammatory Biomarkers Including Beta-Hexosaminidase, but Low Levels of Vitamin A and Immunoglobulins

et al. 2020

View full text Add to dashboard Cite

show abstract

“…HMGB1‐TLR4 interplay drives clinical conditions such as sepsis, arthritis , cancer and potentially asthma (reviewed by Imbalzano et al . ). S100 proteins are another type of endogenous proteins with various intracellular functions, but which also act as DAMPs when excreted in the extracellular milieu.…”

Section: Endogenous Triggersmentioning

confidence: 97%

“…It has been shown to lead to calcium mobilization and increases the excitability of primary DRG neurons [221], driving pain hypersensitivity [222][223][224]. HMGB1-TLR4 interplay drives clinical conditions such as sepsis, arthritis [225,226], cancer [227,228] and potentially asthma [229][230][231] (reviewed by Imbalzano et al [232]). S100 proteins are another type of endogenous proteins with various intracellular functions, but which also act as DAMPs when excreted in the extracellular milieu.…”

Section: Dampsmentioning

confidence: 99%

Profiling of how nociceptor neurons detect danger – new and old foes

et al. 2019

View full text Add to dashboard Cite

The host evolves redundant mechanisms to preserve physiological processing and homeostasis. These functions range from sensing internal and external threats, creating a memory of the insult and generating reflexes, which aim to resolve inflammation. Impairment in such functioning leads to chronic inflammatory diseases. By interacting through a common language of ligands and receptors, the immune and sensory nervous systems work in concert to accomplish such protective functions. Whilst this bidirectional communication helps to protect from danger, it can contribute to disease pathophysiology. Thus, the somatosensory nervous system is anatomically positioned within primary and secondary lymphoid tissues and mucosa to modulate immunity directly. Upstream of this interplay, neurons detect danger, which prompts the release of neuropeptides initiating (i) defensive reflexes (ranging from withdrawal response to coughing) and (ii) chemotaxis, adhesion and local infiltration of immune cells. The resulting outcome of such neuro‐immune interplay is still ill‐defined, but consensual findings start to emerge and support neuropeptides not only as blockers of TH1‐mediated immunity but also as drivers of TH2 immune responses. However, the modalities detected by nociceptors revealed broader than mechanical pressure and temperature sensing and include signals as various as cytokines and pathogens to immunoglobulins and even microRNAs. Along these lines, we aggregated various dorsal root ganglion sensory neuron expression profiling datasets supporting such wide‐ranging sensing capabilities to help identifying new danger detection modalities of these cells. Thus, revealing unexpected aspects of nociceptor neuron biology might prompt the identification of novel drivers of immunity, means to resolve inflammation and strategies to safeguard homeostasis.

show abstract

“…High-mobility group box 1 (HMGB1) is synthesized and secreted by activated immunocytes, such as monocytes and macrophages, and has been considered as one of the important inflammatory inducers. After binding with receptor for advanced glycation end products (RAGE), HMGB1 activates the nuclear factor κB signaling [ 7 ]. Thus, the expression levels pro-inflammatory cytokines including tumor necrosis factor α (TNFα), interleukin 6 (IL6), and transforming growth factor β1 (TGFβ1) are upregulated [ 8 – 10 ].…”

Section: Introductionmentioning

confidence: 99%

Curcumin Attenuates Pulmonary Inflammation in Lipopolysaccharide Induced Acute Lung Injury in Neonatal Rat Model by Activating Peroxisome Proliferator-Activated Receptor γ (PPARγ) Pathway

Cheng¹,

Yang²,

Hu³

et al. 2018

Med Sci Monit

View full text Add to dashboard Cite

BackgroundThis study aimed to investigate the therapeutic effect of curcumin in lipopolysaccharide (LPS) induced neonatal acute lung injury (ALI) and the possibly associated molecular mechanisms.Material/MethodsALI neonatal animal model was established by using LPS. Curcumin and/or peroxisome proliferator-activated receptor γ (PPARγ) inhibitor BADGE (bisphenol A diglycidyl ether) were administrated to animals. Lung edema was evaluated by PaO2 and lung wet/dry weight ratio (W/D) measurements. EMSA was used to determine the PPARγ activity. Levels of high-mobility group box 1 (HMGB1), secretory receptor for advanced glycation end products (RAGE), tumor necrosis factor α (TNFα), interleukin 6 (IL6), and transforming growth factor β1 (TGFβ1) in bronchoalveolar lavage fluid (BALF) were examined by ELISA. Western blotting was used to evaluate the expression levels of HMGB1, RAGE, heme oxygenase 1 (HO1), TNFα, IL6, and TGFβ1 in lung tissue.ResultsCurcumin administration significantly improved lung function by increasing PaO2 and decreasing W/D in neonatal ALI rats. Curcumin treatment upregulated the PPARγ activity and expression level of HO1 which were suppressed in lung tissue of neonatal ALI rats. Elevated levels of HMGB1, RAGE, TNFα, IL6, and TGFβ1 in both lung tissue and BALF from neonatal ALI rats were decreased dramatically by curcumin treatment. PPARγ inhibitor BADGE administration impaired curcumin’s alleviation on lung edema, inhibitory effects on inflammatory cytokine expression and recovery of PPARγ/HO1 signaling activation.ConclusionsCurcumin alleviated lung edema in LPS-induced ALI by inhibiting inflammation which was induced by PPARγ/HO1 regulated-HMGB1/RAGE pro-inflammatory pathway.

show abstract

Association between HMGB1 and asthma: a literature review

Cited by 52 publications

References 37 publications

Questioning Cause and Effect: Children with Severe Asthma Exhibit High Levels of Inflammatory Biomarkers Including Beta-Hexosaminidase, but Low Levels of Vitamin A and Immunoglobulins

Questioning Cause and Effect: Children with Severe Asthma Exhibit High Levels of Inflammatory Biomarkers Including Beta-Hexosaminidase, but Low Levels of Vitamin A and Immunoglobulins

Profiling of how nociceptor neurons detect danger – new and old foes

Curcumin Attenuates Pulmonary Inflammation in Lipopolysaccharide Induced Acute Lung Injury in Neonatal Rat Model by Activating Peroxisome Proliferator-Activated Receptor γ (PPARγ) Pathway

Contact Info

Product

Resources

About