Background Interleukin 16 （IL-16） can be detected by ELISA in pleural effusion （PE） and its concentration is higher than in serum. This study investigated the cellular sources of IL-16 in PE. Methods The samples o...Background Interleukin 16 （IL-16） can be detected by ELISA in pleural effusion （PE） and its concentration is higher than in serum. This study investigated the cellular sources of IL-16 in PE. Methods The samples of PE were collected from 34 patients who were newly diagnosed having PE in the pleural cavity We performed cell culture to purify the pleural mesothelial cells （PMC）, Wright staining to count the purity and immunocytochemical stain to identify the cultured cells. The intracellular IL-16 expression was detected by flow cytometry （FCM）. The different cells in PE were first separated by magnetic cell sorting （MCAS） then the separated cells were cultured in RPMI1640 with 10% fetal calf serum （FCS）. We extracted the supernatant and detected IL-16 concentration by ELISA. The IL-16 protein was detected by immunohistochemistry and double immunofluorescence staining. Results The percentages of cells which secreted IL-16 were： CD3^＋CD8^- cells （（74.27±15.56）%, n=34）; CD3^＋CD8^＋ cells （（69.86±18.55）%, n=34）; CD19^＋ cells （（45.30±18.77）%, n=15）; CD14^＋ cells （（16.91＋16.69）%, n=15）; and PMC （（2.05±1.85）%, n=7）. The concentrations of IL-16 in the supernatant from cultured cells were： CD4^＋ cells （（102.50±42.51） ng/L, n=5）; CD8^＋ cells （（92.58±18.34） ng/L, n=5）; CD19^＋ cells （（79.85±5.62） ng/L, n=5）; CD14^＋ cells （（58.51±25.38） ng/L, n=5）; and PMC （（18.14±8.37） ng/L, n=5）. In lymphocytes, monocytes/macrophages and PMC, we could observe the cells that expressed IL-16 protein. In paraffin-embedded sections, we also could observe by immunohistochemistry the CD4^＋I L-16^＋ cells, CD8^＋IL-16^＋ cells, CD19^＋IL-16^＋ cells, and CD14^＋IL-16^＋ cells. Conclusions IL-16 in PE is mainly secreted by T lymphocytes, including CD3^＋CD8^- cells and CD^3＋CD^8＋ cells. CD19^＋ cells and CD14^＋ cells can also secrete IL-16, but the percentage of PMC that can secrete IL-16 is very low.展开更多
AIM: To investigate gene variants in a large Italian inflammatory bowel disease (IBD) cohort, and to analyze the correlation of sub-phenotypes (including age at diagnosis) and epistatic interaction with other IBD gene...AIM: To investigate gene variants in a large Italian inflammatory bowel disease (IBD) cohort, and to analyze the correlation of sub-phenotypes (including age at diagnosis) and epistatic interaction with other IBD genes. METHODS: Total of 763 patients with Crohn's disease (CD, 189 diagnosed at age < 19 years), 843 with ulcerative colitis (UC, 179 diagnosed <19 years), 749 healthy controls, and 546 healthy parents (273 trios) were included in the study. The rs2241880 [autophagy-related 16-like 1 (ATG16L1)], rs11209026 and rs7517847 [interleukin 23 receptor (IL23R)], rs2066844, rs2066845, rs2066847 (CARD15), rs1050152 (OCTN1), and rs2631367 (OCTN2) gene variants were genotyped. RESULTS: The frequency of G allele of ATG16L1 SNP (Ala197Thr) was increased in patients with CD compared with controls (59% vs 54% respectively) (OR = 1.25, CI = 1.08-1.45, P = 0.003), but not in UC (55%). The frequency of A and G (minor) alleles of Arg381Gln, rs11209026 and rs7517847 variants of IL23R were reduced significantly in CD (4%, OR = 0.62, CI = 0.45-0.87, P = 0.005; 28%, OR = 0.64, CI = 0.55-0.75, P < 0.01), compared with controls (6% and 38%, respectively). The A allele (but not G) was also reduced signifi cantly in UC (4%, OR = 0.69, CI = 0.5-0.94, P = 0.019). No association was demonstrated with sub-phenotypes and interaction with CARD15 , and OCTN1/2 genes, although both gene variants were associated with pediatric-onset disease. CONCLUSION: The present study confirms the association of IL23R polymorphisms with IBD, and ATG16L1 with CD, in both adult- and pediatric-onset subsets in our study population.展开更多
目的探讨血清细胞因子信号转导负调控因子-3(suppressor of cytokine signaling 3,SOCS-3)、肿瘤坏死因子-α(tumor necrosis factor-α,TNF-α)、白细胞介素-16(interleukin-16,IL-16)及T辅助细胞1/T辅助细胞2(Th1/Th2)与妊娠期高血压...目的探讨血清细胞因子信号转导负调控因子-3(suppressor of cytokine signaling 3,SOCS-3)、肿瘤坏死因子-α(tumor necrosis factor-α,TNF-α)、白细胞介素-16(interleukin-16,IL-16)及T辅助细胞1/T辅助细胞2(Th1/Th2)与妊娠期高血压疾病(HDCP)的关系。方法选取2014年1月-2016年6月本院妇产科收治的妊娠期高血压疾病患者182例,其中妊娠期高血压组51例,轻度子痫前期组69例,重度子痫前期组62例。另选择同期分娩健康孕妇65例作为对照组。采用ELISA法检测各组孕妇血清SOCS-3、TNF-α、IL-16及Th1/Th2水平,分析重度子痫前期患者不良妊娠结局与各指标的关系。采用Spearman相关分析各组HDCP患者血清SOCS-3水平与TNF-α、IL-16及Th1/Th2的相关性。结果与对照组比较,轻度子痫前期组和重度子痫前期组血清SOCS-3水平均明显降低(0.59±0.12 vs 0.14±0.03和0.08±0.01;P均<0.05)。各组TNF-α、IL-16及Th1/Th2水平均高于对照组,且重度子痫前期组较轻度子痫前期组升高更明显[TNF-α(ng/L):12.58±2.37 vs 34.75±6.42和61.53±9.26;IL-16(ng/L):108.47±35.24 vs 187.63±81.47和284.62±113.58;Th1/Th2:9.27±2.38 vs20.15±4.82和26.48±6.13;P均<0.05]。重度子痫前期患者中,SOCS-3低表达组胎儿宫内窘迫综合征、胎儿生长受限及新生儿窒息的发生率均显著高于高表达组(P均<0.05),TNF-α、IL-16、Th1/Th2高表达组早产及胎儿生长受限的发生率均显著高于低表达组(P均<0.05)。相关分析显示,妊娠期高血压患者血清SOCS-3水平与TNF-α、IL-16、Th1/Th2均呈负相关(r=-0.528,r=-0.506,r=-0.126;P均<0.05)。结论监测孕妇血清SOCS-3、TNF-α、IL-16及Th1/Th2对妊娠期高血压疾病尤其是重度子痫前期的早发现、早诊断、早治疗具有一定的临床指导意义。展开更多
文摘Background Interleukin 16 （IL-16） can be detected by ELISA in pleural effusion （PE） and its concentration is higher than in serum. This study investigated the cellular sources of IL-16 in PE. Methods The samples of PE were collected from 34 patients who were newly diagnosed having PE in the pleural cavity We performed cell culture to purify the pleural mesothelial cells （PMC）, Wright staining to count the purity and immunocytochemical stain to identify the cultured cells. The intracellular IL-16 expression was detected by flow cytometry （FCM）. The different cells in PE were first separated by magnetic cell sorting （MCAS） then the separated cells were cultured in RPMI1640 with 10% fetal calf serum （FCS）. We extracted the supernatant and detected IL-16 concentration by ELISA. The IL-16 protein was detected by immunohistochemistry and double immunofluorescence staining. Results The percentages of cells which secreted IL-16 were： CD3^＋CD8^- cells （（74.27±15.56）%, n=34）; CD3^＋CD8^＋ cells （（69.86±18.55）%, n=34）; CD19^＋ cells （（45.30±18.77）%, n=15）; CD14^＋ cells （（16.91＋16.69）%, n=15）; and PMC （（2.05±1.85）%, n=7）. The concentrations of IL-16 in the supernatant from cultured cells were： CD4^＋ cells （（102.50±42.51） ng/L, n=5）; CD8^＋ cells （（92.58±18.34） ng/L, n=5）; CD19^＋ cells （（79.85±5.62） ng/L, n=5）; CD14^＋ cells （（58.51±25.38） ng/L, n=5）; and PMC （（18.14±8.37） ng/L, n=5）. In lymphocytes, monocytes/macrophages and PMC, we could observe the cells that expressed IL-16 protein. In paraffin-embedded sections, we also could observe by immunohistochemistry the CD4^＋I L-16^＋ cells, CD8^＋IL-16^＋ cells, CD19^＋IL-16^＋ cells, and CD14^＋IL-16^＋ cells. Conclusions IL-16 in PE is mainly secreted by T lymphocytes, including CD3^＋CD8^- cells and CD^3＋CD^8＋ cells. CD19^＋ cells and CD14^＋ cells can also secrete IL-16, but the percentage of PMC that can secrete IL-16 is very low.
基金The National Minister of Health grant, No. RC0702GA35
文摘AIM: To investigate gene variants in a large Italian inflammatory bowel disease (IBD) cohort, and to analyze the correlation of sub-phenotypes (including age at diagnosis) and epistatic interaction with other IBD genes. METHODS: Total of 763 patients with Crohn's disease (CD, 189 diagnosed at age < 19 years), 843 with ulcerative colitis (UC, 179 diagnosed <19 years), 749 healthy controls, and 546 healthy parents (273 trios) were included in the study. The rs2241880 [autophagy-related 16-like 1 (ATG16L1)], rs11209026 and rs7517847 [interleukin 23 receptor (IL23R)], rs2066844, rs2066845, rs2066847 (CARD15), rs1050152 (OCTN1), and rs2631367 (OCTN2) gene variants were genotyped. RESULTS: The frequency of G allele of ATG16L1 SNP (Ala197Thr) was increased in patients with CD compared with controls (59% vs 54% respectively) (OR = 1.25, CI = 1.08-1.45, P = 0.003), but not in UC (55%). The frequency of A and G (minor) alleles of Arg381Gln, rs11209026 and rs7517847 variants of IL23R were reduced significantly in CD (4%, OR = 0.62, CI = 0.45-0.87, P = 0.005; 28%, OR = 0.64, CI = 0.55-0.75, P < 0.01), compared with controls (6% and 38%, respectively). The A allele (but not G) was also reduced signifi cantly in UC (4%, OR = 0.69, CI = 0.5-0.94, P = 0.019). No association was demonstrated with sub-phenotypes and interaction with CARD15 , and OCTN1/2 genes, although both gene variants were associated with pediatric-onset disease. CONCLUSION: The present study confirms the association of IL23R polymorphisms with IBD, and ATG16L1 with CD, in both adult- and pediatric-onset subsets in our study population.
文摘目的探讨血清细胞因子信号转导负调控因子-3(suppressor of cytokine signaling 3,SOCS-3)、肿瘤坏死因子-α(tumor necrosis factor-α,TNF-α)、白细胞介素-16(interleukin-16,IL-16)及T辅助细胞1/T辅助细胞2(Th1/Th2)与妊娠期高血压疾病(HDCP)的关系。方法选取2014年1月-2016年6月本院妇产科收治的妊娠期高血压疾病患者182例,其中妊娠期高血压组51例,轻度子痫前期组69例,重度子痫前期组62例。另选择同期分娩健康孕妇65例作为对照组。采用ELISA法检测各组孕妇血清SOCS-3、TNF-α、IL-16及Th1/Th2水平,分析重度子痫前期患者不良妊娠结局与各指标的关系。采用Spearman相关分析各组HDCP患者血清SOCS-3水平与TNF-α、IL-16及Th1/Th2的相关性。结果与对照组比较,轻度子痫前期组和重度子痫前期组血清SOCS-3水平均明显降低(0.59±0.12 vs 0.14±0.03和0.08±0.01;P均<0.05)。各组TNF-α、IL-16及Th1/Th2水平均高于对照组,且重度子痫前期组较轻度子痫前期组升高更明显[TNF-α(ng/L):12.58±2.37 vs 34.75±6.42和61.53±9.26;IL-16(ng/L):108.47±35.24 vs 187.63±81.47和284.62±113.58;Th1/Th2:9.27±2.38 vs20.15±4.82和26.48±6.13;P均<0.05]。重度子痫前期患者中,SOCS-3低表达组胎儿宫内窘迫综合征、胎儿生长受限及新生儿窒息的发生率均显著高于高表达组(P均<0.05),TNF-α、IL-16、Th1/Th2高表达组早产及胎儿生长受限的发生率均显著高于低表达组(P均<0.05)。相关分析显示,妊娠期高血压患者血清SOCS-3水平与TNF-α、IL-16、Th1/Th2均呈负相关(r=-0.528,r=-0.506,r=-0.126;P均<0.05)。结论监测孕妇血清SOCS-3、TNF-α、IL-16及Th1/Th2对妊娠期高血压疾病尤其是重度子痫前期的早发现、早诊断、早治疗具有一定的临床指导意义。
