Multiplex cytokine analysis of Werner syndrome

Goto, Makoto; Hayata, Koichiro; Chiba, Junji; Matsuura, M.; Iwaki-Egawa, Sachiko; Watanabe, Yasuhiro

doi:10.5582/irdr.2015.01035

Cited by 20 publications

(16 citation statements)

References 33 publications

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“…The body initiates the immune response by secreting proinflammatory cytokines such as IL‐2, IL‐6, and IL‐8. As an innovative cytokine detection technique, the Luminex bead array system allows us to quantitatively detect multiple cytokines in a single test using a minimal level of samples . In the present study, cytokine responses to HTNV infection were monitored and the patient cytokine profiles were used to access the outcome of HFRS treatment.…”

Section: Introductionmentioning

confidence: 99%

Cytokine response to Hantaan virus infection in patients with hemorrhagic fever with renal syndrome

Guo

Wang

et al. 2017

Journal of Medical Virology

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Hantaan virus (HTNV) infection of the human body causes a severe acute infectious disease known as hemorrhagic fever renal syndrome (HFRS). The aim of this study was to correlate patient cytokine profiles to HFRS severity. In this study, we discuss the clinical significance of evaluating HFRS treatment outcomes using cytokine information. The levels of 18 cytokines were quantitatively determined in three groups: 34 HTNV IgM+ cases, 63 HTNV IgM- negative cases, and 78 healthy volunteers. The level of 14 serum cytokines were higher in the patient group than that in the healthy control group. In the 34 HTNV IgM+ patient sera, a set of 27 cytokines was further assessed. The cytokines of TNF-β, IL-1ra, and IL-6 were detected at higher level in the IgM+ group than that in the IgM- group. The deterioration of HFRS was accompanied with multiple cytokines increased, such as IL-1ra, IL-12p70, IL-10, IP-10, IL-17, IL-2, and IL-6. Our data indicate that serum cytokine levels are associated with the progression of HFRS.

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Section: Introductionmentioning

confidence: 99%

Cytokine response to Hantaan virus infection in patients with hemorrhagic fever with renal syndrome

Guo

Wang

et al. 2017

Journal of Medical Virology

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“…As the recent WS gene (WRN) knock-out mice study suggested an induction of immune dysfunction followed by chronic inflammation (30), we would like to speculate that the loss-of-function mutation of WRN may lead to some immune dysfunction leading to more susceptibility to CMV infection in WS than normal aging populations. Because natural killer cell function declined significantly in WS and WS patients produced more auto-antibodies compared with the normal aging population as we already reported (4,5,8,9,(31)(32)(33)(34)(35). Obviously, this is a highly speculative idea and further study may be needed to clarify the pathogenesis of mild inflammation: inflammageing in healthy aging and also in WS.…”

Section: Discussionmentioning

confidence: 73%

“…Chronic elevation of hsCRP in the normal elderly population may probably be associated with agingrelated pathological conditions including diabetes mellitus (DM), sarcopenia, osteoporosis, cancer, atherosclerosis, cognitive decline and finally death (6,7). Aging-related persistent, systemic, minimal and asymptomatic inflammation, termed 'inflammageing', is tightly associated with an imbalance between an increase in pro-and a decrease in anti-inflammatory substances including cytokines/chemokines (8)(9)(10)(11). Inflammation is widely recognized as a pathophysiologically fundamental metabolism to generate energy with thermogenesis, leading to wound healing and tissue destruction during healthy development and aging (6,12,13).…”

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confidence: 99%

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Aging-associated latent herpes viral infection in normal Japanese individuals and patients with Werner syndrome

Goto

Chiba

Matsuura

et al. 2018

IRDR

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Human aging is probably controlled by a combination of intrinsic/genetic factors including metabolism/ catabolism functions (1), and extrinsic/environmental factors such as infections (2). The possible intrinsic/ genetic factors include genetically-determined progeroid syndrome genes such as WRN for Werner syndrome (WS) (3). WS has been proposed as the representative human natural ageing model. Because patients with WS, transmitted autosomal-recessively by the homozygous mutation of WRN (RecQ3 DNA helicase), usually manifest their premature aging phenotypes immediately after adulthood. Typical aging signs and symptoms in WS include voice change, bilateral cataracts, gray hair/alopecia, skin atrophy, skin pigmentation, type II diabetes mellitus, central obesity, atherosclerosis, hyperlipidemia, skin ulcer, renal dysfunction, osteoporosis, and cancer/sarcoma. The Summary A series of our "inflammageing" study examining serum samples from a maximum of 217 healthy Japanese individuals aged between 1 and 100 years and mutation-proven 40 patients with Werner syndrome (WS) indicated normal aging-associated elevations of highly sensitive CRP (hsCRP) and matrix metalloproteinase-9 (MMP-9). To further study the contribution of environmental factors such as persistent herpes viral infection to inflammageing, IgG antibodies against varicella/zoster virus (VZV) and cytomegalovirus (CMV) were examined in the same serum samples as has been done for hsCRP and MMP-9 analyses. The mean levels of serum IgG viral antibodies were comparable between normal (mean ± SE: 31.0 ± 4.3 unit) and WS (38.6 ± 7.6) for CMV, and between normal (42.0 ± 12.2) and WS (29.8 ± 3.8) for VZV, respectively. Significant associations of aging with IgG anti-CMV antibody were in normal aging (p = 0.023) and WS (p = 0.037), but not with IgG VZV in both conditions. Aging-associated change of IgG anti-CMV antibody titer in WS increased significantly (1.32 times higher) compared with normal aging (p = 0.037). IgG anti-CMV level was significantly elevated in the male gender than female in both conditions (p = 0.006). Elevated hsCRP level was significantly associated with IgG anti-CMV (p = 0.016) and IgG anti-VZV (p = 0.008) antibodies in normal aging, but not in WS. Serum MMP-9 was significantly associated with IgG anti-CMV level (p = 0.0002) in normal aging, but not in WS. Persistent herpes viral infection may constitute a part of "inflammageing" in normal aging and WS.

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“…Inflammation alters intercellular communication owing to the accumulation of cytokines increasing with aging. Patients with WS have elevated cytokine levels of interleukin-2 (IL-2), IL-4, IL-6, tumor necrosis factor alpha (TNF-α), interferon gamma (IFNγ), and monocyte chemoattractant protein-1 (MCP-1) 18 .…”

Section: Introductionmentioning

confidence: 99%

Recent Advances in Understanding Werner Syndrome

et al. 2017

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Aging, the universal phenomenon, affects human health and is the primary risk factor for major disease pathologies. Progeroid diseases, which mimic aging at an accelerated rate, have provided cues in understanding the hallmarks of aging. Mutations in DNA repair genes as well as in telomerase subunits are known to cause progeroid syndromes. Werner syndrome (WS), which is characterized by accelerated aging, is an autosomal-recessive genetic disorder. Hallmarks that define the aging process include genomic instability, telomere attrition, epigenetic alterations, loss of proteostasis, deregulation of nutrient sensing, mitochondrial dysfunction, cellular senescence, stem cell exhaustion, and altered intercellular communication. WS recapitulates these hallmarks of aging and shows increased incidence and early onset of specific cancers. Genome integrity and stability ensure the normal functioning of the cell and are mainly guarded by the DNA repair machinery and telomeres. WRN, being a RecQ helicase, protects genome stability by regulating DNA repair pathways and telomeres. Recent advances in WS research have elucidated WRN’s role in DNA repair pathway choice regulation, telomere maintenance, resolution of complex DNA structures, epigenetic regulation, and stem cell maintenance.

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Multiplex cytokine analysis of Werner syndrome

Cited by 20 publications

References 33 publications

Cytokine response to Hantaan virus infection in patients with hemorrhagic fever with renal syndrome

Cytokine response to Hantaan virus infection in patients with hemorrhagic fever with renal syndrome

Aging-associated latent herpes viral infection in normal Japanese individuals and patients with Werner syndrome

Recent Advances in Understanding Werner Syndrome

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