Home About us Contact
|
Home About us Contact | ||
|
|
||
Surfactant Protein (surfactant + protein)
Selected AbstractsProteomic analysis of pulmonary sclerosing hemangiomaPROTEINS: STRUCTURE, FUNCTION AND BIOINFORMATICS, Issue 17 2006Lian-Jin Jin Abstract Sclerosing hemangioma (SH) is a rare benign pulmonary tumor derived from the primitive respiratory epithelium. However, the pathogenesis of SH has not yet been clear. Surfactant protein, thyroid transcription factor-1, epithelial membrane antigen, cytokeratin, and vimentin have been identified in SH by immunohistochemistry and electron microscopy. To identify proteins specifically regulated in SH, 2-D PAGE was performed using SH and paired normal tissues. Ten selected differentially expressed protein spots were identified by PMF, MALDI-TOF-MS, and database searching. Apolipoprotein,A-1, antizyme inhibitor, heat shock 27-kDa protein,1, and antioxidant proteins, such as peroxiredoxin,II (Prx,II) and GST, were identified among the down-regulated proteins in SH. Western blot and immunohistochemistry confirmed reduced expressions of Prx,II and GST in SH versus normal lung tissue. This study is the first report on the reduced expressions of Prx,II and GST in SH. [source] Surfactant protein A and D gene polymorphisms and protein expression in victims of sudden infant deathACTA PAEDIATRICA, Issue 1 2009Arne Stray-Pedersen Abstract Aim: To investigate the innate immune components surfactant protein A (SP-A) and D (SP-D) in victims of sudden infant death syndrome (SIDS). Methods: Ten common single nucleotide polymorphisms (SNPs) in the exons of SP-A1, SP-A2 and SP-D genes were analysed in 42 cases of SIDS and 46 explained sudden infant deaths. SP-A and SP-D protein expression in tissue from the aerodigestive tract was semi-quantitatively evaluated by immunohistochemistry. Results: SP-D immunoreactivity was found in lungs and tissue from submandibular gland, palatine tonsils and duodenum. Positive SP-A immune staining was found exclusively in lung tissue. Neither the allele nor the haplotype distribution of the SP-A and SP-D genes was significantly different in SIDS compared to explained deaths. The most common SP-A haplotype, 6A2/1A0, tended to be overrepresented in the cases with low immunohistochemical SP-A expression (61%) compared to cases with high expression (49%), p = 0.08. The SP-D expression was not influenced by the 11 C/T or 160 A/G polymorphisms. Conclusion: No significant association between the common genetic variants of SP-A and SP-D and SIDS is disclosed by the present study. However, low SP-A protein expression may possibly be determined by the 6A2/1A0 SP-A haplotype, this should be subject for further investigation. [source] NKX2-1 mutations leading to surfactant protein promoter dysregulation cause interstitial lung disease in "Brain-Lung-Thyroid Syndrome",HUMAN MUTATION, Issue 2 2010Loïc Guillot Abstract NKX2-1 (NK2 homeobox 1) is a critical regulator of transcription for the surfactant protein (SP)-B and -C genes (SFTPB and SFTPC, respectively). We identified and functionally characterized two new de novo NKX2-1 mutations c.493C>T (p.R165W) and c.786_787del2 (p.L263fs) in infants with closely similar severe interstitial lung disease (ILD), hypotonia, and congenital hypothyroidism. Functional analyses using A549 and HeLa cells revealed that NKX2-1-p.L263fs induced neither SFTPB nor SFTPC promoter activation and had a dominant negative effect on wild-type (WT) NKX2-1. In contrast,NKX2-1-p.R165W activated SFTPC, to a significantly greater extent than did WTNKX2-1,whileSFTPB activation was only significantly reduced in HeLa cells. In accordance with our in vitro data, we found decreased amounts of SP-B and SP-C by western blot in bronchoalveolar lavage fluid (patient with p.L263fs) and features of altered surfactant protein metabolism on lung histology (patient with NKX2-1-p.R165W). In conclusion, ILD in patients with NKX2-1 mutations was associated with altered surfactant protein metabolism, and both gain and loss of function of the mutated NKX2-1 genes on surfactant protein promoters were associated with ILD in "Brain-Lung-Thyroid syndrome". © 2009 Wiley-Liss, Inc. [source] Surfactant protein expression is increased in the ipsilateral but not contralateral lungs of fetal sheep with left-sided diaphragmatic hernia,PEDIATRIC PULMONOLOGY, Issue 4 2005Marcus G. Davey PhD Abstract Congenital diaphragmatic hernia (CDH) impairs fetal lung growth and increases the density of alveolar epithelial type 2 (AE2) cells. There is controversy whether surfactant protein (SP) expression is altered in CDH. The primary aim of this study was to assess SP expression (mRNA and protein) in the left and right lungs of fetal sheep with and without a diaphragmatic hernia (DH). Left-sided DH was created in four fetal sheep at 65 days of gestational age (g.a.). Sham-operated animals were used as controls. At 138 days g.a., lungs were harvested and the following parameters were measured: SP-A, -B, and -C mRNA expression (Northern blot), SP-A and -B expression (Western blot), and AE2 cell density (immunohistochemistry). The lung weight-to-body weight ratio was reduced by 42% in DH animals. The left-to-right lung weight ratio was lower in DH animals (0.47,±,0.03 vs. 0.69,±,0.03), indicative of asymmetric lung growth. SP-A, -B, and -C mRNA expression were increased by 61.7%, 32.9%, and 75.5%, respectively, in the left lungs of DH animals. SP-A and SP-B were also increased in DH. In the right lung, SP expression (mRNA and protein) was not different between groups. AE2 cell density was higher (by 67%) in the left but not right lungs of DH animals. Although DH in fetal sheep results in significant lung hypoplasia, SP expression is not reduced. On the contrary, SP expression was increased in the ipsilateral lung of fetuses with left-sided DH. Furthermore, AE2 cell density is increased in DH, suggesting that the increase in SP mRNA and protein levels is due to increases AE2 cell number. Our data further support the premise that fetal lung hypoplasia favors an AE2 phenotype. Pediatr Pulmonol. 2005; 39:359,367. © 2005 Wiley-Liss, Inc. [source] Hypersensitivity pneumonitis caused by Penicillium citrinum, not enoki sporesAMERICAN JOURNAL OF INDUSTRIAL MEDICINE, Issue 12 2007Sumiko Yoshikawa MD Abstract Background Flammulina velutipes is called the Enoki mushroom in Japanese and is cultivated indoors. Mushroom workers face occupational exposure to a tremendous number of fungi and organic antigens capable of causing hypersensitivity pneumonitis (HP). One worker employed at an Enoki farm developed HP due to Penicillium citrinum. This study investigated new cases of HP among the workers cultivating Enoki. Methods Serum Krebs von der Lungen-6 (KL-6), surfactant protein (SP)-A and SP-D were measured. Lymphocyte stimulation tests (LST) and double immunodiffusion tests (DIT) were performed to identify P. citrinum. Workers showing high levels of KL-6, SP-A, or SP-D and a high LST value or positive DIT were identified and then were further examined by chest computed tomography, bronchoalveolar lavage and transbronchial lung biopsy. The initial patient and new HP patients were defined as the HP group and the other participants were defined as the non-HP group. Results Forty-eight Enoki workers participated in the study. Four of nine workers who met the criteria for further examinations were diagnosed as having HP due to P. citrinum. In comparison between non-HP group and HP group, KL-6, SP-D and LST values were significantly higher in HP group. There was a strong correlation between KL-6 and SP-D. DIT had high sensitivity and high specificity. Conclusions KL-6, SP-D, LST, and DIT were useful for detecting HP patients. KL-6 was the most useful predictor of HP in this study. DIT was useful not only as a predictor of HP but also as a detector of the causative antigen. Am. J. Ind. Med. 50:1010,1017, 2007. © 2007 Wiley-Liss, Inc. [source] Characterization of bovine surfactant proteins B and C by electrospray ionization mass spectrometryRAPID COMMUNICATIONS IN MASS SPECTROMETRY, Issue 2 2008Suya Liu Bovine surfactant proteins B (SP-B) and C (SP-C) were analyzed by nano-electrospray ionization mass spectrometry (nano-ESI-MS). The observed molecular masses showed discrepancies compared to the calculated molecular masses using the published amino acid sequences. The number of cysteine residues in the published bovine SP-B amino acid sequences also failed to match the observed mass shift upon reduction of the SP-B dimer. To determine the amino acid sequences of two proteins, SP-B was first digested with trypsin and analyzed by liquid chromatography/tandem mass spectrometry (LC/MS/MS), while SP-C was analyzed by MS/MS in its intact form. The amino acid sequence of bovine SP-B determined here matches the observed molecular mass. The sequence is almost identical to the sheep SP-B except for two amino acid residues, consistent with the proximity of the two species. The correct sequence contains seven cysteine residues. Bovine SP-B exists as dimers and all cysteines are oxidized to form disulfide bonds in physiological conditions, which is in agreement with the observed mass shift upon reduction of the SP-B dimer. These cysteine residues are completely conserved across all species indicating their importance for the biological functions of this surfactant protein. The sequence of SP-C determined here also reveals an L to V substitution at its position 22 compared with the published bovine SP-B sequence. Copyright © 2007 John Wiley & Sons, Ltd. [source] Elevated serum surfactant protein A and D in pulmonary alveolar microlithiasisRESPIROLOGY, Issue 3 2006Hiroki TAKAHASHI Abstract: Pulmonary alveolar microlithiasis (PAM) is a rare disease characterized by widespread localization of calcispherites in the alveolar spaces. The authors report two cases of PAM, with markedly elevated sera concentrations of surfactant protein-A and surfactant protein-D, which showed a tendency to increase as the disease progressed. Therefore, surfactant protein-A and surfactant protein-D may function as serum markers to monitor the disease activity and progression of PAM. [source] Surfactant protein A and D gene polymorphisms and protein expression in victims of sudden infant deathACTA PAEDIATRICA, Issue 1 2009Arne Stray-Pedersen Abstract Aim: To investigate the innate immune components surfactant protein A (SP-A) and D (SP-D) in victims of sudden infant death syndrome (SIDS). Methods: Ten common single nucleotide polymorphisms (SNPs) in the exons of SP-A1, SP-A2 and SP-D genes were analysed in 42 cases of SIDS and 46 explained sudden infant deaths. SP-A and SP-D protein expression in tissue from the aerodigestive tract was semi-quantitatively evaluated by immunohistochemistry. Results: SP-D immunoreactivity was found in lungs and tissue from submandibular gland, palatine tonsils and duodenum. Positive SP-A immune staining was found exclusively in lung tissue. Neither the allele nor the haplotype distribution of the SP-A and SP-D genes was significantly different in SIDS compared to explained deaths. The most common SP-A haplotype, 6A2/1A0, tended to be overrepresented in the cases with low immunohistochemical SP-A expression (61%) compared to cases with high expression (49%), p = 0.08. The SP-D expression was not influenced by the 11 C/T or 160 A/G polymorphisms. Conclusion: No significant association between the common genetic variants of SP-A and SP-D and SIDS is disclosed by the present study. However, low SP-A protein expression may possibly be determined by the 6A2/1A0 SP-A haplotype, this should be subject for further investigation. [source] Role of Lung Surfactant in Respiratory Disease: Current Knowledge in Large Animal MedicineJOURNAL OF VETERINARY INTERNAL MEDICINE, Issue 2 2009U. Christmann Lung surfactant is produced by type II alveolar cells as a mixture of phospholipids, surfactant proteins, and neutral lipids. Surfactant lowers alveolar surface tension and is crucial for the prevention of alveolar collapse. In addition, surfactant contributes to smaller airway patency and improves mucociliary clearance. Surfactant-specific proteins are part of the innate immune defense mechanisms of the lung. Lung surfactant alterations have been described in a number of respiratory diseases. Surfactant deficiency (quantitative deficit of surfactant) in premature animals causes neonatal respiratory distress syndrome. Surfactant dysfunction (qualitative changes in surfactant) has been implicated in the pathophysiology of acute respiratory distress syndrome and asthma. Analysis of surfactant from amniotic fluid allows assessment of fetal lung maturity (FLM) in the human fetus and exogenous surfactant replacement therapy is part of the standard care in premature human infants. In contrast to human medicine, use and success of FLM testing or surfactant replacement therapy remain limited in veterinary medicine. Lung surfactant has been studied in large animal models of human disease. However, only a few reports exist on lung surfactant alterations in naturally occurring respiratory disease in large animals. This article gives a general review on the role of lung surfactant in respiratory disease followed by an overview of our current knowledge on surfactant in large animal veterinary medicine. [source] Altered expression of antimicrobial molecules in cigarette smoke-exposed emphysematous mice lungsRESPIROLOGY, Issue 7 2008Yoko SHIBATA Background and objective: The natural history of COPD, a disease usually caused by cigarette smoking, is associated with frequent respiratory infections. Consistent with human COPD, bacterial clearance in the lungs has been reported to be impaired in mice exposed to cigarette smoke. In the airways, several antimicrobial molecules such as surfactant proteins (SP), beta-defensins (BD), secretory leucocyte protease inhibitor (SLPI) and lysozyme play important roles in the defence against invading pathogens. This study evaluated the expression of antimicrobial molecules in mice lungs with cigarette smoke-induced emphysematous changes. Methods: Six B6C3F1 mice were exposed to cigarette smoke (2 cigarettes/day/mouse for 6 months) or room air. Gene expression within the lungs of mice in both groups was assessed by RT-PCR. Results: The expression of SP-A, BD2, BD3 and SLPI was significantly elevated in the lungs of cigarette smoke-exposed mice compared with air-exposed mice. BD1 expression decreased in the smoke-exposed mice and lysozyme expression was unchanged. Conclusions: Chronic cigarette smoke exposure did not suppress the expression of antimicrobial molecules in the lung. Altered expression of antimicrobial molecules in this mouse model does not explain the impaired host defence against respiratory microbes seen in patients with COPD. [source] Binding and entry of respiratory syncytial virus into host cells and initiation of the innate immune responseCELLULAR MICROBIOLOGY, Issue 10 2003James Harris Summary Respiratory syncytial virus (RSV) is the most common cause of severe lower respiratory tract infection in infants and the elderly. There is currently no effective antiviral treatment for the infection, but advances in our understanding of RSV uptake, especially the role of surfactant proteins, the attachment protein G and the fusion protein F, as well as the post-binding events, have revealed potential targets for new therapies and vaccine development. RSV infection triggers an intense inflammatory response, mediated initially by the infected airway epithelial cells and antigen-presenting cells. Humoral and cell-mediated immune responses are important in controlling the extent of infection and promoting viral clearance. The initial innate immune response may play a critical role by influencing the subsequent adaptive response generated. This review summarizes our current understanding of RSV binding and uptake in mammalian cells and how these initial interactions influence the subsequent innate immune response generated. [source] | ||||||||||||||||