Study on neutrophil functions in infectious diseases in a allergic diseases and analysis of intracelluar signal transmission

(1)慢性肉芽肿病患者CD4+CD29+（记忆T）细胞减少。慢性肉芽肿病（Chronic granulomatous disease， CGD）是一种具有代表性的遗传性吞噬细胞疾病，迄今为止从吞噬细胞的角度对其进行了广泛的评价，但在淋巴细胞功能方面的研究尚不充分。我们的研究显示了CGD患者淋巴细胞亚群的差异，这可能对阐明该病的病理生理有一定的贡献。(2)甲氧苄啶-磺胺甲恶唑治疗1例高免疫球蛋白E综合征患者成功。高免疫球蛋白E综合征是一种独特的综合征，特别是在感染和过敏方面，其病因尚不清楚。我们的病人有反复发作的细菌感染，这是传统的抗微生物药物耐药。磺胺甲恶唑-甲氧苄啶（ST）治疗在大多数CGD患者中已建立临床疗效，该患者已成功应用。临床改善还与一些中性粒细胞功能的正常化以及血清IgE水平明显升高的降低有关。虽然它是小和轶事，这项研究当然可以帮助了解这种神秘综合征的本质。(3)粪诱导肺泡巨噬细胞活化介导的肺损伤。为了阐明胎粪诱导的细胞损伤机制，我们研究了胎粪对兔肺泡巨噬细胞（AM）的影响。AM与胎粪共同培养时，AM的超氧阴离子产量显著增加。结合其他一系列实验结果，我们的结果表明，粪诱导的肺损伤可能是通过肺泡巨噬细胞的激活而发生的，巨噬细胞-上皮细胞轴可能在粪诱导的肺损伤的发病机制中起重要作用。(4)兔肺泡巨噬细胞超氧阴离子生成的成熟变化。了解与年龄相关的细胞功能的变化对于解释新生儿的一些生物学现象是重要的。利用兔肺泡巨噬细胞，我们发现即使在幼兔中，通过直接刺激蛋白激酶C. Less的趋化肽，超氧化物的产生能力也得到了充分的发展

(1) Decreased CD4+CD29+ (memory T) cells in patients with chronic granulomatous disease.Chronic granulomatous disease (CGD) , a representative hereditary phagocyte disorder, has so far been extensively evaluated from the aspect of phagocytes but has not been duly studied in terms of lymphocyte functions. Our study has demonstrated differences in lymphocyte subsets in patients with CGD,which may hopefully be of some contribution in clarifying pathophysiology of the disease.(2) Successful trimethoprim-sulfamethoxazole therapy in a patient with hyperimmunoglobulin E syndrome.Hyperimmunoglobulin E syndrome, of which etiology still remaines to be elucidated, is one of the unique syndromes especially in terms of infections as well as allergy. The patient we experienced had repeated episodes of bacterial infections which were resistant to conventional antimicrobial medications. Sulfamethoxazole-trimethoprim (ST) therapy, of which clinical efficacy has been established in the majority of CGD p … More atients, has been successfully employed in this patient. Clinical improvement was also associated with normalization in some neutrophil functions as well as a decrease in markedly elevated serum IgE level. Although it was small and anecdotal, this study can certainly be of help in understanding the nature of this enigmatic syndrome.(3) Meconium-induced lung injury mediated by activation of alveolar macrophages.To clarify the machanism of meconium-induced cellular injury, we examined the effect of meconium on the rabbit alveolar macrophages (AM) . Superoxide anion production of AM significantly increased when AM were cultured with meconium. When combined with those of a series of other experiments, our results suggest that meconium-induced lung injury may occur through an activation of alveolar macrophages and that the macrophage-epithelial cell axis may be important for the pathogenesis of meconium-induced injuries.(4) Maturational changes in superoxide anion production of rabbit alveolar macrophages.Understanding of changes of age-related celluar functions are important in interpreting a number of biological phenomena in newborns. Using rabbit alveolar macrophages, we showed that the ability of superoxide production is sufficiently developed even in young rabbits with a chemotactic peptide which directly stimulates protein kinase C. Less