Role Of Nuclear Factor Kappa Research Articles

Targeting Nuclear Factor-Kappa B Signaling Pathway by Curcumin: Implications for the Treatment of Multiple Sclerosis.

Multiple sclerosis (MS) is a chronic inflammatory disease of the central nervous system, which involves an auto-immune mechanism that leads to perivascular demyelination. The role of nuclear factor-kappa B (NF-κB) signaling pathway in the pathogenesis of MS has been suggested by genome-wide association studies. Therefore, strategies targeting this pathway could be potentially beneficial. Curcumin is the active component of turmeric and a phenolic phytochemical. This phytochemical has anti-inflammatory properties and has been shown by multiple studies to downregulate NF-κB and its downstream gene targets including cyclooxygenase-2, tumor necrosis factor-α, interleukin-1, and interleukin-6. This review discusses the modulatory effects of curcumin on the NF-κB signaling pathway and its downstream effectors, and the therapeutic implications of this modulation on MS.

Role of Nuclear Factor Kappa B (NF-κB) Signalling in Neurodegenerative Diseases: An Mechanistic Approach.

A transcriptional regulatory nuclear factor kappa B (NF-KB) protein is a modulator of cellular biological activity via binding to a promoter region in the nucleus and transcribing various protein genes. The recent research implicated the intensive role of nuclear factor kappa B (NF-KB) in diseases like autoimmune disorder, inflammatory, cardiovascular and neurodegenerative diseases. Therefore, targeting the nuclear factor kappa B (NF-KB) protein offers a new opportunity as a therapeutic approach. Activation of IKB kinase/NF-KB signaling pathway leads to the development of various pathological conditions in human beings, such as neurodegenerative, inflammatory disorders, autoimmune diseases, and cancer. Therefore, the transcriptional activity of IKB kinase/NF-KB is strongly regulated at various cascade pathways. The nuclear factor NF-kB pathway plays a major role in the expression of pro-inflammatory genes, including cytokines, chemokines, and adhesion molecules. In response to the diverse stimuli, the cytosolic sequestered NF-KB in an inactivated form by binding with an inhibitor molecule protein (IkB) gets phosphorylated and translocated into the nucleus further transcribing various genes necessary for modifying various cellular functions. The various researches confirmed the role of different family member proteins of NF-KB implicated in expressing various genes products and mediating various cellular cascades. MicroRNAs, as regulators of NF- KB microRNAs play important roles in the regulation of the inflammatory process. Therefore, the inhibitor of NF-KB and its family members plays a novel therapeutic target in preventing various diseases. Regulation of NF- KB signaling pathway may be a safe and effective treatment strategy for various disorders.

Friedelin Protects Against Alveolar Epithelial Cells Apoptosis in Lps-Induced Acute Pneumonia in Neonatal Rats by Suppressing NF-κB Activation

Neonatal pneumonia is caused by inflammation mediated by lipopolysaccharide from gram negative bacteria. This type of pneumonia is characterized by inflammatory and apoptotic responses. In this study, we have examined the effect of friedelin on lipopolysaccharide-induced pneumonia and the role of nuclear factor kappa B in this process. Also, using the human pulmonary alveolar epithelial cells as a model we examined the effect of lipopolysaccharide on the cell apoptosis and its protection by friedelin. The results show that friedelin prevented lipopolysaccharide-induced acute pneumonia in neonatal rats and cellular apoptosis by suppressing the nuclear factor kappa B signaling pathway. In summary, this study shows that the friedelin exhibits a remarkable protective effect on lung tissues exposed to lipopolysaccharides.

Medicinal Plant Polyphenols Attenuate Oxidative Stress and Improve Inflammatory and Vasoactive Markers in Cerebral Endothelial Cells during Hyperglycemic Condition.

Blood-brain barrier endothelial cells are the main targets of diabetes-related hyperglycemia that alters endothelial functions and brain homeostasis. Hyperglycemia-mediated oxidative stress may play a causal role. This study evaluated the protective effects of characterized polyphenol-rich medicinal plant extracts on redox, inflammatory and vasoactive markers on murine bEnd3 cerebral endothelial cells exposed to high glucose concentration. The results show that hyperglycemic condition promoted oxidative stress through increased reactive oxygen species (ROS) levels, deregulated antioxidant superoxide dismutase (SOD) activity, and altered expression of genes encoding Cu/ZnSOD, MnSOD, catalase, glutathione peroxidase (GPx), heme oxygenase-1 (HO-1), NADPH oxidase 4 (Nox4), and nuclear factor erythroid 2-related factor 2 (Nrf2) redox factors. Cell preconditioning with inhibitors of signaling pathways highlights a causal role of nuclear factor kappa B (NFκB), while a protective action of AMP-activated protein kinase (AMPK) on redox changes. The hyperglycemic condition induced a pro-inflammatory response by elevating NFκB gene expression and interleukin-6 (IL-6) secretion, and deregulated the production of endothelin-1 (ET-1), endothelial nitric oxide synthase (eNOS), and nitric oxide (NO) vasoactive markers. Importantly, polyphenolic extracts from Antirhea borbonica, Ayapana triplinervis, Dodonaea viscosa, and Terminalia bentzoe French medicinal plants, counteracted high glucose deleterious effects by exhibiting antioxidant and anti-inflammatory properties. In an innovative way, quercetin, caffeic, chlorogenic and gallic acids identified as predominant plant polyphenols, and six related circulating metabolites were found to exert similar benefits. Collectively, these findings demonstrate polyphenol protective action on cerebral endothelial cells during hyperglycemic condition.

P53 vs NF-κB: the role of nuclear factor-kappa B in the regulation of p53 activity and vice versa.

The onco-suppressor p53 is a transcription factor that regulates a wide spectrum of genes involved in various cellular functions including apoptosis, cell cycle arrest, senescence, autophagy, DNA repair and angiogenesis. p53 and NF-κB generally have opposing effects in cancer cells. While p53 activity is associated with apoptosis induction, the stimulation of NF-κB has been demonstrated to promote resistance to programmed cell death. Although the transcription factor NF-κB family is considered as the master regulator of cancer development and maintenance, it has been mainly studied in relation to its ability to regulate p53. This has revealed the importance of the crosstalk between NF-κB, p53 and other crucial cell signaling pathways. This review analyzes the various mechanisms by which NF-κB regulates the activity of p53 and the role of p53 on NF-κB activity.

NF-κB "decoy" inhibits COX-2 expression in epileptic rat brain.

There is a need to investigate the role of nuclear factor kappa B in the regulation of cyclooxygenase-2 expression in the epileptic rat brain and cultured hippocampal neurons. Immunofluorescence and polymerase chain reaction was used to detect the expression of nuclear factor kappa B and cyclooxygenase-2. In cultured hippocampal neurons and rat brain: the control group compared with the normal group, nuclear factor kappa B expression in the hippocampal dentate gyrus, cerebral cortex, the piriform cortex brain regions were significantly increased (P < 0.01). This is accompanied by a significant increase in cyclooxygenase-2 protein and mRNA expressions in the hippocampus (P < 0.01). In the experimental group compared to the control group, the nuclear factor-kappa B expression in the hippocampal dentate gyrus, cerebral cortex, piriform cortex, and other brain regions was significantly lower (P < 0.01), with the accompanying decrease in cyclooxygenase-2 protein and mRNA expression (P < 0.01) in the hippocampus. In conclusion, κB-decoy can inhibit nuclear factor kappa B activation in epileptic rat brain and cyclooxygenase-2 overexpression.

Potential role of NF-κB pathway in the immuno-inflammatory responses during human cystic echinococcosis

Cystic echinococcosis (CE) induces in the human host innate and adaptive immune response that plays an important role in controlling the immunopathogenesis. Due to the crucial role of nuclear factor kappa B (NF-κB) in regulating immuno-inflammatory processes, we investigated its potential contribution in systemic and local immuno-inflammatory responses in primary CE patients and relapsed patients. The expression of NF-κB and inducible nitric oxide synthase (iNOS) was analyzed in peripheral blood mononuclear cells (PBMC) as well as in pericystic layer of pulmonary hydatid cysts from Algerian primary CE patients and relapsed patients. Tumor necrosis factor alpha (TNF-α) and nitric oxide (NO) production was evaluated in plasma samples. Our results showed high iNOS and NF-κB expression in both PBMCs and pericystic histiocytes from primary CE patients. In addition, substantial amounts of systemic NO and TNF-α were detected in the same patients. Remarkably, relapsed patients exhibited a low NF-κB and iNOS expression associated with low amounts of plasmatic TNF-α and NO. Collectively, NF-κB/iNOS pathway is involved in the host defense mechanisms at the systemic and local level during primary CE. Our results indicate that the inhibition of this pathway in relapsed patients will attenuate protective immunity and promote parasite escape. This study allowed to identify a novel predictive biomarkers of hydatidosis.

Role of nuclear factor-kappa B in feline injection site sarcoma

BackgroundChronic inflammation has been implicated in sarcomagenesis. Among various factors, activation of nuclear factor-kappa B (NF-κB) signaling pathway has been documented being able to target genes associated with tumor progression and up-regulate the expression of tumor-promoting cytokines and survival genes in several human solid tumors. Feline injection sites sarcomas (FISS) are malignant entities derived from the mesenchymal origin. The disease has been considered to be associated with vaccine adjuvant, aluminum, which serves as a stimulus continuously inducing overzealous inflammatory and immunologic reactions. To understand the contribution of NF-κB in FISS, detection of activated NF-κB in paraffin-embedded specimens, in vitro establishment of primary cells derived from FISS, and evaluation of the effects of the NF-κB inhibitor, dehydroxymethylepoxyquinomicin (DHMEQ), on primary tumor cells were conducted.ResultsIn this study, nuclear expression of NF-κB p65 was detected in 83.3% of FISS cases and not correlated with tumor grading, sex, and age. Primary cells derived from FISS in three cats exhibiting same immunohistochemical characteristics as their original tumor were successfully established. The NF-κB inhibitor, DHMEQ, was able to prevent nuclear translocation of NF-κB p65, inhibit cell proliferation, migration, and colonization in dosage-dependent manners, and induce cell apoptosis in these primary FISS cells.ConclusionsHigh expression rate of nuclear NF-κB p65 in FISS cases and dose-dependent inhibitory effects on the growth of FISS primary cells treated with NF-κB inhibitor suggested that NF-κB might be a potential molecular therapeutic target for FISS.

Research progress in the role of nuclear factor-kappa B in neuropathic pain

Chronic pain is a worldwide public health problem in which neuropathic pain (NP) caused by nerve damage is the most common chronic pain. At present, NP lacks effective treatment for any reason. In recent years, increasing studies have shown that neuroimmunity and neuroinflammation play a key role in mediating NP, and nuclear factor-kappa B (NF-κB) plays the most important role in the expression of pain inducers and effectors in the immune and inflammatory systems. NF-κB promotes transcriptional up-regulation by a promoter that links to a variety of inflammatory factors. Therefore, this paper reviews the research status of the role of NF-κB in NP. Key words: NF-κappa B; Neuralgia; Neuroimmunomodulation; Review

Refining the dermatological spectrum in primary immunodeficiency: mucosa‐associated lymphoid tissue lymphoma translocation protein 1 deficiency mimicking Netherton/Omenn syndromes

The proteinase mucosa-associated lymphoid tissue lymphoma translocation protein 1 (MALT1), which forms part of the caspase recruitment domain-containing protein 11-B-cell lymphoma 10-MALT1 signalosome complex, plays a direct role in nuclear factor kappa B activation. Here, we describe the case of a female infant with severe immune dysregulation leading to recurrent systemic infections, failure to thrive and severe crises of ichthyosiform erythroderma with high levels of serum IgE. Hence, initial symptoms indicated Netherton syndrome or Omenn syndrome. Surprisingly, sequence analyses of SPINK5 and RAG1/RAG2, respectively, excluded these diseases. During the hospital stay the patient's health deteriorated, despite intensive care therapy, and she died. In order to delineate the diagnosis, whole-exome sequencing was performed. Two compound heterozygous mutations in MALT1 were found and verified by Sanger sequencing (exon 2 c.245T>C, exon 2 c.310dup), which led to a MALT1 deficiency at the protein level. Based on these results, an immunological analysis was performed, as was immunofluorescence staining of key skin proteins, to confirm a diagnosis of MALT1 deficiency. This case report provides a closer description of the clinical and histological skin phenotype of MALT1 deficiency, and we conclude that MALT1 deficiency must be considered a possible differential diagnosis of Netherton and Omenn syndromes. What's already known about this topic? Mucosa-associated lymphoid tissue lymphoma translocation protein 1 (MALT1) deficiency is a combined immunodeficiency. MALT1 is part of the caspase recruitment domain-containing protein 11-B-cell lymphoma 10-MALT1 signalosome complex, which is essential for nuclear factor kappa B activation. Current publications describe a phenotype of recurrent systemic infections; only in a few cases has an inflammatory involvement of the integument been described. What does this study add? A closer description of the cutaneous phenotype of MALT1 deficiency in a patient with two novel MALT1 mutations. Immune mapping of follicular epidermis shows lympho-epithelial Kazal-type-related inhibitor is reduced in MALT1 deficiency and absent on interfollicular staining. Clinically, MALT1 deficiency mimics Netherton syndrome and Omenn syndrome, and should be considered a differential diagnosis.

The NF-KB pathway and endocrine therapy resistance in breast cancer

Breast cancer is a heterogeneous disease, which over time acquires various adaptive changes leading to more aggressive biological characteristics and development of treatment resistance. Several mechanisms of resistance have been established; however, due to the complexity of oestrogen receptor (ER) signalling and its crosstalk with other signalling networks, various areas still need to be investigated. This article focusses on the role of nuclear factor kappa B (NF-KB) as a key link between inflammation and cancer and addresses its emerging role as a key player in endocrine therapy resistance. Understanding the precise mechanism of NF-KB-driven endocrine therapy resistance provides a possible opportunity for therapeutic intervention.

Роль ядерного фактора каппа-В (NF-kB) в патогенезе рака легкого

Роль ядерного фактора каппа-В (NF-kB) в патогенезе рака легкого

The role of NF-κB-mediated JNK pathway in cognitive impairment in a rat model of sleep apnea.

The aim of this study is to determine the role of nuclear factor kappa B (NF-κB)-mediated c-Jun N-terminal kinase (JNK) pathway in cognitive impairment induced by chronic intermittent hypoxia (CIH). Ninety-six male Sprague-Dawley rats were randomly divided into 8 groups: sham group, sustained hypoxia (SH) group, CIH group, CIH + melatonin group, CIH + vitamin E group, CIH + DMSO group, CIH + BAY 11-7082 group and CIH + normal saline (NS) group. Rats were exposed to normoxia, CIH (21% O2 for 60 s and 10% O2 for 60 s, cyclically repeated for 10 h/day) or SH (10% O2 for 10 h/day) for 14 days. Afterwards, Morris water maze test was conducted, and serum and hippocampus tissues were subjected to molecular biological and biochemical analyses. Compared with the Sham and SH group, oxidative stress was induced by CIH in rat hippocampus with the high level of malondialdehyde (MDA) and 8-iso-PGF2α and the low level of superoxide dismutase (SOD) and glutathione (GSH). Activated NF-κB and its downstream products including tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6) and inducible nitric oxide synthase (iNOS) were highly expressed in CIH rats. These changes were attenuated by pretreatment of the rats with melatonin and vitamin E. CIH also resulted in hippocampus neuron apoptosis with increased caspase 3 level, dUIP nick end labeling (TUNEL)-positive neurons number and cognitive impairment verified by prolonged latency and shortened time in the target quadrant in Morris water maze test. JNK and its downstream transcriptional factors including c-Jun, activating transcription factor 2 (ATF2), and JunD were all significantly phosphorylated in CIH rats. However, pretreatment of NF-κB inhibitor BAY 11-7082 inhibited the activation of NF-κB under CIH condition and also significantly reduced the phosphorylation of JNK as well as c-Jun, ATF2, and JunD. Moreover, hippocampus neuron apoptosis and cognitive impairment were significantly improved with the pretreatment of BAY 11-7082 in rats subjected to CIH. These findings suggest that NF-κB-mediated JNK pathway is at least partially implicated in CIH-induced hippocampus neuron apoptosis and cognitive impairment. Inhibition of NF-κB activation provided a therapeutic potential for cognitive impairment in sleep apnea (SA).

Role of nuclear factor kappa B in cognitive decline in aged mice with sepsis

Objective To evaluate the role of nuclear factor kappa B (NF-κB) in cognitive decline in aged mice with sepsis. Methods Forty-five SPF healthy aged female C57BL/6 mice, aged 10-12 months, weighing 20-30 g, were assigned into 3 groups (n=15 each) using a random number table: control group (group C), sepsis group (group Sep)and NF-κB selective inhibitor pyrrolidine dithiocarbamate (PDTC) group (group PDTC). Lipopolysaccharide 250 μg/kg was injected intraperitoneally once a day for 7 consecutive days in Sep and PDTC groups, and in addition PDTC 50 mg/kg was injected intraperitoneally at 30 min before lipopolysaccharide injection once a day for 7 consecutive days in group PDTC.The equal volume of normal saline was given in group C. Five mice in each group were sacrificed at 2 h after the last administration, cardiac puncture was performed and blood samples were collected, and then the mice were sacrificed and hippocampi were harvested for determination of the levels of tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β) and IL-6 in plasma and hippocampal tissues using enzyme-linked immunosorbent assay.Cognitive function was assessed using open field, elevated plus maze and Morris water maze tests at 24 h after the last administration in the other mice left in each group. Results Compared with group C, the levels of TNF-α, IL-1β and IL-6 in plasma and hippocampal tissues were significantly increased, the time of movement at the central region was shortened, the percentage of time spent in the open arms and number of entries into the open and closed arms were decreased, the escape latency was prolonged, the time of staying at the original platform quadrant was shortened, and the frequency of crossing the platform was decreased in group Sep (P<0.05). Compared with group Sep, the levels of TNF-α, IL-1β and IL-6 in plasma and hippocampal tissues were significantly decreased, the time of movement at the central region was prolonged, the percentage of time spent in the open arms and number of entries into the open and closed arms were increased, the escape latency was shortened, and the time of staying at the original platform quadrant was prolonged in group PDTC (P<0.05). Conclusion NF-κB is involved in cognitive decline in aged mice with sepsis. Key words: NF-kappa B; Sepsis; Cognition disorders; Aged

Survival of Cancer Stem-Like Cells Under Metabolic Stress via CaMK2α-mediated Upregulation of Sarco/Endoplasmic Reticulum Calcium ATPase Expression.

Purpose: Cancer cells grow in an unfavorable metabolic milieu in the tumor microenvironment and are constantly exposed to metabolic stress such as chronic nutrient depletion. Cancer stem-like cells (CSC) are intrinsically resistant to metabolic stress, thereby surviving nutrient insufficiency and driving more malignant tumor progression. In this study, we aimed to demonstrate the potential mechanisms by which CSCs avoid Ca2+-dependent apoptosis during glucose deprivation.Experimental Design: We investigated cell viability and apoptosis under glucose deprivation, performed genome-wide transcriptional profiling of paired CSCs and parental cells, studied the effect of calcium/calmodulin-dependent protein kinase 2 alpha (CaMK2α) gene knockdown, and investigated the role of nuclear factor kappa B (NFκB) in CSCs during time-dependent Ca2+-mediated and glucose deprivation-induced apoptosis. We also observed the effect of combined treatment with 2-deoxy-d-glucose, a metabolic inhibitor that mimics glucose deprivation conditions in mouse xenograft models, and thapsigargin, a specific inhibitor of sarco/endoplasmic reticulum Ca2+-ATPase (SERCA).Results: We demonstrated the coordinated upregulation of SERCA in CSCs. SERCA, in turn, is transcriptionally regulated by CaMK2α via NFκB activation. Combined treatment with 2-deoxy-d-glucose and thapsigargin, a specific inhibitor of SERCA, significantly reduced tumor growth compared with that in untreated control animals or those treated with the metabolic inhibitor alone.Conclusions: The current study provides compelling evidence that CaMK2α acts as a key antiapoptosis regulator in metabolic stress-resistant CSCs by activating NFκB. The latter induces expression of SERCA, allowing survival in glucose-deprived conditions. Importantly, our combination therapeutic strategy provides a novel approach for the clinical application of CSC treatment. Clin Cancer Res; 24(7); 1677-90. ©2017 AACR.

Inhaled Cryptococcus neoformans elicits allergic airway inflammation independent of Nuclear Factor Kappa B signalling in lung epithelial cells.

Pulmonary challenge with the ubiquitous fungus Cryptococcus neoformans results in allergic airway inflammation (AAI) characterized by robust recruitment of eosinophils and T cells producing type 2 cytokines to the lungs. Previous studies have demonstrated a critical role for Nuclear Factor Kappa B (NF-κB) activation within lung epithelial cells (LECs) in driving AAI in response to protein allergens, yet the role of LEC-intrinsic NF-κB in promoting AAI following exposure to C. neoformans is poorly understood. To investigate the role of LEC-intrinsic NF-κB in promoting AAI following C. neoformans challenge, we used IKK∆LEC mice, which lack canonical NF-κB activation specifically within LECs. IKK∆LEC and littermate control mice were intranasally challenged with 106 CFU of C. neoformans strain 52D, and lung tissues were collected at 7, 14 and 21 days post infection to assess the development of AAI. Notably, the absence of epithelial NF-κB signalling did not affect the magnitude or kinetics of lung eosinophilia when compared with the response in wild-type control mice. The total numbers of lung T cells producing the type 2 cytokines interleukin-5 and interleukin-13 were also unchanged in IKK∆LEC mice. Furthermore, IKK∆LEC mice showed no defect in the recruitment of protective interferon-γ-producing CD4 T cells to the lungs, fungal clearance, or host survival compared with control mice. Immunofluorescence imaging surprisingly revealed no evidence of nuclear localization of NF-κB in LECs in response to C. neoformans challenge, indicating that NF-κB is not activated within these cells. Taken together, these data strongly suggest that NF-κB signalling within LECs does not promote AAI observed in response to C. neoformans.

The role of Nuclear Factor-kappa B signaling in human cervical cancer.

Background The Nuclear Factor kappaB (NF-kB) family consists of transcription factors that play a complex and essential role in the regulation of immune responses and inflammation. NF-kB has recently generated considerable interest as it has been implicated in human cancer initiation, progression and resistance to treatment. In the present comprehensive review the different aspects of NF-kB signaling in the carcinogenesis of cancer of the uterine cervix are discussed. NF-kB functions as part of a network, which determines the pattern of its effects on the expression of several other genes (such as crosstalks with reactive oxygen species, p53, STAT3 and miRNAS) and thus its function. Activation of NF-kB triggered by a HPV infection is playing an important role in the innate and adaptive immune response of the host. The virus induces down regulation of NF-kB to liquidate the inhibitory activity for its replication triggered by the immune system leading a status of persistant HPV infection. During the progression to high grade intraepithelial neoplasia and cervical cancer NF-KB becomes constitutionally activated again. Mutations in NF-kB genes are rare in solid tumors but mutations of upstream signaling molecules such as RAS, EGFR, PGF, HER2 have been implicated in elevated NF-kB signaling. NF-kB can stimulate transcription of proliferation regulating genes (eg. cyclin D1 and c-myc), genes involved in metastasis, VEGF dependent angiogenesis and cell immortality by telomerase. NF-kB activation can also induce the expression of activation-induced cytodine deaminase (AID) and the APOBEC proteins, providing a mechanistic link between the NF-kB pathway and mutagenic characteristic of cervical cancer. Inhibition of NF-kB has the potential to be used to reverse resistance to radiotherapy and systemic anti-cancer medication, but currently no clinicaly active NF-kB targeting strategies are available.

The role of nuclear factor kappa B and helicobacter pylori associated protein A in the pathogenesis of idiopathic thrombocytopenic purpura

Objective To detect and analyze nuclear factor kappa B (NF-κB), Helicobacter pylori (HP), Helicobacter pylori cytotoxin associated protein A (CagA), platelet (PLT) and platelet associated IgG (PA IgG) in 224 patients with idiopathic thrombocytopenic purpur(ITP) from three urban hospitals of Shaoxing, in order to explore the role of NF-κB and CagA in the pathogenesis of ITP, then to improve the prognosis of ITP. Methods SABC method was used to detect the NF-κB, 13C breath test for the determination of the Hp infection.CagA and PA-IgG were tested by enzyme linked immunosorbent assay.Automatic blood cell analyzer was used to measure PLT.According to the test results, the patients were divided into Hp+ cagA+ NF-κB+ , Hp+ cagA+ NF-κB-, Hp+ cagA-NF-κB+ , Hp+ cagA-NF-κB-, Hp-NF-κB+ , Hp-NF-κB-PLT groups, and PA-IgG, PLT of the six groups were statistically analyzed. Results Of 224 cases with ITP, 175 cases of HP positive, the positive rate was 78.13%.CagA+ 91 cases in 175 cases of Hp+ , accounting for 52%, overall 43.63%.NF-kappa B+ 108 cases, the positive rate was 46.21%, 78 cases were found in Hp+ cagA+ , accounting for 85.71% in cagA+ .In 84 cases of Hp+ cagA-, there were 21 cases NF-κB+ , the positive rate was 25%.In 49 of HP-, 9 cases with NF-kappa B+ , accounting for 18.37%.PLT and PA-IgG were compared among the groups.The count of PLT of group Hp+ , group Hp+ cagA+ and group NF-κB+ was lower than group Hp-, group Hp+ cagA- and group NF-κB-.However, the level of PA-IgG of group Hp+ , group Hp+ cagA+ and group NF-κB+ was higher than group Hp-, group Hp+ cagA- and group NF-κB-, the difference was statistically significant(P<0.05). Conclusion CagA maybe directly or through the activation of NF-kappa B take part in the immune response of ITP, cause PA-IgG increased and thrombocytopenia. Key words: Helicobacter pylori; Cytotoxin-associated protein; Nuclear factor-kappa B; Purpur, thrombocytopenic

Role of nuclear factor kappa- b (nf-kb) and its interactionWith hsamicrorna 146A in esophageal cancer

Role of nuclear factor kappa- b (nf-kb) and its interactionWith hsamicrorna 146A in esophageal cancer

Shall we blame CD4 T cells for everything?

Persistent inflammatory conditions in the liver promote chronic liver damage and liver fibrosis ultimately leading to hepatocellular carcinoma (HCC). Multiple cytokines have been investigated in the context of acute and chronic liver damage. Interleukin 17 (IL-17) is a proinflammatory cytokine produced by a subset of CD4 T cells (T helper 17 (Th17) cells). IL-17 recruits other immune cells such as monocytes and neutrophils to the site of inflammation in response to invasion by pathogens. It can promote inflammation and has been linked to various autoimmune disorders.1 In the liver, Th17 responses have been shown in non-alcoholic steatohepatitis, cholestatic liver diseases, liver fibrosis and antimicrobial defences.2 In this issue, Nadine Kuttkat from the Trautwein group investigated Th17 cells in a murine model of liver injury and HCC development.3 Following a previous report on the role of nuclear factor-kappa B (NF-κB) signalling events in hepatocytes using liver parenchymal cell-specific Nemo knockout (NemoLPC-KO or NemoΔHep) mice that develop steatohepatitis followed …