脐血SP-D测定及其与自发早产儿预后的关系

目的测定自发早产儿脐血SP-D的浓度,随访早产儿住院时间,探讨脐带血SP-D浓度与早产儿住院时间的相关性.方法母孕23至32周分娩的早产儿165名,和46名健康足月儿入选本实验.利用酶联免疫吸附试验(ELISA)技术测定其脐带血中SP-D浓度.随访早产儿住院时间.结果自发早产儿脐带血SP-D浓度明显升高,差异具有统计学意义;早产儿脐带血SP-D浓度和ICU住院时间呈正相关.结论新生儿血清SP-D浓度的升高可能参与了自发早产的过程,脐带血SP-D浓度可作为判断早产儿严重程度的指标之一.     

Decidual expression and localization of human surfactant protein SP-A and SP-D,and complement protein C1q

Surfactant proteins SP-A and SP-D, and complement protein C1q are soluble innate immune pattern recognizing molecules. SP-A, SP-D and C1q have an overall similar structure composed of an N-terminal triple-helical collagen region that is followed by a trimeric globular domain. While SP-A and SP-D belong to the collectin family (collagen containing lectin), C1q is the first recognition subcomponent of the classical pathway of the complement system. Recently, SP-A, SP-D and C1q have been considered to play important roles in early and late pregnancy. However, their expression in early human decidua has not been examined. Here, we investigated whether SP-A, SP-D and C1q are expressed within first trimester decidua in humans and their expression is associated with trophoblasts and decidual stromal cells. Decidual samples from women undergoing elective vaginal termination of pregnancy during first trimester were obtained from 25 subjects. Immunohistochemical studies using anti-human SP-A, anti-human SP-D and anti-human C1q antibodies were performed on decidual tissue sections along with anti-vimentin and cytokeratin-7 antibodies to identify stromal cells and trophoblasts. The expression was also examined by immunostaining and PCR using decidual and stromal cells. C1q expression was significantly higher when compared to SP-A and SP-D in the first trimester human decidua. Double immunostaining revealed that all stromal cells and trophoblasts expressed SP-A, SP-D and C1q, while only few invasive trophoblasts expressed C1q. Thus, expression of SP-A, SP-D and C1q in human decidua during first trimester suggests potential role of SP-A, SP-D and C1q during the early stages of pregnancy including implantation, trophoblast invasion and placental development.     

Chard (Beta vulgaris var. cicla) extract improved hyperglycemia-induced oxidative stress and surfactant-associated protein alterations in rat lungs

Abstract

Context: Chard is used as an antidiabetic agent by the diabetic patients in Turkey.

Objective: The effect of chard extract [Beta vulgaris L. var. cicla (Chenopodiaceae)] on the antioxidant system and the expression of surfactant-associated proteins (SP) in the lungs of hyperglycemic rats were examined.

Materials and methods: Hyperglycemia was induced by a single dose of streptozotocin (60?mg/kg) provided intraperitoneally. Fourteen days after the rats were rendered hyperglycemic, the chard (2?g/kg/d), insulin (6?U/kg/d), and chard plus insulin (as mentioned above) were administered to rats for 45?d. On day 60, rats’ lungs were removed. Oxidative stress parameters and SP expression were assayed.

Results: The lungs of hyperglycemic rats were characterized by the induced lipid and protein oxidation, elevated myeloperoxidase and xanthine oxidase activities, decreased glutathione levels, and reduced tissue factor and antioxidant enzymes activities (catalase, superoxide dismutase, glutathione peroxidase, and glutathione-S-transferase). Chard treatment alone and chard treatment combined with insulin were capable of achieving a regression of pulmonary oxidative stress, by inhibiting lipid and protein oxidation, and restoring the antioxidant system of hyperglycemic rats. SP-A expressions were significantly unchanged in all groups, whereas pro-SP-C and SP-D expressions were reduced in hyperglycemic rats. Pro-SP-C and SP-D levels were increased by chard and insulin administrations alone and combined in hyperglycemic rats.

Discussion and conclusion: All treatments have a positive effect on the surfactant and antioxidant systems of the lungs of hyperglycemic rats. The best therapeutic effect was provided by treatment with chard extract alone in the compensation of hyperglycemic symptoms.     

The immunoregulatory roles of lung surfactant collectins SP-A, and SP-D, in allergen-induced airway inflammation

It has become increasingly evident that pulmonary surfactant proteins, SP-A and SP-D, present in the alveolar and bronchial epithelial fluid linings, not only play significant functions in the innate defense mechanism against pathogens, but also are involved in immunomodulatory roles, which result in the protection against, and resolution of, allergen-induced airway inflammation. Studies on allergen-sensitized murine models, and asthmatic patients, show that SP-A and SP-D can: specifically bind to aero-allergens; inhibit mast cell degranulation and histamine release; and modulate the activation of alveolar macrophages and dendritic cells during the acute hypersensitive phase of allergic response. They also can alleviate chronic allergic inflammation by inhibiting T-lymphocyte proliferation as well as increasing phagocytosis of DNA fragments and clearance of apoptotic cell debris. Furthermore, it has emerged, from the studies on SP-D-deficient mice, that, when these mice are challenged with allergen, they develop increased eosinophil infiltration, and abnormal activation of lymphocytes, leading to the production of Th2 cytokines. Intranasal administration of SP-D significantly attenuated the asthmatic-like symptoms seen in allergen-sensitized wild-type, and SP-D-deficient, mice. These important findings provide a new insight of the role that surfactant proteins play in handling environmental stimuli and in their immunoregulation of airway inflammatory disease.     

The SARS coronavirus spike glycoprotein is selectively recognized by lung surfactant protein D and activates macrophages

The severe acute respiratory syndrome coronavirus (SARS-CoV) infects host cells with its surface glycosylated spike-protein (S-protein). Here we expressed the SARS-CoV S-protein to investigate its interactions with innate immune mechanisms in the lung. The purified S-protein was detected as a 210 kDa glycosylated protein. It was not secreted in the presence of tunicamycin and was detected as a 130 kDa protein in the cell lysate. The purified S-protein bound to Vero but not 293T cells and was itself recognized by lung surfactant protein D (SP-D), a collectin found in the lung alveoli. The binding required Ca(2+) and was inhibited by maltose. The serum collectin, mannan-binding lectin (MBL), exhibited no detectable binding to the purified S-protein. S-protein binds and activates macrophages but not dendritic cells (DCs). It suggests that SARS-CoV interacts with innate immune mechanisms in the lung through its S-protein and regulates pulmonary inflammation.     

Regulation of surfactant protein D in the mouse female reproductive tract in vivo

Surfactant protein D (SP-D) plays a role in innate immunity in the lung and is expressed at many other mucosal surfaces throughout the human body. In this study, we show that SP-D mRNA and protein are present in the murine female reproductive tract; i.e. in the vagina, cervix, uterus and oviduct. SP-D protein is primarily localized to epithelial cells lining the genital tract and is also present in secretory material within the lumen of the uterus and cervix. The levels of SP-D mRNA in the uterus vary by a factor of 10 during the estrous cycle with peak levels present at estrus and the lowest levels at diestrus. In contrast, SP-D mRNA levels in the lung do not change during the estrous cycle. Since SP-D is an innate host defense protein present in the mouse reproductive tract, we studied the influence of infection on SP-D levels in vivo. We found that Chlamydia muridarum infection caused an increase in the SP-D protein content of reproductive tract epithelial cells. These data are suggestive that SP-D may play a role in innate immunity in the female reproductive tract in vivo.     

Acute inflammatory and immunologic responses against antigen in chronic bird-related hypersensitivity pneumonitis

BackgroundHypersensitivity pneumonitis (HP) is an immune-mediated lung disease induced by the inhalation of a wide variety of antigens and a persistent antigen exposure induces inevitably pulmonary fibrosis in chronic HP. Although neutrophils, Th1 and Th17 cells contribute to lung inflammation in acute phase of HP, there is no clear explanation as to how the immunological reaction occurs just after the inhalation of causative antigens in the chronic phase of HP.MethodsWe examined the inflammatory and immunologic profiles before and after the inhalation provocation test (IPT) in serum and bronchoalveolar lavage fluid (BALF) from patients with chronic bird-related HP (BRHP) and other interstitial lung diseases (ILDs). We analyzed BALF samples from 39 patients (19 BRHP and 20 other ILDs) and serum samples from 25 consecutive patients (20 BRHP and 5 other ILDs) who underwent the IPT.ResultsA significant increase of neutrophils was observed in the BALF from the BRHP patients following the IPT. Neutrophil chemoattractants, namely, granulocyte colony-stimulating factor, IL-6, IL-8, IL-17, and CXCL2 significantly increased in both the serum and BALF of the BRHP patients after the IPT. Serum IFN-γ and CXCL10, cytokines/chemokines that contributed to Th1 inflammation, were also significantly increased in BRHP following the IPT.ConclusionsThis study demonstrated the exposure to the causative antigen provoked acute neutrophilic and Th1 immunologic responses similar to acute HP even in the chronic phase of HP.