Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0017168 (gastroesophageal reflux disease)
 11,783 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Children with gastroesophageal reflux often suffer from chronic, severe lung damage and recurrent infections. The mechanisms may involve reflux induced lung injury with alterations of the surfactant proteins (SP) SP-A and SP-D, which bind specifically to various microbes and increase their elimination by granular leukocytes and macrophages. In 20 children with gastroesophageal reflux disease (GERD) the bronchoalveolar lavage content and macromolecular organization of SP-A and SP-D was determined by enzyme linked immunosorbent assay and gel chromatography. For comparison, lavages from 17 children without respiratory diseases were investigated. Both, SP-A and SP-D were significantly reduced in children with GERD-median (25, 75 percentiles) SP-A: 362 (169, 494) ng/ml versus 867 (656, 1,761) in control subjects and SP-D: 174 (73, 456) ng/ml versus 518 (295, 748) ng/ml in control subjects. The more active, higher molecular weight oligomers of SP-A and especially those of SP-D were diminished, whereas the smaller sized forms of SP-D were markedly increased. In children with GERD, significantly reduced amounts of SP-A and SP-D and an altered structural organization of the surfactant protein oligomers were demonstrated. Such impairments of central components of the innate host defense system may contribute to the pathogenesis of the chronic lung disease commonly observed in these children.
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PMID:Surfactant proteins A and D in children with pulmonary disease due to gastroesophageal reflux. 1204 31

Gastro-esophageal reflux and related pulmonary bile acid aspiration were prospectively investigated as possible contributors to postlung transplant bronchiolitis obliterans syndrome (BOS). We also studied the impact of aspiration on pulmonary surfactant collectin proteins SP-A and SP-D and on surfactant phospholipids--all important components of innate immunity in the lung. Proximal and distal esophageal 24-h pH testing and broncho-alveolar lavage fluid (BALF) bile acid assays were performed prospectively at 3-month posttransplant in 50 patients. BALF was also assayed for SP-A, SP-D and phospholipids expressed as ratio to total lipids: phosphatidylcholine; dipalmitoylphosphatidylcholine; phosphatidylglycerol (PG); phosphatidylinositol; sphingomyelin (SM) and lysophosphatidylcholine. Actuarial freedom from BOS was assessed. Freedom from BOS was reduced in patients with abnormal (proximal and/or distal) esophageal pH findings or BALF bile acids (Log-rank Mantel-Cox p < 0.05). Abnormal pH findings were observed in 72% (8 of 11) of patients with bile acids detected within the BALF. BALF with high levels of bile acids also had significantly lower SP-A, SP-D, dipalmitoylphosphatidylcholine; PG and higher SM levels (Mann-Whitney, p < 0.05). Duodeno-gastro-esophageal reflux and consequent aspiration is a risk factor for the development of BOS postlung transplant. Bile acid aspiration is associated with impaired lung allograft innate immunity manifest by reduced surfactant collectins and altered phospholipids.
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PMID:The effect of reflux and bile acid aspiration on the lung allograft and its surfactant and innate immunity molecules SP-A and SP-D. 1688 47