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1.
Takahisa Koyama Shin Kariya Yasuharu Sato Yuka Gion Takaya Higaki Takenori Haruna Tazuko Fujiwara Akira Minoura Soshi Takao Yorihisa Orita Kengo Kanai Masami Taniguchi Kazunori Nishizaki Mitsuhiro Okano 《Allergology international》2019,68(2):216-224
Background
IgG4 production is regulated by type 2 (IL-4 and IL-13) and regulatory (IL-10) cytokines involved in the pathophysiology of chronic rhinosinusitis (CRS). We sought to determine the pathophysiological characteristics of IgG4-positive cells in sinonasal tissues in CRS, especially eosinophilic CRS (ECRS).Methods
IgG4-positive cells in uncinate tissues (UT) and nasal polyps (NP) were examined by immunohistochemistry. Associations between the number of IgG4-positive cells and clinicopathological factors were analyzed. Receiver operating characteristics (ROC) analysis was performed to determine the cut-off value of IgG4-positive cells in tissue that can predict the post-operative course.Results
IgG4 was mainly expressed in infiltrating plasma and plasmacytoid cells, and the number of IgG4-positive cells was significantly higher in NP, especially those from severe ECRS patients, than in UT. In CRS patients, the number of IgG4-positive cells significantly and positively correlated with blood and tissue eosinophilia, radiological severity, and serum level of total IgE. The number of infiltrating IgG4-positive cells was significantly higher in patients with a poor post-operative course (sustained sinus shadow 6 months after surgery) than in those with a good one. The number of IgG4-positive cells in NP could discriminate patients with a good or a poor post-operative course (area under the curve: 0.769). Also, 73.3% sensitivity and 82.5% specificity were achieved when the cut-off value was set at 17 cells/high-power field.Conclusions
Our results suggest that the local expression of IgG4 on cells may be used as a biomarker that reflects the pathophysiology of CRS, including the post-operative course. 相似文献2.
Yasuyuki Noyama Mitsuhiro Okano Tazuko Fujiwara Shin Kariya Takaya Higaki Takenori Haruna Sei-ichiro Makihara Kengo Kanai Takahisa Koyama Masami Taniguchi Jun-ichi Ishitoya Akira Kanda Yoshiki Kobayashi Mikiya Asako Koichi Tomoda Kazunori Nishizaki 《Allergology international》2017,66(1):42-51
Background
IL-22 is an IL-10-family cytokine that regulates chronic inflammation. We investigated the role of IL-22 and its receptor, IL-22R1, in the pathophysiology of chronic rhinosinusitis with nasal polyps (CRSwNP).Methods
IL-22 and IL-22R1 protein and mRNA expression in NP and in uncinate tissues (UT) from CRS and non-CRS patients was examined using immunohistochemistry and real-time PCR, respectively. Dispersed NP and UT cells were cultured with the Staphylococcus aureus exotoxins, staphylococcal enterotoxin B and alpha-toxin, following which exotoxin-induced IL-22 levels and their association with clinicopathological factors were analyzed. Effects of IL-22 on MUC1 expression and cytokine release in NP cells were also determined.Results
IL-22 and IL-22R1 in NP were mainly expressed in infiltrating inflammatory cells and in epithelial cells, respectively. IL-22 mRNA levels in NP were significantly higher than those in UTs from non-CRS patients whereas IL-22R1 levels were conversely lower in NPs. NP cells produced substantial amounts of IL-22 in response to exotoxins. Exotoxin-induced IL-22 production by NP cells significantly and negatively correlated with the degree of local eosinophilia and postoperative computed tomography (CT) score, whereas conversely it positively correlated with the forced expiratory volume in 1s (FEV1)/forced vital capacity (FVC) ratio. IL-22 significantly enhanced MUC1 mRNA expression in NP cells. IL-22-induced MUC1 mRNA levels were significantly and positively correlated with IL-22R1 mRNA levels in NPs.Conclusions
These data suggest that imbalance of IL-22/IL-22R1 signaling regulates the pathogenesis of CRSwNP, including local eosinophilia, via alteration of MUC1 expression. 相似文献3.
Tomohisa Kato Hideaki Kouzaki Koji Matsumoto Junichi Hosoi Takeshi Shimizu 《Allergology international》2017,66(2):281-289
Background
Calprotectin is a heterodimer complex of the S100A8 and S100A9 proteins, and has various functions as an innate mediator at the sites of inflammation.The aim of this study was to elucidate the roles of calprotectin in the eosinophilic chronic rhinosinusitis (ECRS).Methods
Allergen-induced production of calprotectin was evaluated in cultured normal human bronchial epithelial (NHBE) cells by ELISA and RT-PCR. We then examined the roles of calprotectin on Alternaria alternata (Alternaria)-induced production of thymic stromal lymphopoietin (TSLP) and IL-25 in NHBE cells. The extracellular concentration and allergen-induced secretion of calprotectin in cultured primary nasal epithelial (PNE) cells were examined and compared between patients with ECRS and non-eosinophilic chronic rhinosinusitis (NECRS).Results
Alternaria, house dust mites, protease from Staphylococcus aureus, papain, trypsin, polyinosinic:polycytidylic acid and lipopolysaccharide stimulated calprotectin production in the cultured NHBE cells. The combination of calprotectin and ATP stimulated the production of TSLP and IL-25 in NHBE cells, and calprotectin stimulated Alternaria-induced production of TSLP and IL-25, which was suppressed by blocking P2 purinergic receptors and by treatment with siRNA for S100A8, S100A9 or calprotectin receptors (Toll-like receptor 4 or receptor for advanced glycation end products). Allergen-induced calprotectin production was significantly stimulated in PNE cells from patients with ECRS.Conclusions
These results indicate that calprotectin enhances the allergen-induced Th2-type inflammatory responses in airway epithelial cells via the secretion of TSLP and IL-25, and that calprotectin secreted by the epithelial cells may be involved in the pathogenesis of ECRS. 相似文献4.
Kanako Yoshida Tetsuji Takabayashi Yoshimasa Imoto Masafumi Sakashita Norihiko Narita Shigeharu Fujieda 《Allergology international》2019,68(2)
Background
In Eosinophilic chronic rhinosinusitis (ECRS), it is difficult to estimate the refractoriness and recurrence risk for each patient. Fraction of exhaled nitric oxide (FeNO) is known as a biomarker of eosinophilic inflammation in lower airway. It has been reported that nasal NO has some crucial functions in the upper and lower airways. However, in upper airway, paranasal sinuses, the usefulness of NO measurement remains controversial. The purpose of this study is to identify the usefulness of nasal NO measurement in ECRS and the involvement of nasal NO in the pathogenesis of ECRS.Methods
We compared the nasal NO levels of ECRS, non-ECRS, and normal control groups. Correlation between nasal NO levels and clinical findings were observed. Then, we compared nasal NO levels before and after endoscopic sinus surgery (ESS). We also examine whether nasal NO levels might discriminate ECRS by the receiver operating characteristic (ROC) curve analysis.Results
Nasal NO levels were significantly decreased in ECRS compared to the other two groups. Moreover, nasal NO levels in ECRS significantly and negatively correlated with eosinophil levels and CT score. However, they did not correlate with the nasal polyp score. Nasal NO levels were not upregulated soon after opening the sinus ostium by ESS. The ROC curves for nasal NO levels were used to discriminate all CRS patients and ECRS patients from normal controls.Conclusions
Nasal NO may be useful as a marker of ECRS severity and low nasal NO levels in ECRS may contribute to its pathogenesis. 相似文献5.
Tomoe Nishimura Osamu Kaminuma Mayumi Saeki Noriko Kitamura Minoru Gotoh Akio Mori Takachika Hiroi 《Allergology international》2018
Background
We have recently demonstrated that T cell-mediated nasal hyperresponsiveness (NHR) is a representative pathophysiological feature of allergic rhinitis (AR). Although several anti-allergic drugs are used for the treatment of AR, the efficacy of these drugs on T cell-mediated NHR have not been elucidated. In these studies we investigated the effects of dexamethasone (Dex), montelukast (Mk), and chlorpheniramine (Chl) on NHR in antigen-immunized and antigen-specific Th2 cell-transferred mice.Methods
OVA-immunized BALB/c mice were treated with Dex, Mk, or Chl and challenged intranasally with OVA. We then assessed NHR, the number of inflammatory cells in the nasal lavage fluid (NALF), mRNA expression of Th2 cytokines in the nasal tissue, the population of CD3+CD4+ cells in the nasal lymphoid tissue (NALT), and antigen-specific serum IgE and IgG levels. Antigen-induced NHR and changes in antigen-specific T cells in the NALT were investigated in OVA-specific Th2 cell-transferred mice.Results
Dex significantly suppressed antigen-induced NHR, inflammatory cell infiltration, and IL-4, IL-5, IL-6, and IL-13 expression in immunized mice. Chl was completely ineffective, and only IL-13 expression was suppressed by Mk. None of these drugs affected IgE and IgG production. Antigen-induced NHR and the increase in antigen-specific T cells in the NALT of Th2 cell-transferred mice were inhibited by Dex, but not by Mk or Chl.Conclusions
Steroids are effective for the reduction of NHR in AR by suppressing the accumulation of inflammatory cells, especially antigen-specific T cells. 相似文献6.
Koji Matsumoto Hideaki Kouzaki Hirotaka Kikuoka Tomohisa Kato Ichiro Tojima Shino Shimizu Takeshi Shimizu 《Allergology international》2018
Background
Epithelial cell-derived IL-33 has an important role in the initiation and activation of innate allergic inflammation. IL-33 acts as a cytokine through the ST2 receptor (ST2L) and it stimulates the production of Th2 cytokines. Soluble ST2 (sST2) may regulate Th2 responses by neutralizing the activity of IL-33. Basophils express ST2L and produce IL-5 in response to IL-33. However, the role of the epithelial cell–basophil interaction and sST2 in IL-5 production remains unclear.Methods
Cultured human bronchial epithelial (hBE33) cells, that contained the human IL-33 gene (i.e., hBE33 cells) and a human basophilic cell line, KU812 cells, were used to study the epithelial cell–basophil interaction in the production of IL-5 induced by HDM.Results
At 15 min after incubation, HDM stimulated the rapid release of IL-33 from cultured hBE33 cells. IL-33 and the supernatant of HDM-treated hBE33 cells stimulated IL-5 production from KU812 cells. Anti-IL-33 antibody and anti-ST2 antibody treatment of KU812 cells suppressed IL-5 production, which had been induced by the supernatant of HDM-treated hBE33 cells. The hBE33 cells secreted sST2 in a time-dependent manner. The production of sST2 by KU812 cells co-cultured with hBE33 cells was significantly increased, compared with KU812 cells cultured with the supernatant of hBE33 cells. Soluble ST2 suppressed IL-5 production by KU812 cells, which was induced by the supernatant of HDM-treated hBE33 cells.Conclusions
Epithelial cell-derived IL-33 promoted IL-5 production by KU812 cells. The subsequently produced sST2 has important roles in regulating Th2 responses. 相似文献7.
8.
Masato Tamari Keisuke Orimo Kenichiro Motomura Ken Arae Akio Matsuda Susumu Nakae Hirohisa Saito Hideaki Morita Kenji Matsumoto 《Allergology international》2018,67(3):380-387
Background
Direct contact of food proteins with eczematous lesions is thought to be the main cause of epicutaneous sensitization. To further investigate the development and pathogenesis of food allergy in vivo, a good mouse model of epicutaneous sensitization is needed. However, a fundamental problem in that regard is that the optimal age for epicutaneous sensitization of mice is unknown. In this study, we attempted to elucidate that optimal age.Methods
Dorsal skin of wild-type BALB/c female mice (1, 3, 8 and 24 weeks old) was shaved, depilated and tape-stripped. A Finn chamber containing a 20-μl-aliquot of 20-mg/ml (OVA) was applied to the tape-stripped skin on 3 consecutive days/week, for 3 weeks. The body temperature was measured after intraperitoneal OVA challenge. Serum OVA-specific IgE titers and OVA-induced cytokine production by spleen cells were measured by ELISA. Dendritic cells (DCs) that migrated to the draining lymph nodes were quantified by FITC-labeled OVA and flow cytometry. The mRNA expression levels in the dorsal skin were measured by qPCR.Results
A significant age-dependent body temperature decline was observed after OVA challenge. The serum OVA-specific IgE titer, OVA-induced cytokine production (i.e., IL-4, IL-5 and IL-13) by spleen cells, and number of FITC-OVA-engulfing DCs increased with age. In addition, mRNA for IL-33, but not TSLP or IL-25, was significantly induced in the skin by tape-stripping and increased with age.Conclusions
Twenty-four-week-old mice showed the greatest DC migration, Th2 polarization, IgE production and body temperature decline. Skin-derived IL-33 is likely to play key roles in those changes. 相似文献9.
Soichi Sano Kosei Oshima Ying Wang Susan MacLauchlan Yasufumi Katanasaka Miho Sano María A. Zuriaga Minoru Yoshiyama David Goukassian Matthew A. Cooper José J. Fuster Kenneth Walsh 《Journal of the American College of Cardiology》2018,71(8):875-886
Background
Recent studies have shown that hematopoietic stem cells can undergo clonal expansion secondary to somatic mutations in leukemia-related genes, thus leading to an age-dependent accumulation of mutant leukocytes in the blood. This somatic mutation-related clonal hematopoiesis is common in healthy older individuals, but it has been associated with an increased incidence of future cardiovascular disease. The epigenetic regulator TET2 is frequently mutated in blood cells of individuals exhibiting clonal hematopoiesis.Objectives
This study investigated whether Tet2 mutations within hematopoietic cells can contribute to heart failure in 2 models of cardiac injury.Methods
Heart failure was induced in mice by pressure overload, achieved by transverse aortic constriction or chronic ischemia induced by the permanent ligation of the left anterior descending artery. Competitive bone marrow transplantation strategies with Tet2-deficient cells were used to mimic TET2 mutation-driven clonal hematopoiesis. Alternatively, Tet2 was specifically ablated in myeloid cells using Cre recombinase expressed from the LysM promoter.Results
In both experimental heart failure models, hematopoietic or myeloid Tet2 deficiency worsened cardiac remodeling and function, in parallel with increased interleukin-1beta (IL-1β) expression. Treatment with a selective NLRP3 inflammasome inhibitor protected against the development of heart failure and eliminated the differences in cardiac parameters between Tet2-deficient and wild-type mice.Conclusions
Tet2 deficiency in hematopoietic cells is associated with greater cardiac dysfunction in murine models of heart failure as a result of elevated IL-1β signaling. These data suggest that individuals with TET2-mediated clonal hematopoiesis may be at greater risk of developing heart failure and respond better to IL-1β–NLRP3 inflammasome inhibition. 相似文献10.
Mariola Sliwinska-Mosson Grzegorz Marek Zygmunt Grzebieniak Halina Milnerowicz 《Pancreatology》2018,18(8):885-891
Objectives
The aim of the analysis is to determine dynamic changes in somatostatin (SS) and interleukin-6 (IL-6) concentrations during in acute pancreatitis (AP).Methods
The influence of tobacco smoking on IL-6 and SS levels in the serum of non-smoking (n?=?10) and smoking (n?=?27) patients with diagnosed AP and control group: non-smoking (n?=?44), smoking (n?=?42) and passive smoking (n?=?29) healthy persons was proved. The concentration of IL-6 and SS was determined by means of ELISA. Differences between the groups analyzed were tested using the U Mann Whitney test. The Spearman rank correlation analysis was used to evaluate the correlations.Results
The concentrations of IL-6 and SS were significantly higher in smoking patients with AP and healthy persons when compared with non-smoking population on every day (1 day: p?=?0.0002, p?=?0.015; 3 day: p?=?0.005, p?=?0.001 and 7 day: p?=?0.025, p?=?0.038). Dynamic changes in concentrations of IL-6 and SS in the serum of patients with AP were demonstrated in the ensuing days of the disease. In case of non-smoking and smoking patients, significant positive correlations between IL-6 and SS was observed.Conclusions
These findings suggest that some of the antiinflammatory effects of SS against acute pancreatitis may be mediated by reducing the local proinflammatory cytokine secretion in the pancreas. 相似文献11.
Takenori Haruna Shin Kariya Tazuko Fujiwara Atsushi Yuta Takaya Higaki Pengfei Zhao Yukiko Ogawa Kengo Kanai Yuji Hirata Aiko Oka Kazunori Nishizaki Mitsuhiro Okano 《Allergology international》2019,68(1):82-89
Background
The development of methods to predict the clinical effectiveness of sublingual immunotherapy (SLIT) for allergic diseases is a crucial matter. We sought to determine whether whole saliva, which is the first body component that contacts allergen extracts during SLIT, is associated with the clinical effectiveness of SLIT in Japanese cedar pollinosis.Methods
Blood monocytes or monocytic THP-1 cells were cultured in the presence or absence of either whole saliva or pure saliva with or without treatments including filtration and blockade of TLR2 and/or TLR4 signaling. IL-10 levels in the supernatants were then measured. Whole saliva-induced IL-10 production by THP-1 cells was compared between asymptomatic and disease-onset patients during peak pollen dispersal after SLIT.Results
Both monocytes and THP-1 cells produced substantial amounts of IL-10 in response to whole saliva. IL-10 production was significantly reduced in response to pure saliva and 0.2 μm-filtered saliva. Simultaneous treatment with polymyxin B and TL2.1, a neutralizing antibody against TLR2, also reduced IL-10 production. IL-10 levels produced by THP-1 cells in response to whole saliva collected prior to SLIT were significantly higher in asymptomatic patients determined by symptom-medication scores than disease-onset patients following SLIT. Such differences were not seen in saliva collected 3 months after the initiation of SLIT or saliva collected during peak pollen dispersal.Conclusions
Our results provide a basis for why the sublingual route is effective and preferable in allergen immunotherapy. Saliva-induced IL-10 levels produced by THP-1 cells may be a predictive marker for clinical remission after SLIT. 相似文献12.
Background
Severe acute pancreatitis (SAP) is characterised by two distinct clinical phases. Organ dysfunction and death is initially as a result of a systemic inflammatory response syndrome (SIRS). Systemic sepsis from infected pancreatic necrosis characterises the second phase, the so called 'second hit' of acute pancreatitis (AP). An immune imbalance during the second hit is postulated to contribute to the formation of the septic complications that occur in these patients. The pro-inflammatory T-helper (Th) 17 pathway has been shown to be an initiator of early SIRS in AP, however to date its role has not been established in the second hit in AP.Methods
Thirty-six patients with mild (n?=?16), moderate (n?=?10) and severe (n?=?10) acute pancreatitis were enrolled. Peripheral blood samples were drawn on days 7, 9, 11 and 13 of illness for analysis of routine clinical markers as well as cytokine analysis. Flow cytometry and a IL-17A ELISA was performed to determine cytokine concentrations.Results
There were no significant differences between days 7, 9, 11 and 13 for either the mild/moderate or SAP groups for IL-17A (CBA assay or ELISA), IFN-γ, TNF-α, IL-2 or IL-4. For each of the study days, the mean IL-6 and IL-10 concentrations were significantly higher in the SAP group compared to the mild/moderate group. WCC, CRP and PCT were all significantly higher in severe acute pancreatitis over the study days.Conclusions
An immune imbalance exists in patients with SAP, however secreted IL-17A is not responsible for the second hit in AP. 相似文献13.
14.
Takahiro Kawauchi Kayoko Ishimaru Yuki Nakamura Nobuhiro Nakano Mutsuko Hara Hideoki Ogawa Ko Okumura Shigenobu Shibata Atsuhito Nakao 《Allergology international》2017,66(3):472-478
Background
Interleukin-33 (IL-33) is an alarmin cytokine that binds to the interleukin 1 receptor-like 1 protein ST2. Clock is a key circadian gene that is essential for endogenous clockworks in mammals. This study investigated whether Clock temporally regulated IL-33-mediated responses in mast cells.Methods
The kinetics of IL-33-mediated IL-6, IL-13, and TNF-α productions were compared between bone marrow-derived mast cells (BMMCs) from wild-type and Clock-mutated mice (ClockΔ19/Δ19 mice). The kinetics of the neutrophil influx into the peritoneal cavity or expression of IL-13 and Gob-5 in the lung in response to IL-33 were compared between wild-type and ClockΔ19/Δ19 mice. We also examined the kinetics of ST2 expression in mast cells and its association with Clock expression.Results
There was a time-of-day-dependent variation in IL-33-mediated IL-6, IL-13, and TNF-α production in wild-type BMMCs, which was absent in Clock-mutated BMMCs. IL-33-induced neutrophil infiltration into the peritoneal cavity also showed a time-of-day-dependent variation in wild-type mice, which was absent in ClockΔ19/Δ19 mice. Furthermore, IL-33-induced IL-13 and Gob-5 expression in the lung exhibited a time-of-day-dependent variation in wild-type mice. These temporal variations in IL-33-mediated mast cell responses were associated with temporal variations of ST2 expression in mast cells. In addition, CLOCK bound to the promoter region of ST2 and Clock deletion resulted in down-regulation of ST2 expression in mast cells.Conclusions
CLOCK temporally gates mast cell responses to IL-33 via regulation of ST2 expression. Our findings provide novel insights into IL-33/mast cell-associated physiology and pathologies. 相似文献15.
Takehito Kobayashi Kazuyuki Nakagome Toru Noguchi Kiyoko Kobayashi Yutaka Ueda Tomoyuki Soma Kenji Ikebuchi Hidetomo Nakamoto Makoto Nagata 《Allergology international》2017
Background
Recent evidence has suggested that the innate immune response may play a role in the development of eosinophilic airway inflammation. We previously reported that uric acid (UA) and adenosine triphosphate (ATP), two important damage-associated molecular pattern molecules (DAMPs), activate eosinophil functions, suggesting that these molecules may be involved in the development of eosinophilic airway inflammation. The objective of this study was to measure the concentrations of DAMPs including UA and ATP in the bronchoalveolar lavage fluid (BALF) of patients with eosinophilic pneumonia (EP).Methods
BAL was performed in patients with EP including acute and chronic eosinophilic pneumonia, and in patients with hypersensitivity pneumonia, and sarcoidosis. UA, ATP, and cytokine concentrations in the BALF were then measured.Results
The UA concentration was increased in the BALF of EP patients. UA concentrations correlated with eosinophil numbers, and with eosinophil-derived neurotoxin and interleukin (IL)-5 concentrations. Furthermore, the ATP concentration was increased in the BALF of EP patients and ATP concentrations correlated with UA concentrations. Moreover, IL-33 was increased in EP patients and IL-33 concentrations correlated with UA and ATP concentrations.Conclusions
The UA and ATP concentration was increased in the BALF of EP patients. UA concentrations correlated with eosinophil numbers, and with ATP and IL-33 concentrations. Our findings suggest that DAMPs such as UA and ATP play a role in the pathogenesis of EP. 相似文献16.
Annukka Holster Johanna Teräsjärvi Eero Lauhkonen Sari Törmänen Merja Helminen Petri Koponen Matti Korppi Ville Peltola Qiushui He Kirsi Nuolivirta 《Allergology international》2018,67(1):109-113
Background
Interleukin-17 (IL-17A) is a mainly pro-inflammatory cytokine, and IL-17 signaling implicates in the development of allergic asthma. The polymorphism rs2275913 in the promoter region of the IL-17A gene has in previous studies been associated with asthma susceptibility. The objective was to evaluate the association between IL-17A rs2275913 (-197G>A) polymorphism and post-bronchiolitis asthma and/or allergic rhinitis in a prospective 11–13 years post-bronchiolitis follow-up.Methods
166 previously healthy full-term infants, hospitalized for bronchiolitis at age less than 6 months, were invited to follow-up visits at the ages of 5–7 years and 11–13 years. Asthma diagnoses and presumptive symptoms, allergic rhinitis and use of inhaled corticosteroids (ICS) were registered. Blood samples for IL-17A rs2275913 (-197G>A) polymorphism were obtained during hospitalization or at the 5–7 years control visit.Results
There were no significant differences between children with the wild GG and variant GA or AA genotype in the severity of bronchiolitis during hospitalization or in the outcomes until the age 5–7 years. At 11–13 years of age, children with the variant GA or AA genotype had significantly less often current asthma, use of ICSs during last 12 months or allergic rhinitis than those with the wild GG genotype. The ICS use during last 12 months retained the statistical significance in adjusted analyses (adjusted OR 0.25), whereas current asthma and allergic rhinitis marginally lost it.Conclusions
The IL-17A rs2275913 (-197G>A) polymorphism decreased the risk of post-bronchiolitis asthma at 11–13 years of age, but not earlier in life, in the present prospective, long-term follow-up study. 相似文献17.
Hiromi Mizutani Risa Tamagawa-Mineoka Naomi Nakamura Koji Masuda Norito Katoh 《Allergology international》2017,66(3):440-444
Background
Interleukin (IL)-21 is a member of the type I cytokine family and plays a role in the pathogenesis of T helper type 2 allergic diseases. It has been reported that IL-21 expression is upregulated in acute skin lesions in atopic dermatitis (AD) patients; however, little is known about the serum IL-21 levels of AD patients. The aim of this study was to quantify the serum IL-21 levels of AD patients and to evaluate the relationships between the serum IL-21 level and disease severity, laboratory markers, and eruption type in AD patients.Methods
We measured the serum IL-21 levels of adult AD patients and healthy control subjects using an enzyme-linked immunosorbent assay.Results
The adult AD patients exhibited significantly higher serum IL-21 levels than the healthy control subjects. A comparison of the patients' serum IL-21 levels based on the clinical severity of their AD revealed that the patients with severe AD demonstrated significantly higher serum IL-21 levels than those with mild AD and the healthy control subjects. The serum IL-21 levels were significantly correlated with the skin severity score, and especially with the degree of acute lesions such as erythema and edema/papules. The serum IL-21 level was not associated with laboratory markers, such as the serum IgE level, the serum thymus and activation-related chemokine level, blood eosinophilia, and the serum lactate dehydrogenase level.Conclusions
These results suggest that IL-21 might be involved in the pathogenesis of AD, especially the development of acute skin lesions. 相似文献18.
Yiyin Chen Marjorie Funk Jia Wen Xianghua Tang Guixiang He Hong Liu 《Heart & lung : the journal of critical care》2018,47(1):24-31
Background
Multidisciplinary disease management programs (MDMP) for patients with heart failure (HF) have been delivered, but evidence of their effectiveness in China is limited.Objective
To determine if a MDMP improves quality of life (QoL), physical performance, depressive symptoms, self-care behaviors and mortality or rehospitalization in patients with HF in China.Methods
This is a randomized controlled single center trial in which patients with HF received either MDMP with discharge education, physical training, follow-up visits and telephone calls for 180 days (n = 31) or standard care (SC, n = 31).Results
Compared with SC, QoL, depressive symptoms, and self-care behaviors were significantly improved by MDMP from baseline to 180 days (37% vs 66%, 20% vs 61%, and 8% vs 33%, respectively, all p < 0.001). There were no differences in physical performance and mortality or rehospitalization during follow-up.Conclusions
A HF MDMP can improve QoL, depressive symptoms and self-care behaviors in China. 相似文献19.
Audrey R. Roberson Angela Starkweather Catherine Grossman Edmund Acevedo Jeanne Salyer 《Heart & lung : the journal of critical care》2018,47(1):1-9
Background
Muscle strength may be one indicator of readiness to mobilize that can be used to guide decisions regarding early mobility efforts and to progressively advance mobilization.Objectives
To provide a synthesis of current measures of muscle strength in the assessment of early mobilization in critically ill adult patients who are receiving MV therapy.Methods
Research studies conducted between 2000-2015 were identified using PubMed, CINHAL, MEDLINE, and the Cochrane Database of Systematic Reviews databases using the search terms “muscle strength”, “intensive care”, “mechanical ventilation” and “muscle weakness”.Results
Nine articles used manual muscle testing, the Medical Research Council scale and/or hand-held dynamometer to provide objective measures for assessing muscle strength in the critically ill adult patient population.Conclusions
Further research is needed to examine the application of standardized measures of muscle strength for guiding decisions regarding early and progressive advancement of mobility goals in adult ICU patients on MV. 相似文献20.