The important role played by chemokines influence the clinical outcome of Helicobacter pylori infection

Jafarzadeh, Abdollah; Nemati, Maryam; Jafarzadeh, Sara

doi:10.1016/j.lfs.2019.116688

Cited by 31 publications

(38 citation statements)

References 181 publications

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“…Autoantibodies against proteins in the retina and/or the optic nerve, resulting from the possible molecular mimicry between H. pylori and ocular proteins, might be involved in glaucomatous neuropathy of the optic nerve [63,64]. More specifically, H. pylori antigens stimulate the production of specific antibodies which recognize homologous host protein sequences, such as in glycoproteins, heat-shock proteins (Hsps), H + /K + ATPase, H + /K + -adenosine triphosphatase, Human leukocyte antigens (HLA), chemokine receptors, Lewis antigens, and act as autoantibodies [58,[67][68][69][70]. In this regard, an example could be autoimmune gastritis, in which similarities of H + , K + -ATPase and bacterial epitopes may result in the production of antibodies against parietal cells, thereby suggesting that bacterial infection may be the trigger of an autoimmune mucosal inflammation resulting to mucosa atrophy in patients with chronic H. pylori gastritis [71].…”

Section: Discussionmentioning

confidence: 99%

Association between Active Helicobacter pylori Infection and Glaucoma: A Systematic Review and Meta-Analysis

et al. 2020

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Background: Glaucoma is the second most common cause of blindness worldwide affecting almost 70 million individuals. Helicobacter pylori (H. pylori) is a widespread pathogen with systematic pathogenicity. This meta-analysis aimed to estimate the contradictory data regarding a potential association between active H. pylori infection and glaucoma. Materials and Methods: A research in MEDLINE/PubMed and Google Scholar was conducted and original studies investigating the relationship between H. pylori infection and glaucoma were included. Analysis was performed with random effects model. The main outcome was the odds ratio (OR) with 95% confidence intervals (CI) of H. pylori infection as a risk factor for glaucoma. A parallel analysis studied the role of active infection as indicated by histology and the titer of anti-H. pylori antibodies. For the anti-H. pylori antibody titers, weighted mean differences (WMD) were estimated between patients and controls. Results: Fifteen studies were included, with 2664 participants (872 patients with glaucoma and 1792 controls), divided into primary open-angle glaucoma (POAG), normal tension glaucoma (NTG) and pseudo-exfoliation glaucoma (PEG). The association between H. pylori infection and overall glaucoma was significant (OR = 2.08, CI 95% 1.48–2.93) with moderate heterogeneity (I2 = 61.54%). After stratification by glaucoma subtype, heterogeneity was eliminated in the NTG subgroup. Studies with healthy controls, and controls with anemia yielded very low or no heterogeneity, respectively. Gastric biopsy to document active H. pylori infection yielded the highest OR (5.4, CI: 3.17–9.2, p < 0.001) and null heterogeneity. For anti-H. pylori antibody titers, there was a significant difference in WMD between patients and controls (WMD 15.98 IU/mL; 95% CI: 4.09–27.87; p = 0.008); values were greater in glaucoma patients, with high heterogeneity (I2: 93.8%). Meta-regression analysis showed that mean age had a significant impact on glaucoma (p = 0.037). Conclusions: Active H. pylori infection may be associated with glaucoma with null heterogeneity, as, beyond histology, quantified by anti-H. pylori titers and increases with age.

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Section: Discussionmentioning

confidence: 99%

Association between Active Helicobacter pylori Infection and Glaucoma: A Systematic Review and Meta-Analysis

et al. 2020

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“…It seems that pathological macrophages mainly derive from circulating monocytes that massively infiltrate the lungs and other organs rather than from tissue-resident macrophage populations. The targeting of monocyte/macrophage-attracting chemokines using small-molecule antagonists, neutralizing monoclonal antibodies and siRNA can modulate the monocyte/macrophage recruitment to the inflamed organ and prevent tissue injury [106]. The circulating CD14 + monocytes accumulate in inflamed tissues using the chemokine receptor CCR2 [107].…”

Section: Monocytes and Macrophages As Targets For Therapeutic Intervementioning

confidence: 99%

Contribution of monocytes and macrophages to the local tissue inflammation and cytokine storm in COVID-19: Lessons from SARS and MERS, and potential therapeutic interventions

et al. 2020

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The COVID-19-, SARS-and MERS-related coronaviruses share many genomic and structural similarities. However, the SARS-CoV-2 is less pathogenic than SARS-CoV and MERS-CoV. Despite some differences in the cytokine patterns, it seems that the cytokine storm plays a crucial role in the pathogenesis of COVID-19-, SARSand MERS. Monocytes and macrophages may be infected by SARS-CoV-2 through ACE2-dependent and ACE2independent pathways. SARS-CoV-2 can effectively suppress the anti-viral IFN response in monocytes and macrophages. Since macrophages and dendritic cells (DCs) act as antigen presenting cells (APCs), the infection of these cells by SARS-CoV-2 impairs the adaptive immune responses against the virus. Upon infection, monocytes migrate to the tissues where they become infected resident macrophages, allowing viruses to spread through all organs and tissues. The SARS-CoV-2-infected monocytes and macrophages can produce large amounts of numerous types of pro-inflammatory cytokines and chemokines, which contribute to local tissue inflammation and a dangerous systemic inflammatory response called cytokine storm. Both local tissue inflammation and the cytokine storm play a fundamental role in the development of COVID-19-related complications, such as acute respiratory distress syndrome (ARDS), which is a main cause of death in COVID-19 patients. Here, we describe the monocytes and macrophage responses during severe coronavirus infections, while highlighting potential therapeutic interventions to attenuate macrophage-related inflammatory reactions in possible approaches for COVID-19 treatment. 1. Introduction The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2)mediated COVID-19 has emerged during the late 2019 and caused a serious public health threat, forcing the WHO to announce the SARS-CoV-2 outbreak as a pandemic [1]. SARS-CoV-2, as a member of the coronavirus family, is an enveloped virus containing a positive-sense single-stranded RNA molecule

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“…Tumor necrosis factor (TNF)-α is considered to be an effective pro-inflammatory mediator, which promotes the expression of other inflammatory cytokines and adhesion molecules as well as increasing the apoptosis of vascular smooth muscle cells, thus promoting AS and plaque instability (9). Chemotactic factors are small molecule proteins that recruit leukocytes from circulation in the blood to inflammatory injury sites (10). In chronic inflammatory diseases such as AS, the binding of monocyte chemotactic protein (MCP)-1 and its receptor, C-C motif chemokine receptor-2, induces monocyte chemotaxis to the inflammatory site, leading to aggravation of the inflammatory response (11).…”

Section: Introductionmentioning

confidence: 99%

Curcumin affects ox‑LDL‑induced IL‑6, TNF‑α, MCP‑1 secretion and cholesterol efflux in THP‑1 cells by suppressing the TLR4/NF‑κB/miR33a signaling pathway

Zhong

Liu²,

Feng

et al. 2020

Exp Ther Med

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The aim of the present study was to study the molecular mechanism of how curcumin decreases the formation of ox-LDL induced human monocyte macrophage foam cells, promotes the efflux of cholesterol and reduces the secretion of inflammatory cytokines. In vitro cultured THP-1 cells were induced to become macrophages using phorbol-12-myristate-13-acetate. The cells were then pre-treated with curcumin before inducing the foam cell model by addition of oxidized low-density lipoprotein (ox-LDL). Western blot assays were used to detect expression levels of toll-like receptor (TLR)4, nuclear factor κB (NF-κB), NF-κB inhibitor α (IκBα), phosphorylated-IκBα and ATP binding cassette transporter (ABC)A1. Reverse transcription-quantitative PCR was employed to examine mRNA levels of TLR4, microRNA (miR)33a and ABCA1. ELISAs were used to detect inflammatory factors, including tumor necrosis factor (TNF)-α, monocyte chemotactic protein (MCP)-1 and interleukin (IL)-6. ox-LDL successfully induced the foam cell model, promoted phosphorylation of IκBα, promoted nuclear translocation of NF-κB, promoted the expression of TLR4 and miR33a, and promoted the secretion of TNF-α, MCP-1 and Il-6. Additionally, ox-LDL reduced the expression of ABCA1 and cholesterol efflux. However, pretreatment with curcumin increased the expression of ABCA1 and cholesterol efflux and suppressed secretion of TNF-α, MCP-1 and Il-6. TLR4 antibodies, the NF-κB blocker, PDTC, and the miR33a inhibitor also reduced the abnormal transformations induced by ox-LDL. Curcumin promoted cholesterol efflux by suppressing the TLR4/NF-κB/miR33a signaling pathway, and reduced the formation of foam cells and the secretion of inflammatory factors.

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The important role played by chemokines influence the clinical outcome of Helicobacter pylori infection

Cited by 31 publications

References 181 publications

Association between Active Helicobacter pylori Infection and Glaucoma: A Systematic Review and Meta-Analysis

Association between Active Helicobacter pylori Infection and Glaucoma: A Systematic Review and Meta-Analysis

Contribution of monocytes and macrophages to the local tissue inflammation and cytokine storm in COVID-19: Lessons from SARS and MERS, and potential therapeutic interventions

Curcumin affects ox‑LDL‑induced IL‑6, TNF‑α, MCP‑1 secretion and cholesterol efflux in THP‑1 cells by suppressing the TLR4/NF‑κB/miR33a signaling pathway

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