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TRIF Deficiency does not Affect Severity of Ovalbumin-induced Airway Inflammation in Mice.

Tae Hyoun KIM ; Dong Jae KIM ; Jae Hak PARK ; Jong Hwan PARK

Immune Network.2014;14(5):249-254. doi:10.4110/in.2014.14.5.249

Allergic asthma is a chronic pulmonary inflammatory disease characterized by reversible airway obstruction, hyperresponsiveness and eosinophils infiltration. Toll-like receptors (TLRs) signaling are closely associated with asthma and have emerged as a novel therapeutic target in allergic disease. The functions of TLR3 and TLR4 in allergic airway inflammation have been studied; however, the precise role of TIR-domain-containing adapter-inducing interferon-beta (TRIF), the adaptor molecule for both TLR3 and TLR4, is not yet fully understood. To investigate this, we developed a mouse model of OVA-induced allergic airway inflammation and compared the severity of allergic airway inflammation in WT and TRIF-/- mice. Histopathological assessment revealed that the severity of inflammation in airway inflammation in TRIF-deficient mice was comparable to that in WT mice. The total number of cells recovered from bronchoalveolar lavage fluid did not differ between WT and TRIF-deficient mice. Moreover, TRIF deficiency did not affect Th1 and Th2 cytokine production in lung tissue nor the level of serum OVA-specific IgE, IgG1 and IgG2c. These findings suggest that TRIF-mediated signaling may not be critical for the development of allergic airway inflammation.
Airway Obstruction ; Animals ; Asthma ; Bronchoalveolar Lavage Fluid ; Eosinophils ; Immunoglobulin E ; Immunoglobulin G ; Inflammation* ; Interferon-beta ; Lung ; Mice* ; Toll-Like Receptors

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5-aminoimidazole-4-carboxamide Riboside Induces Apoptosis Through AMP-activated Protein Kinase-independent and NADPH Oxidase-dependent Pathways.

Sae Mi WI ; Ki Young LEE

Immune Network.2014;14(5):241-248. doi:10.4110/in.2014.14.5.241

It is debatable whether AMP-activated protein kinase (AMPK) activation is involved in anti-apoptotic or pro-apoptotic signaling. AICAR treatment increases AMPK-alpha1 phosphorylation, decreases intracellular reactive oxygen species (ROS) levels, and significantly increases Annexin V-positive cells, DNA laddering, and caspase activity in human myeloid cell. AMPK activation is therefore implicated in apoptosis. However, AMPK-alpha1-knockdown THP-1 cells are more sensitive to apoptosis than control THP-1 cells are, suggesting that the apoptosis is AMPK-independent. Low doses of AICAR induce cell proliferation, whereas high doses of AICAR suppress cell proliferation. Moreover, these effects are significantly correlated with the downregulation of intracellular ROS, strongly suggesting that AICAR-induced apoptosis is critically associated with the inhibition of NADPH oxidase by AICAR. Collectively, our results demonstrate that in AICAR-induced apoptosis, intracellular ROS levels are far more relevant than AMPK activation.
AMP-Activated Protein Kinases ; Apoptosis* ; Cell Proliferation ; DNA ; Down-Regulation ; Humans ; Lymphocytes ; Myeloid Cells ; NADP* ; NADPH Oxidase ; Phosphorylation ; Reactive Oxygen Species

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Contrasting Roles of Different Endoglin Forms in Atherosclerosis.

Young Saeng JANG ; In Hong CHOI

Immune Network.2014;14(5):237-240. doi:10.4110/in.2014.14.5.237

Endoglin (also known as CD105 or TGF-beta type III receptor) is a co-receptor involved in TGF-beta signaling. In atherosclerosis, TGF-beta signaling is crucial in regulating disease progression owing to its anti-inflammatory effects as well as its inhibitory effects on smooth muscle cell proliferation and migration. Endoglin is a regulator of TGF-beta signaling, but its role in atherosclerosis has yet to be defined. This review focuses on the roles of the various forms of endoglin in atherosclerosis. The expression of the two isoforms of endoglin (long-form and short-form) is increased in atherosclerotic lesions, and the expression of the soluble forms of endoglin is upregulated in sera of patients with hypercholesterolemia and atherosclerosis. Interestingly, long-form endoglin shows an atheroprotective effect via the induction of eNOS expression, while short-form and soluble endoglin enhance atherogenesis by inhibiting eNOS expression and TGF-beta signaling. This review summarizes evidence suggesting that the different forms of endoglin have distinct roles in atherosclerosis.
Atherosclerosis* ; Disease Progression ; Humans ; Hypercholesterolemia ; Myocytes, Smooth Muscle ; Protein Isoforms ; Transforming Growth Factor beta

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Regulatory T Cells in B Cell Follicles.

Jae Hoon CHANG ; Yeonseok CHUNG

Immune Network.2014;14(5):227-236. doi:10.4110/in.2014.14.5.227

Understanding germinal center reactions is crucial not only for the design of effective vaccines against infectious agents and malignant cells but also for the development of therapeutic intervention for the treatment of antibody-mediated immune disorders. Recent advances in this field have revealed specialized subsets of T cells necessary for the control of B cell responses in the follicle. These cells include follicular regulatory T cells and Qa-1-restricted cluster of differentiation (CD)8+ regulatory T cells. In this review, we discuss the current knowledge related to the role of regulatory T cells in the B cell follicle.
Germinal Center ; Immune System Diseases ; T-Lymphocytes ; T-Lymphocytes, Helper-Inducer ; T-Lymphocytes, Regulatory* ; Vaccines

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Cross-Reactivity of Porcine Immunoglobulin A Antibodies with Fecal Immunoglobulins of Wild Boar (Sus scrofa) and Other Animal Species.

Sang Won SEO ; Sung J YOO ; Sunyoung SUNWOO ; Bang hun HYUN ; Young S LYOO

Immune Network.2016;16(3):195-199. doi:10.4110/in.2016.16.3.195

Fecal samples obtained from wild boar habitats are useful for the surveillance of diseases in wild boar populations; however, it is difficult to determine the species of origin of feces collected in natural habitats. In this study, a fecal IgA ELISA was evaluated as a method for identifying the porcine species from fecal samples. Both domestic pigs (Sus scrofa domestica) and wild boars (Sus scrofa coreanus) showed significantly higher levels of fecal IgA than other animal species. Additionally, age dependent changes in the level of Ig A in wild boars and domestic pigs were identified; Titers of Ig A were highest in suckling period and lowest in weanling period.
Animals* ; Antibodies* ; Ecosystem ; Enzyme-Linked Immunosorbent Assay ; Feces ; Immunoglobulin A* ; Immunoglobulins* ; Methods ; Sus scrofa*

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Differential Chemokine Signature between Human Preadipocytes and Adipocytes.

Rosa Mistica C IGNACIO ; Carla R GIBBS ; Eun Sook LEE ; Deok Soo SON

Immune Network.2016;16(3):189-194. doi:10.4110/in.2016.16.3.189

Obesity is characterized as an accumulation of adipose tissue mass represented by chronic, low-grade inflammation. Obesity-derived inflammation involves chemokines as important regulators contributing to the pathophysiology of obesity-related diseases such as cardiovascular disease, diabetes and some cancers. The obesity-driven chemokine network is poorly understood. Here, we identified the profiles of chemokine signature between human preadipocytes and adipocytes, using PCR arrays and qRT-PCR. Both preadipocytes and adipocytes showed absent or low levels in chemokine receptors in spite of some changes. On the other hand, the chemokine levels of CCL2, CCL7-8, CCL11, CXCL1-3, CXCL6 and CXCL10-11 were dominantly expressed in preadipocytes compared to adipocytes. Interestingly, CXCL14 was the most dominant chemokine expressed in adipocytes compared to preadipocytes. Moreover, there is significantly higher protein level of CXCL14 in conditioned media from adipocytes. In addition, we analyzed the data of the chemokine signatures in adipocytes obtained from healthy lean and obese postmenopausal women based on Gene Expression Omnibus (GEO) dataset. Adipocytes from obese individuals had significantly higher levels in chemokine signature as follows: CCL2, CCL13, CCL18-19, CCL23, CCL26, CXCL1, CXCL3 and CXCL14, as compared to those from lean ones. Also, among the chemokine networks, CXCL14 appeared to be the highest levels in adipocytes from both lean and obese women. Taken together, these results identify CXCL14 as an important chemokine induced during adipogenesis, requiring further research elucidating its potential therapeutic benefits in obesity.
Adipocytes* ; Adipogenesis ; Adipose Tissue ; Cardiovascular Diseases ; Chemokines ; Culture Media, Conditioned ; Dataset ; Female ; Gene Expression ; Hand ; Humans* ; Inflammation ; Obesity ; Polymerase Chain Reaction ; Receptors, Chemokine

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Induction of Nuclear Enlargement and Senescence by Sirtuin Inhibitors in Glioblastoma Cells.

Kyoung B YOON ; Kyeong R PARK ; Soo Y KIM ; Sun Young HAN

Immune Network.2016;16(3):183-188. doi:10.4110/in.2016.16.3.183

Sirtuin family members with lysine deacetylase activity are known to play an important role in anti-aging and longevity. Cellular senescence is one of the hallmarks of aging, and downregulation of sirtuin is reported to induce premature senescence. In this study, we investigated the effects of small-molecule sirtuin inhibitors on cellular senescence. Various small molecules such as tenovin-1 and EX527 were employed for direct sirtuin activity inhibition. U251, SNB-75, and U87MG glioblastoma cells treated with sirtuin inhibitors exhibited phenotypes with nuclear enlargement. Furthermore, treatment of rat primary astrocytes with tenovin-1 also increased the size of the nucleus. The activity of senescence-associated β-galactosidase, a marker of cellular senescence, was induced by tenovin-1 and EX527 treatment in U87MG glioblastoma cells. Consistent with the senescent phenotype, treatment with tenovin-1 increased p53 expression in U87MG cells. This study demonstrated the senescence-inducing effect of sirtuin inhibitors, which are potentially useful tools for senescence research.
Aging* ; Animals ; Astrocytes ; Cell Aging ; Down-Regulation ; Glioblastoma* ; Humans ; Longevity ; Lysine ; Phenotype ; Rats

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Roles of RUNX1 and PU.1 in CCR3 Transcription.

Su Kang KONG ; Byung Soo KIM ; Sae Mi HWANG ; Hyune Hwan LEE ; Il Yup CHUNG

Immune Network.2016;16(3):176-182. doi:10.4110/in.2016.16.3.176

CCR3 is a chemokine receptor that mediates the accumulation of allergic inflammatory cells, including eosinophils and Th2 cells, at inflamed sites. The regulatory sequence of the CCR3 gene, contains two Runt-related transcription factor (RUNX) 1 sites and two PU.1 sites, in addition to a functional GATA site for transactivation of the CCR3 gene. In the present study, we examined the effects of the cis-acting elements of RUNX1 and PU.1 on transcription of the gene in EoL-1 eosinophilic cells and Jurkat T cells, both of which expressed functional surface CCR3 and these two transcription factors. Introduction of RUNX1 siRNA or PU.1 siRNA resulted in a modest decrease in CCR3 reporter activity in both cell types, compared with transfection of GATA-1 siRNA. Cotransfection of the two siRNAs led to inhibition in an additive manner. EMSA analysis showed that RUNX1, in particular, bound to its binding motifs. Mutagenesis analysis revealed that all point mutants lacking RUNX1- and PU.1-binding sites exhibited reduced reporter activities. These results suggest that RUNX1 and PU.1 participate in transcriptional regulation of the CCR3 gene.
Eosinophils ; Mutagenesis ; RNA, Small Interfering ; T-Lymphocytes ; Th2 Cells ; Transcription Factors ; Transcriptional Activation ; Transfection

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Immunomodulatory Effects of Ambroxol on Airway Hyperresponsiveness and Inflammation.

Katsuyuki TAKEDA ; Nobuaki MIYAHARA ; Shigeki MATSUBARA ; Christian TAUBE ; Kenichi KITAMURA ; Astushi HIRANO ; Mitsune TANIMOTO ; Erwin W GELFAND

Immune Network.2016;16(3):165-175. doi:10.4110/in.2016.16.3.165

Ambroxol is used in COPD and asthma to increase mucociliary clearance and regulate surfactant levels, perhaps through anti-oxidant and anti-inflammatory activities. To determine the role and effect of ambroxol in an experimental model of asthma, BALB/c mice were sensitized to ovalbumin (OVA) followed by 3 days of challenge. Airway hyperresponsiveness (AHR), lung cell composition and histology, and cytokine and protein carbonyl levels in bronchoalveolar lavage (BAL) fluid were determined. Ambroxol was administered either before the first OVA challenge or was begun after the last allergen challenge. Cytokine production levels from lung mononuclear cells (Lung MNCs) or alveolar macrophages (AM) were also determined. Administration of ambroxol prior to challenge suppressed AHR, airway eosinophilia, goblet cell metaplasia, and reduced inflammation in subepithelial regions. When given after challenge, AHR was suppressed but without effects on eosinophil numbers. Levels of IL-5 and IL-13 in BAL fluid were decreased when the drug was given prior to challenge; when given after challenge, increased levels of IL-10 and IL-12 were detected. Decreased levels of protein carbonyls were detected in BAL fluid following ambroxol treatment after challenge. In vitro, ambroxol increased levels of IL-10, IFN-γ, and IL-12 from Lung MNCs and AM, whereas IL-4, IL-5, and IL-13 production was not altered. Taken together, ambroxol was effective in preventing AHR and airway inflammation through upregulation of Th1 cytokines and protection from oxidative stress in the airways.
Ambroxol* ; Animals ; Asthma ; Bronchoalveolar Lavage ; Cytokines ; Eosinophilia ; Eosinophils ; Goblet Cells ; In Vitro Techniques ; Inflammation* ; Interleukin-10 ; Interleukin-12 ; Interleukin-13 ; Interleukin-4 ; Interleukin-5 ; Lung ; Macrophages, Alveolar ; Metaplasia ; Mice ; Models, Theoretical ; Mucociliary Clearance ; Neutrophils ; Ovalbumin ; Ovum ; Oxidative Stress ; Pulmonary Disease, Chronic Obstructive ; Up-Regulation

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Roles of IL-33 in Resistance and Tolerance to Systemic Candida albicans Infections.

Sang Jun PARK ; Hong Rae CHO ; Byungsuk KWON

Immune Network.2016;16(3):159-164. doi:10.4110/in.2016.16.3.159

IL-33 is a multifunctional cytokine that is released in response to a variety of intrinsic and extrinsic stimuli. The role of IL-33 in Candida albicans infections is just beginning to be revealed. This cytokine has beneficial effects on host defense against systemic C. albicans infections, and it promotes resistance mechanisms by which the immune system eliminates the invading fungal pathogens; and it also elevates host tolerance by reducing the inflammatory response and thereby, potentially, tissue damage. Thus, IL-33 is classified as a cytokine that has evolved functionally to protect the host from damage by pathogens and immunopathology.
Candida albicans* ; Candida* ; Immune System ; Interleukin-33*

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