Chih-I Chen

Oral administration of a combination of select lactic acid bacteria strains to reduce the Salmonella invasion and inflammation of broiler chicks

One-day-old chicks are susceptible to infection by strains of Salmonella enterica subspecies. Because multistrain probiotics are suggested to be more effective than monostrain probiotics due to the additive and synergistic effects, in this study, we prepared a multistrain formula A (MFA) consisting of 4 lactic acid bacteria (LAB) strains selected by enhancing the TNF-α production for mouse macrophage 264.7 cells. The antagonistic effect of this MFA against the cecal colonization, viscera invasiveness, as well as the inflammation of 1-d-old chicks challenged with Salmonella Typhimurium were then assayed. One-day-old chicks were fed with MFA from d 1 to d 3, and on d 4, chicks were challenged with Salmonella Typhimurium (200 μL, 10(6) cfu/mL). The livers, spleens, and cecal tonsils of chicks were then removed on d 3 and 6 postinfection. Compared with the multistrain formula B (MFB) which consisted of LAB strains selected at random, the efficacy of MFA to reduce the Salmonella counts recovered from the cecal tonsils, spleens, and livers of chicks were significantly higher. Moreover, when the levels of proinflammatory cytokines, such as IL-1β, IL-6, interferon (IFN)-γ, and anti-inflmmatory cytokine, that is, IL-10, in cecal tonsils were measured by reverse-transcription real-time quantitative PCR; it was found that chicks fed with MFA for 3 d had lower levels of IL-1β, IL-6, IFN-γ and a higher level of IL-10 in the cecal tonsils of chicks as compared with those of the chicks fed with MFB or without LAB. These results suggest that multistrain probiotics consisting of LAB strains selected by immunomodulatory activity and adherence are more effective than those consisting of strains selected at random in antagonistic effect against Salmonella colonization, invasion, and the induced inflammation.

Characteristics of the photosynthesis microbial fuel cell with a Spirulina platensis biofilm.

A novel design of a photosynthetic microbial fuel cell (PMFC) is constructed. It is a membrane-less and mediator-free apparatus with a gilding gold mesh as an anode and a graphite carbon cloth as a cathode. The electrode spacing is 4 cm. Spirulina platensis is aggregated and deposited on the anode to form a thin biofilm. Results show that the chlorophyll (Chl) content of the biofilm attributed the PMFCs electricity performance. The open circuit voltage (OCV) reading of PMFC is proportional to Chl content when the Chl was below 0.5mg. The maximal OCV of PMFC is 0.49 V. When the PMFC was connected to an external resistance of 1 kΩ, a maximum power density of 10 mW m(-2) was obtained. This designed PMFC yielded competitively high OCV and power density as compared to other microbial fuel cells reported in the literature.

Obesity-associated cardiac pathogenesis in broiler breeder hens: Development of metabolic cardiomyopathy2,3

&NA; Feed intake is typically restricted (R) in broiler hens to avoid obesity and improve egg production and livability. To determine whether improved heart health contributes to improved livability, fully adult 45‐week‐old R hens were allowed to consume feed to appetite (ad libitum; AL) up to 10 wk (70 d). Mortality, contractile functions, and morphology at 70 d, and measurements of cardiac hypertrophic remodeling at 7 d and 21 d were made and compared between R and AL hens. Outcomes for cardiac electrophysiology and mortality, reported separately, found increased mortality in AL hens in association with cardiac pathological hypertrophy and contractile dysfunction. The present study aimed to delineate metabolic cardiomyopathies underlying the etiology of obesity‐associated cardiac pathology. Metabolic measurements were made in hens continued on R rations or assigned to AL feeding after 7 d and 21 days. AL feeding increased plasma insulin, glucose, and non‐esterified fatty acid (NEFA) concentrations by 21 d (P < 0.05). Metabolic cardiomyopathy in AL‐hens was confirmed by cardiac triacylglycerol (TG) and ceramide accumulation consistent with up‐regulation of related enzyme gene expressions, and by increased indices of oxidation stress (P < 0.05). In contrast to R hens, cardiac pyruvate dehydrogenase (PDH) activity and glucose transporter (GLUT) gene expressions increased progressively while carnitine palmitoyltransferase‐1 (CPT‐1) transcript levels in AL hens declined from 7 d to 21 d (P < 0.05), reflecting a shift from an oxidative to a more glycolytic metabolism, a typical metabolic derangement associated with cardiac hypertrophic remodeling. Cardiac pathogenesis in AL hens was further indicated by increased leukocyte infiltrates, interleukin‐1&bgr; (IL‐1&bgr;) and IL‐6 production, cellular apoptosis, interstitial fibrosis, and expression of the heart failure marker myosin heavy chain (MHC‐&bgr;; cardiac muscle beta) (P < 0.05). Results support the conclusion that diabetic conditions, cardiac inflammation and lipotoxic metabolic derangements act as pathological cues to trigger pathogenic changes along cardiac hypertrophy in AL hens.

Obesity-associated cardiac pathogenesis in broiler breeder hens: Pathological adaption of cardiac hypertrophy1,2

&NA; Broiler hens consuming feed to appetite (ad libitum; AL) show increased mortality. Feed restriction (R) typically improves reproductive performance and livability of hens. Rapidly growing broilers can exhibit increased mortality due to cardiac insufficiency but it is unknown whether the increased mortality of non‐R broiler hens is also due to cardiac compromise. To assess cardiac growth and physiology in fully mature birds, 45‐week‐old hens were either continued on R rations or assigned to AL feeding for 7 or 21 days. AL hens exhibited increased bodyweight, adiposity, absolute and relative heart weight, ventricular hypertrophy, and cardiac protein/DNA ratio by d 21 (P < 0.05). Increased heart weights due to hypertrophic growth was attributed to enhanced IGF‐1‐Akt‐FoxO1 signaling and its downstream target, translation initiation factor 4E‐BP1 in conjunction with down‐regulation of ubiquitin ligase atrogin‐1/MAFbx (P < 0.05). Reduced activation of cardiac AMPK and downstream activation of ACC‐1 in parallel with increased cardiac nitric oxide levels, calcineurin activity, and MAPK activation in AL hens (P < 0.05) suggested that metabolic derangement develops along the cardiovascular remodeling. These indictors of cardiac maladaptive hypertrophic growth were further supported by uregulation of heart failure markers, BNP and MHC‐&bgr; (P < 0.05). Hens allowed AL feeding for 70 d exhibited a higher incidence of mortality (40% vs. 10%) in association with ascites, pericardial effusion, and ventricle dilation. A higher incidence of irregular ECG patterns and rhythmicity consistent with persistently elevated systolic blood pressure and ventricle fibrosis were observed in AL hens (P < 0.05). These observations support the conclusion that AL feeding in broiler hens results in maladaptive cardiac hypertrophy that progresses to overt pathogenesis in contractility and thereby increases mortality. Feed restriction provides clear physiological benefit to heart function of adult broiler hens.