反复呼吸道感染患儿锌治疗前后红细胞CD35分子表达和血清炎性因子的变化

目的检测反复呼吸道感染（recurrent respiratory tract infection,RRTI）患儿红细胞表面CD。分子的表达,研究循环免疫复合物（CIC）和血清炎性因子在感染反复发生中的机制,并观察锌治疗的临床效果。方法将116例RRTI患儿根据不同感染部位分为上呼吸道感染组和下呼吸道感染组,随机选择同期发病的急性呼吸道感染患儿40例和50名健康儿童作为对照,检测红细胞膜CD35分子表达、CIC阳性率,以及IL-6、IL-8和TNF-α的含量。从116例RRTI患儿中选取68例患儿,随机分成锌治疗组（38例）和对照组（30例）,治疗结束时和结束后12周再次检测上述指标。结果RRTI患儿（上呼吸道感染组和下呼吸道感染组）红细胞膜CD35分子表达明显低于健康对照组（t值分别为6．17和6．46,P值均〈0．01）,而CIC阳性率及其他炎性因子则较健康对照组明显升高,且这些指标在下呼吸道感染中变化更为明显。感染缓解期的RRTI患儿较急性呼吸道感染患儿红细胞CD35表达明显降低（t=20．307,P〈0．01）。经过锌治疗后,RRTI患儿的各项指标明显改善。结论红细胞膜CD,,分子表达低下和CIC等血清炎性因子的过量产生可能是RRTI患儿反复呼吸道感染的重要免疫病理机制之一。锌治疗对上述指标的改善有一定的作用。     

芙露饮对频发感染患儿免疫力提升的疗效研究

目的探究芙露饮对频发呼吸道感染的患儿治疗效果及免疫力影响。方法选取2012年6月至2013年7月于本院就诊的反复呼吸道感染的患儿108例,依据分层随机分组法将患者分为治疗组及对照组,每组各54例;对照组给予常规抗感染等方法进行治疗;治疗组患儿在对照组治疗方案基础上加用口服芙露饮进行治疗,观察比较两组患儿治疗疗效、反复呼吸道感染的预防效果以及药物不良反应情况。结果治疗前两组患儿的免疫球蛋白G（Ig G）、免疫球蛋白A（Ig A）、免疫球蛋白M（Ig M）、C-反应蛋白（CRP）及血细胞沉降速率（ESR）比较差异均无统计学意义（P均〉0.05）;治疗1周后治疗组患儿的CRP、ESR及体温均显著低于对照组,差异具有统计学意义（P均〈0.05）;治疗2个月后治疗组患儿Ig G为（10.42±3.87）g/L、Ig A为（1.96±0.78）g/L及Ig M为（1.15±0.57）g/L,分别显著高于对照组的（8.13±3.46）g/L、（1.27±0.53）g/L和（0.82±0.46）g/L,差异均具有统计学意义（P均〈0.05）;治疗期间治疗组患者出现寒战及喘息例数显著低于对照组,差异有统计学意义（P均〈0.05）;治疗期间两组患儿出现头痛、恶心、腹泻及皮疹等不良反应的例数比较差异无统计学意义（P均〉0.05）。结论应用芙露饮辅助反复呼吸道感染患儿的治疗,可明显提高感染控制效果,提高患儿的免疫力。     

Immune responses and prediction of major infection in patients undergoing transhiatal or transthoracic esophagectomy for cancer

OBJECTIVE: To investigate alterations in immune responses after transhiatal versus transthoracic esophageal resection and to evaluate the role of preoperative immune functions in predicting postoperative infectious complications. SUMMARY BACKGROUND DATA: Impaired immune defense is associated with a decreased resistance to infection. Patients undergoing esophageal resection via a transhiatal or transthoracic approach are prone to develop infectious complications. There are no randomized data on immune responses after two major surgical interventions. METHODS: The study group consisted of 20 patients who were randomly allocated to a limited transhiatal or extended transthoracic esophagectomy for cancer. Blood samples were taken before the operation and at regular intervals thereafter from day 1 to day 10. Monocyte and T-helper type 1 (Th1) and type 2 (Th2) lymphocyte functions were assessed in stimulated whole blood cultures. RESULTS: Both surgical groups had severely depressed in vitro production of interleukin (IL)-12, IL-10, interferon-gamma, IL-2, IL-4, and IL-13 on postoperative day 1. Depression of Th2-type cytokine production was more profound after transthoracic than after transhiatal esophagectomy (IL-4, P=.005; IL-13,P=.007). Postoperative reduction in Th1-type cytokine production was similar between the two groups (interferon-gamma, P=.40; IL-2, P=.06). Irrespective of the surgical approach, patients who developed major infectious complications after surgery presented with a diminished T-cell cytokine production before the operation compared to those who had a relatively uneventful recovery (IL-4, P=.045; interferon-gamma, P=.064). In regression analysis, the occurrence of postoperative major infection was best predicted by increased duration of anesthesia ( P<.0001) and low preoperative interferon-gamma production ( P=.006). CONCLUSIONS: Both transhiatal and transthoracic esophagectomy induced severely depressed monocyte and T-lymphocyte cytokine production. The extent of the surgical procedure had a differential immunosuppressive impact on Th2-type but not on Th1-type cell activity, indicating that the two Th pathways were downregulated through distinct mechanisms. Preoperative interferon-gamma determination would be useful to anticipate the occurrence of postoperative major infectious complications.     

Impairment of nasal mucociliary clearance after radiotherapy for childhood head cancer

BACKGROUND: Radiotherapy of the head region in children is known to cause long-term sequelae, such as facial, dental, and ocular abnormalities. We investigated whether a decreased nasal mucociliary function occurs after radiotherapy of the head in children. METHODS: A saccharin/charcoal test was performed in 20 children treated with radiotherapy of the head and in 20 controls, age-matched and gender-matched. RESULTS: We found a decreased nasal mucociliary clearance (lower percentage of responses (p = 0083) and longer mucociliary transport times (p =.0001) in the patients compared with the controls. The radiotherapy dosage influenced the response to the test (p =.0046). CONCLUSIONS: Irradiation of the head in children may cause impairment of mucociliary function, even permanently, which may predispose children to upper respiratory infections. We would suggest careful monitoring of such patients to detect as early as possible the clinical effects of the functional changes and to prevent the evolution to chronic diseases.     

Impairment of helper T-cell function following severe head injury.

Major infections, such as sepsis and pneumonia, occur in 50-75% of patients following isolated severe head injury. Previous studies have demonstrated that this high incidence of infection following severe head injury may be related to a decrease in helper T-cell activation and function. The present study was designed to investigate the effect of severe head injury on specific subgroups of helper T cells known to enhance or suppress cellular immune function. Specifically, peripheral blood lymphocytes (PBLs) from 10 head-injured patients and 10 matched controls were evaluated following in vitro stimulation with the T-cell mitogen, phytohemagglutinin (PHA). Subsets of helper T cells evaluated included activated helper (CD4+/CD25+) T cells; helper/inducer (CD4+/CDw29+) T cells, which enhance cellular immune activity; and suppressor/inducer (CD4+/CD45R+) T-cells, which induce suppressor (CD8+) T-cells. In addition, the effect of intraventricular fluid (IVF) on PHA-stimulated in vitro CD4 and CD25 expression was investigated to determine whether severe head injury results in the production of mediators within the central nervous system capable of affecting T-cell activation. The results of this study indicate that isolated severe head injury selectively reduces the ability of PHA-stimulated PBLs to express the helper/inducer (CD4+/CDw29+) T-cell (p = 0.023) and activated helper (CD4+/CD25+) T-cell (P = 0.041) phenotypes. There was no significant change in PHA-stimulated CD4 or CD25 expression following incubation of PBLs with intraventricular fluid (IVF) from head-injured patients. The relationship between these changes in specific helper T-cell subpopulations and the infectious complications of severe head injury are discussed.     

Predominance of type-2 immune response in idiopathic membranous nephropathy. Cytoplasmic cytokine analysis

BACKGROUND: The Th1/Th2 paradigm is proving increasingly useful in the understanding of infectious diseases and many autoimmune diseases. Th1 cells predominantly produce interleukin-2 (IL-2) and interferon-gamma (IFN-gamma) and are instrumental in initiating delayed-type hypersensitivity and activating macrophages. Th2 cells secrete other cytokines, such as IL-4, IL-5, IL-10 and IL-13 that trigger B-cell activation and immunoglobulin synthesis. It has been shown that in patients with membranous nephropathy, there may be a predominance of Th2, because of the presence of IgG, particularly IgG4, which belongs to a subclass of the type-2 immune response, and complement deposits in glomeruli. In this study, we investigated the immunoresponse of helper T cells, i.e. Th predominance in patients with idiopathic membranous nephropathy. METHODS: We used flow cytometry to assess the levels of circulating Th cells in patients with idiopathic membranous nephropathy (n = 8) and in normal individuals (n = 23) based on the expression of intracellular type-1 and type-2 cytokines. Because the production of each of these cytokines has a specific time course, we observed the cytokine synthesis at 3, 6, 9 and 12 h after stimulation. RESULTS: The percentages of IL-2+/CD4+ cells from patients with idiopathic membranous nephropathy were significantly lower than those from normal individuals at 6, 9 and 12 h, with the difference becoming more significant over time. IFN-gamma+/CD4+ cells and IL-4+/CD4+ cells were not significantly different between the two groups. In patients with idiopathic membranous nephropathy, the percentages of IL-10+/CD4+ cells were significantly higher than those in normal individuals at each point in time. CONCLUSION: Increased IL-10-producing Th cells may lead to suppression of delayed-type hypersensitivity and activate suppressor cells and IgG4 synthesis, resulting in idiopathic membranous nephropathy.     

Ataxia-telangiectasia. X,14 translocation, progressive deterioration of lymphocyte numbers and function, and abnormal in vitro immunoglobulin production

Three children with ataxia-telangiectasia have been followed up since their early childhood. Sequential immunological, biochemical and chromosome studies have been performed over the last 7 years. All the children showed progressive cerebellar ataxia and inexorable neurological deterioration. Further evidence for the progressive nature of this condition is the fall in lymphocyte counts, deterioration of lymphocyte transformation responses to mitogens, and an increase in chromosomal translocations and breakage. Elevated serum alpha-fetoprotein levels are a highly characteristic and useful diagnostic finding in this condition. Two of the patients had an X,14 translocation. In vitro studies of immunoglobulin synthesis suggest an intrinsic defect in B-cell synthesis as well as decreased helper T-cell activity. In spite of moderately severe and progressive abnormalities in the immune system, sinopulmonary infections have not been prominent in our patients.     

The effect of surgical site infections on outcomes and resource utilization after liver transplantation

BACKGROUND: Although postoperative infections have a significant impact on morbidity and mortality after orthotopic liver transplantation (OLT), less is known about their economic implications. In this study, we sought to identify risk factors and estimate the impact of surgical site infections on 1-year mortality, graft survival, and resource utilization after OLT. METHODS: We studied 777 first, single-organ liver transplant recipients from the National Institute of Diabetes and Digestive and Kidney Diseases Liver Transplantation Database. Surgical site infections (n = 292, 37.8%) were defined as bacterial or fungal infections of the liver, intestine, biliary tract, surgical wound, or peritoneum within 1 year of transplantation. A subset of these (n = 159) occurred during the transplant hospitalization and were used to estimate excess charges associated with surgical site infections. RESULTS: Leaks in the choledochojejunostomy (odds ratio [OR] = 7.1, P =.001) and choledochocholedochostomy (OR = 2.5, P =.002), extended operation duration in hours (OR = 1.2, P =.002), serum albumin levels in grams per liters (OR = 0.71, P =.009), ascites (OR = 1.43, P =.037), and administration of OKT3 within 7 days (OR = 1.49, P =.039) significantly increased risk of infection. Surgical site infections did not significantly increase 1-year mortality (88.5% vs 91.5%, P =.19) but significantly increased 1-year graft loss (79.8% vs 86.5%, P =.022). Patients with surgical site infections incurred approximately 24 extra hospital days and $159,967 in excess charges (P =.0001). Multivariate analysis reduced the estimate of excess charges to $131,276 (P =.0001). CONCLUSIONS: Liver transplant recipients who develop surgical site infection have significantly higher resource utilization requirements than those who do not. These results imply substantial returns to preventative efforts directed at surgical site infections in patients undergoing OLT.     

Glomerulonephritis and IgA deficiency

A mild self-limiting mesangial proliferative glomerulonephritis is described in 3 patients with selective IgA deficiency (less than 0.05 g/l). In all cases there was irregular thickening of peripheral glomerular capillary loops and paramesangial deposits. Arteriolar hyalinosis was present in two of the three cases. By direct immunofluorescence, and immunoperoxidase techniques in one case, IgM was present in the glomeruli and C3 was present in blood vessel walls. Secretory component was not detected in the glomeruli of any of the patients. The polyethylene glycol (PEG) precipitation immune complex assay was positive for IgM and IgG immune complexes in one patient and weakly positive for IgM immune complexes alone in another. The serum of one patient contained milk precipitins. All three patients had suffered from recurrent upper respiratory tract infections. It is suggested that the glomerular IgM immune complex deposition is related to the IgA deficiency and that, although the immune complexes may be a consequence of antibodies to dietary bovine proteins, this could be due to recurrent upper respiratory tract infections. This type of glomerulonephritis appears to resemble IgM associated glomerulonephritis in some aspects. Careful appraisal is required to establish if this association constitute a specific entity.     

Plasma levels of interleukin-8 and expression of interleukin-8 receptors on circulating neutrophils and monocytes after cardiopulmonary bypass in children

OBJECTIVE: Cardiopulmonary bypass induces a systemic inflammatory response that causes substantial clinical morbidity. This study sought to determine cellular and humoral variables of inflammation. We hypothesized that chemokines are a major source of stimulation of neutrophils and monocytes in pediatric cardiac surgery. METHODS: We performed an observational prospective clinical study of 20 pediatric patients before and after cardiopulmonary bypass. Plasma levels of interleukin-6, interleukin-8, myeloperoxidase, and nitric oxide were measured by immunoassays. Expression of interleukin-8 receptors (CXCR1, CXCR2) and CD14 of circulating neutrophils and monocytes was assessed by flow cytometry. Clinical evaluations included length of inotropic support and mechanical ventilation as well as oxygenation. RESULTS: Two hours after cardiopulmonary bypass, plasma levels of interleukin-6 and interleukin-8 were strongly increased (P =.0001 and P =.0032, respectively). Interleukin-6 and interleukin-8 concentrations correlated with the length of inotropic support, as well as with the length of mechanical ventilation (r >.70, P .62, P 相似文献   

Cell-mediated immune response to influenza vaccination in lung transplant recipients.

BACKGROUND: Lung transplant recipients are susceptible to complications from influenza infection. Antibody responses to influenza vaccination have been shown to be decreased in lung transplant recipients. Cellular immune mechanisms serve an important role in influenza clearance. The cellular immune response to influenza vaccination has not been studied in transplant populations. METHODS: Interleukin-2, interleukin-10, interferon-gamma, and granzyme B levels to the three viral antigens included in the 1999 to 2000 influenza vaccine were measured before and 4 weeks post-vaccination in 43 lung transplant recipients and 21 healthy adult controls. RESULTS: Interleukin-2, interleukin-10, interferon-gamma, and granzyme B levels did not increase from pre- to post-vaccination in the lung transplant group. Both pre- and post-cytokine levels were lower in the transplant group compared to the control group. Pre- and post-granzyme B levels did not differ significantly between the groups. The T-helper response in the control group varied with the different viral strains. A correlation between acute rejection episodes and the absence of both azathioprine and mycophenolate was found. CONCLUSIONS: Influenza vaccination does not stimulate a cell-mediated immune response in lung transplant recipients as judged by interleukin-2, interleukin-10, interferon-gamma, and granzyme B levels. Alternative prevention strategies may be needed.     

Recurrent acute glomerulonephritis

Biopsy-proven recurrent acute glomerulonephritis (AGN) is extremely rare and is usually seen in children with acute, well-defined streptococcal infections. We present here a patient with recurrent AGN in the absence of chronic bacterial infection. The subject, an 80-year-old man, had eight episodes of acute nephritic syndrome following upper respiratory tract infection. No abnormalities were detected during remissions. Renal biopsies during two of those episodes showed typical postinfectious acute exsudative endocapillary glomerulonephritis, while results of another biopsy performed during remission were normal.     

Immunological studies in children with chronic pulmonary infection.

Twenty-three children with chronic pulmonary symptoms following acute lower respiratory tract infection were investigated with a view to establishing their immune status. Cell-mediated immunity was depressed in the majority. Serial testing over some months showed improvement in some and fluctuation or non-recovery in others. The leucocyte function, gamma-globulin and immunoglobulin levels were normal.     

Secretion of A-type and B-type natriuretic peptides into the bloodstream and pericardial space in children with congenital heart disease

OBJECTIVE: To determine the secretion of A-type and B-type natriuretic peptides into the bloodstream and pericardial space in children with congenital heart disease. METHODS: Plasma and pericardial fluid samples were obtained from 77 patients undergoing total correction for congenital heart disease. All patients underwent detailed right-sided and left-sided cardiac catheterization preoperatively. RESULTS: A-type natriuretic peptide levels in pericardial fluid were lower than those in plasma (33.0 +/- 23.1 versus 39.8 +/- 33.6 pg/mL, P <.05), and B-type natriuretic peptide levels in pericardial fluid showed marked elevations compared with those in plasma (231.9 +/- 305.6 versus 19.8 +/- 29.3 pg/mL, P <.0001). The A-type and B-type natriuretic peptide levels in plasma correlated with those in pericardial fluid (R =.522, P <.0001; R =.595, P <.0001). For A-type and B-type natriuretic peptide levels in plasma, the relation with biventricular volume had the highest correlation (R =.669, P <.0001; R =.652, P <.0001). The patients with a pulmonary-to-systemic flow ratio greater than 2 (n = 19) had high levels of natriuretic peptides not only in plasma (58.3 +/- 43.2, 40.5 +/- 49.4 pg/mL, P <.05) but also in pericardial fluid (44.4 +/- 31.5, 287.2 +/- 198.5 pg/mL, P <.05), and higher correlation between A-type and B-type natriuretic peptide plasma levels and left ventricular volume (R =.913, P <.0001; R =.787, P <.0001). CONCLUSIONS: B-type natriuretic peptide is secreted not only into the bloodstream but also into the pericardial space in children with congenital heart disease. Natriuretic peptide levels in plasma correlated well with biventricular volume. The left ventricle was considered to be the main source of secreted natriuretic peptides in the patients with a pulmonary-to-systemic flow ratio greater than 2.     

The role of CC chemokine receptor 5 (CCR5) in islet allograft rejection

Chemokines are important regulators in the development, differentiation, and anatomic location of leukocytes. CC chemokine receptor 5 (CCR5) is expressed preferentially by CD4(+) T helper 1 (Th1) cells. We sought to determine the role of CCR5 in islet allograft rejection in a streptozotocin-induced diabetic mouse model. BALB/c islet allografts transplanted into CCR5(-/-) (C57BL/6) recipients survived significantly longer (mean survival time, 38 +/- 8 days) compared with those transplanted into wild-type control mice (10 +/- 2 days; P < 0.0001). Twenty percent of islet allografts in CCR5(-/-) animals without other treatment survived >90 days. In CCR5(-/-) mice, intragraft mRNA expression of interleukin-4 and -5 was increased, whereas that of interferon-gamma was decreased, corresponding to a Th2 pattern of T-cell activation in the target tissues compared with a Th1 pattern observed in controls. A similar Th2 response pattern was also observed in the periphery (splenocytes responding to donor cells) by enzyme-linked immunosorbent spot assay. We conclude that CCR5 plays an important role in orchestrating the Th1 immune response leading to islet allograft rejection. Targeting this chemokine receptor, therefore, may provide a clinically useful strategy to prevent islet allograft rejection.     

Interleukin-8 and CXCR1 receptor functional polymorphisms and susceptibility to acute pyelonephritis

PURPOSE: We performed a case-control study in children diagnosed by the first episode of upper urinary tract infection with or without vesicoureteral reflux to evaluate the association of functional polymorphism of interleukin-8 (-251A>T and +2767A>G), and its receptor CXCR1 (+2607G>C). MATERIALS AND METHODS: Genomic DNA was obtained from 265 children with a clinical and laboratory diagnosis of urinary tract infection who were recruited in northeast Italy. The children were subdivided as 173 who were dimercapto-succinic acid scan positive with positive static renal scintigraphy in acute conditions, consistent with the diagnosis of acute pyelonephritis, and 92 who were dimercapto-succinic acid scan negative. Genetic analysis for the same polymorphisms was also extended to a control population of 106 umbilical cord DNA samples. RESULTS: Statistical analysis of genotype data showed that 1) the tested populations were in Hardy-Weinberg equilibrium, 2) there were significant differences between the dimercapto-succinic acid scan positive and negative groups (p=0.049), and the dimercapto-succinic acid scan positive group vs controls (p=0.032) in terms of interleukin-8 -251A>T polymorphism frequency, 3) there was also a significant difference in the distribution of IL-8 -251A>T and +2767A>G polymorphisms between dimercapto-succinic acid scan positive and negative children in the subgroup without vesicoureteral reflux (p=0.03 and 0.02, respectively) and 4) no significant differences were found in the frequency of the distribution of CXCR1 +2607G>C polymorphism in all groups. CONCLUSIONS: These data suggest that the gene for the proinflammatory chemokine interleukin-8 is involved in susceptibility to acute pyelonephritis during upper urinary tract infection in children with or without vesicoureteral reflux.     

Composition of IgA-containing circulating immune complexes in IgA nephropathy

Macromolecular IgA is found with a relatively high frequency in the sera of patients with IgA nephropathy (IgAN). This macromolecular IgA consists of polymeric IgA, IgA-containing immune complexes, or both. The presence of polymeric IgA antibodies reflects a recent IgA response. Vaccination data in patients with IgAN suggest that these patients respond more vigorously with their mucosal immune system than do controls. The association of exacerbations with upper respiratory tract infections suggests that the immunogenic stimuli probably are of microbial origin and are presented to mucosal surfaces. Analysis by sucrose density ultracentrifugation has shown that the macromolecular IgA may contain IgG, IgA rheumatoid factor, and C3. The search for the antigen or antigens specifically responsible for IgAN has been unsuccessful. Although IgG and IgA rheumatoid factor may contribute, they do not account for the pathogenesis of the disease in all patients. Alternative mechanisms have to be assumed for patients who do not have detectable levels of IgA-containing immune complexes. They could have polymeric IgA or IgA-containing immune complexes intermittently, as has been shown in children with relapsing IgAN. The binding of circulating IgA antibodies to antigens present in the mesangium can lead to the local formation of deposits in the absence of circulating IgA complexes.     

Th2 cells predominate in idiopathic steroid-sensitive nephrotic syndrome

Background  

Various studies reported a higher incidence of allergic disorders, with an overreactivity of type 2 helper T-cell (Th2) immune mechanisms, in children with idiopathic steroid-sensitive nephrotic syndrome (ISSNS). However, Th2 predominance in ISSNS has not been definitively identified. To determine whether Th2 was predominant in children with ISSNS, we used paired samples to measure the type 1 helper T-cell (Th1)/Th2 ratios and serum cytokine levels secreted by Th1 and Th2.     

Henoch-Schönlein purpura in Wiskott-Aldrich syndrome

Wiskott-Aldrich syndrome (WAS) is a rare immune deficiency disease. Sialophorin glycosylation is defective in WAS. Although it is not very common, renal involvement including IgA nephropathy (IgAN) was reported. Abnormal glycosylation plays a key role in the pathogenesis of IgAN. We present an 8-year-old boy with WAS who had recurrent episodes of Henoch-Schönlein purpura with renal involvement following upper respiratory tract infections. His renal function did not deteriorate. Both IgAN and WAS have glycosylation defects, but there must be some other factors (genetic and environmental) to explain their rare association.