From gastric aspiration to airway inflammation.

The airways are poorly protected from potentially damaging agents contained within gastric contents. While digestive factors are obvious damaging agents, gastric aspiration may also deliver microbial agents, cytokines or food antigens to airway tissues. Direct damage or the triggering of the inflammatory cascade by gastric aspiration is believed to drive airways disease onset and/or progression. Evidence exists from experimental models demonstrating direct instillation of damaging factors to a range of airways epithelia causes damage and/or an inflammatory response. Clinical longitudinal studies have also noted an association between the presence of biomarkers of reflux in airways samples and disease progression. A shared pathophysiology of many chronic airways diseases is a more negative intrathoracic pressure. Such changes would drive an increased abdominothoracic pressure gradient. These changes in respiratory mechanics mean that chronic lung disease patients may be predisposed to reflux and subsequent aspiration. Therefore, it appears that gastric aspiration and airways disease progression may be linked not solely as cause and effect, but seemingly within a vicious cycle. A range of physiological factors govern both occurrence of gastric reflux into the pharynx/larynx and could also increase the susceptibility of certain individuals to disease progression. A range of long-term surgical and pharmacological intervention studies are necessary to test the benefit of such therapies in reducing disease progression or driving symptom improvement. Such studies may be hampered by the reliability of available therapies in halting gastric aspiration and the difficulty in the clinical or biochemical assessment of gastric aspiration.

Carotenoid composition and antioxidant potential of Eucheuma denticulatum, Sargassum polycystum and Caulerpa lentillifera.

Three species of Malaysian edible seaweed (Eucheuma denticulatum, Sargassum polycystum and Caulerpa lentillifera) were analyzed for their carotenoid composition using a combination of high-performance thin layer chromatography (HPTLC) and ultra-high-performance liquid chromatography-electrospray ionization-tandem mass spectrometry (UHPLC-ESI-MS/MS), while the antioxidant capacities were determined by 2,2-diphenyl-1-picrylhydrazyl (DPPH) and oxygen radical absorbance capacity (ORAC) assays. The HPTLC analysis exhibited a distinct carotenoid pattern among the three seaweed groups. The UHPLC-ESI-MS/MS analysis showed fucoxanthin as the major carotenoid present in S. polycystum while lutein and zeaxanthin in E. denticulatum. For C. lentillifera, ß-carotene and canthaxanthin were the major carotenoids. Some of the carotenoids, such as rubixanthin, dinoxanthin, diatoxanthin and antheraxanthin, were also tentatively detected in E. denticulatum and S. polycystum. For antioxidant activity, S. polycystum (20 %) and E. denticulatum (1128 µmol TE/g) showed the highest activity in the DPPH and ORAC assays, respectively. The findings suggest the three edible varieties of seaweeds may provide a good dietary source with a potential to reduce antioxidative stress.

Alginate as a source of dietary fiber.

Alginate, an algal polysaccharide, is widely used in the food industry as a stabilizer, or as a thickening or emulsifying agent. As an indigestible polysaccharide, alginate may also be viewed as a source of dietary fiber. Previous work has suggested that dietary fibres may protect against the onset and continuation of a number of cardiovascular and gastrointestinal diseases. This article aims to examine what is currently understood about the fiber-like activities of alginate, particularly its effects on intestinal absorption and the colon, and therefore aims to gauge the potential use of alginate as a dietary supplement for the maintenance of normal health, or the alleviation of certain cardiovascular or gastrointestinal diseases.

Pepsin like activity in bronchoalveolar lavage fluid is suggestive of gastric aspiration in lung allografts.

BACKGROUND: A biologically plausible link between gastro-oesophageal reflux (GOR), aspiration, and lung allograft dysfunction has been suggested, but there is no systematic evidence indicating the presence of gastric contents in the lung. We have tested the hypothesis that pepsin, as a marker of aspiration, is detectable in bronchoalveolar lavage (BAL) fluid of allograft recipients who had not reported symptoms of GOR. METHODS: Standardised 3 x 60 ml surveillance BAL fluid samples from 13 chronologically sequential stable lung allograft recipients without chronic rejection (10 patients treated with a prophylactic proton pump inhibitor) were studied. Lavage supernatants were assayed by an ELISA based on a monospecific goat antibody for pepsin/pepsinogen. Pepsin levels were compared with those from four normal volunteer controls. RESULTS: Pepsin levels were measurable in all allograft recipients, in keeping with gastric aspiration (median 109 ng/ml (range 35-1375)). In the control group the pepsin levels were below the limit of detection. Treatment with a proton pump inhibitor was not correlated with pepsin levels. There was no correlation between BAL fluid neutrophils and pepsin levels. CONCLUSION: These data demonstrate lung epithelial lining fluid concentrations of pepsin in lung allograft recipients which are much higher than blood reference levels, with no detectable pepsin in controls. This provides direct evidence of gastric aspiration, which is potentially injurious to the allograft.

Enterotoxigenic Escherichia-coli-associated diarrheal disease in Apache children.

A search for intestinal enterotoxigenic Escherichia coli was made in 59 Apache children hospitalized with 64 episodes of acute diarrhea. Esch. coli isolates from acute-phase and convalescent-phase specimens of small-bowel fluid and stool were tested in three currently recognized models: the adult-rabbit ileal loop; infant rabbit; and the adrenal-cell assay. Enterotoxigenic strains were isolated from 10 children during acute diarrheal episodes (16 per cent); none were isolated from convalescent-phase specimens. None of 64 "enteropathogenic" serotypes of Esch. coli from 43 children with diarrhea, however, caused fluid production in the ileal-loop model. These results suggest that enterotoxigenic Esch. coli may be the cause of considerable diarrhea in this population and that the term "enteropathogenic" as applied to serotypes of Esch. coli needs to be redefined.