Source: OREGON STATE UNIVERSITY submitted to
METABOLIC DISEASES IN POULTRY: IS IT AN IMMUNE DISORDER?
Sponsoring Institution
National Institute of Food and Agriculture
Project Status
TERMINATED
Funding Source
Reporting Frequency
Annual
Accession No.
0200054
Grant No.
(N/A)
Project No.
ORE00036
Proposal No.
(N/A)
Multistate No.
(N/A)
Program Code
(N/A)
Project Start Date
Oct 1, 2003
Project End Date
Sep 5, 2005
Grant Year
(N/A)
Project Director
Cherian, G.
Recipient Organization
OREGON STATE UNIVERSITY
(N/A)
CORVALLIS,OR 97331
Performing Department
ANIMAL SCIENCES
Non Technical Summary
Metabolic diseases such as pulmonary hypertension syndrome, ascites, and sudden death syndrome (SDS) are the major cause of mortality in broiler chickens, and cost the U.S. poultry industry over $100 million annually.Despite the high economic loss to the industry, very little research effort has been directed toward investigating the role of diet in minimizing the risk of metabolic diseases in broiler chickens. The current project will examine the role of maternal dietary omega-3 fatty acids in modulating the synthesis of proinflammatroy leukotrienes in the progeny chicks
Animal Health Component
100%
Research Effort Categories
Basic
50%
Applied
40%
Developmental
10%
Classification

Knowledge Area (KA)Subject of Investigation (SOI)Field of Science (FOS)Percent
3023220101060%
3113220109040%
Goals / Objectives
To determine the effect of yolk omega-3 fatty acids on immune cell fatty acid status and leukotriene production in broiler chicks. We hypothesize that the chicks hatched from eggs containing high omega -3 fatty acids will incorporate higher levels of omega-3 fatty acids in heterophils and decrease the production of proinflammatory leukotrienes during growth.
Project Methods
Eggs containing high, medium or low levels of omega-3 fatty acids are produced by feeding appropriate diets to broiler breeder hens. Fish or sunflower oil at different proportions will be used along with a corn-soy diet for altering egg omega-3 omega-6 fatty acid content. Fertilized eggs will be collected and incubated. The hatched chicks will be fed an identical broiler diet containing 22% protein, 3100 kcal ME/kg simulating a commercial broiler diet. At day 7, 14, and 21, a total of 8 birds per treatment will be sacrificed and blood will be collected and heterophils will be separated. Cells harvested from the mononuclear layer will be washed in Hanks balanced salt solution and will be centrifuged 10 min at 1300 RPM. The resultant pellet will be resuspended in approximately 2 ml of phosphate buffered saline. An aliquot of the cell suspension will be used to determine cell numbers. To initiate leukotrien production, calcium ionophore A23187 will be added to each tube containing cells. Control cells will receive DMSO. The quantification of leuokotriene extracted will be done by HPLC using PGB3 as the internal standard. To determine the changes in concentrations of omega-3 fatty acids in progeny due to maternal dietary fat, the fatty acid composition of chick heterophils will be analyzed. Lipids will be extracted from cells using chloroform:methanol mixture. The derivatized fatty acids from heterophils will be analyzed by automated gas chromatography using a fused silica capillary column. A Hewlett-Packard 6890 gas chromatograph with an HP chemstation chromatography data system will be used to integrate peak areas. Fatty acid methyl esters will be identified by comparison with the retention times to those of an authentic standards. The data will be analyzed by two-way ANOVA. Treatment means will be compared by Student-Newman-Keuls multiple comparison test. The statistical significance will be set at P<0.05.

Progress 10/01/03 to 09/05/05

Outputs
Metabolic diseases such as pulmonary hypertension syndrome, ascites, and sudden death syndrome (SDS) are the major cause of mortality in broiler chickens, and cost the U.S. poultry industry over $100 million annually. Despite the high economic loss to the industry, very little research effort has been directed toward investigating the role of diet in minimizing the risk of metabolic diseases in broiler chickens. Eicosanoids are lipid mediators of inflammation. The predominant proinflammatory eicosanoid released is leukotriene B4 (LTB4) which serves as a biological marker of inflammation. Leukotriene B4 is a mediator of smooth muscle contraction, vasodilation and vascular permeability leading to plasma exudation, fluid deposition and ascites. Developing dietary methods to control inflammation by down regulating LTB4 synthesis may help in minimizing the incidence of metabolic diseases. Fatty acids as components of tricaylglycerols are the major source of energy in poultry diets. Normal broiler diets are high in saturated, synthetic trans, omega-6 fatty acids and are low in omega-3 fatty acids. Ester-linked arachidonic acid is potentially biologically active and can be mobilized by phospholipase A2 to generate the free arachidonic acid during stress, infection or when exposed to environmental challenges (dust, ammonia) producing proinflammatory LTB4 through lipooxygenase. Omega-3 fatty acids compete with omega-6 fatty acid in the lipoxygenase pathway producing less proinflammatory LTB5. Thus the current broiler diet rich in n-6 fatty acids shift the physiological state to one that is proinflammatory, leading to metabolic diseases. Given the fact that omega-3 fatty acids are known to manifest a significant positive effect in reducing inflammatory disorders and cardiovascular diseases in humans, it would be important to evaluate the extent to which supplementation of omega-3 fatty acids during growth would influence eicosanoid metabolism and reduce mortality associated with metabolic diseases in broiler birds. The objectives of the current study was to determine the effect of yolk omega-3 fatty acids on immune cell fatty acid status and leukotriene production in broiler chicks. We hypothesize that the chicks hatched from eggs containing high omega-3 fatty acids will incorporate higher levels of omega-3 fatty acids in heterophils and decrease the production of proinflammatory leukotrienes during growth. Our results demonstrated that the content of 20:5(n-3) and 22:6(n-3) omega-3 fatty acids was higher in spleen, platelets and plasma of chicks from hens fed diets containing omega3 (n-3) compared to hens fed no omega-3 diet. The BSA-induced foot pad swelling index was less at 48 hours in hens fed omega-3 diets compared to hens fed no omega-3 diets. Platelets from chicks hatched from hens fed no omega-3 diets produced more proinflamamtory (LTB4) than chicks hatched from hens fed omega-3 diets. These results indicate that altering the (n-6) to (n-3) fatty acid ratio alters LTB4 production, which could reduce inflammatory-related disorders and increase production performance in poultry.

Impacts
Metabolic diseases cost the U.S. poultry industry over $100 million annually. Overall, our study indicates that there is an integral relationship between maternal diet and the fatty acid content of chick immune tissues and inflammatory eicosanoid production. These findings demonstrate that modulating the maternal dietary omega-3 fatty acid composition, and thereby yolk fatty acid composition, can change the type of leukotrienes produced in the progeny during the first few weeks of life. Metabolic diseases (e.g., sudden death and ascites) and inflammatory disorders (e.g., joint abnormalities) are the major causes of mortality in broiler chickens. LeukotrieneB4 is a mediator of smooth muscle contraction, vasodilation and vascular permeability leading to plasma exudation and fluid deposition. Our findings will generate new knowledge about the fundamental relationship between maternal diet, fatty acid metabolism and inflammation mediators in the etiology of metabolic diseases. This will have important practical implications for improving bird health, productivity and will bring increased economic returns to US poultry industry.

Publications

  • S. Jha, J.A. Hall, G. Cherian, L.R. Henry and J.W. Schlipf. 2005. Optimization of assay conditions for leukotriene B4 synthesis by neutrophils or platelets isolated from peripheral blood of monogastric animals. Prostaglandins, Leukotrienes and Essential Fatty Acids. 72:423-430.
  • Jha, S., J.A. Hall., G. Cherian., and L.R. Henry. 2005. Leukotriene Production by platelets in breeder hens and hatched chicks: Effect of dietary fatty acids. Abs#279.2, FASEB, San Diego, CA.


Progress 01/01/04 to 12/31/04

Outputs
Metabolic diseases such as pulmonary hypertension syndrome, ascites, and sudden death syndrome (SDS) are the major cause of mortality in broiler chickens, and cost the U.S. poultry industry over $100 million annually. Despite the high economic loss to the industry, very little research effort has been directed toward investigating the role of diet in minimizing the risk of metabolic diseases in broiler chickens. The commercial broiler chickens are selected for fast growth. The health and survival of broiler birds in part depends on their ability to respond effectively and appropriately to external, internal or other environmental challenges. Inflammation is the response of the body to internal or external injury. Eicosanoids are lipid mediators of inflammation. Neutrophils (or heterophils in birds) are involved in inflammation through eicosanoid production. The predominant proinflammatory eicosanoid released is leukotriene B4 (LTB4) which serves as a biological marker of inflammation. Leukotriene B4 is a mediator of smooth muscle contraction, vasodilation and vascular permeability leading to plasma exudation, fluid deposition and ascites. Developing dietary methods to control inflammation by down regulating LTB4 synthesis may help in minimizing the incidence of metabolic diseases. Fatty acids as components of tricaylglycerols are the major source of energy in poultry diets. Normal broiler diets are high in saturated, synthetic trans, omega-6 fatty acids and are low in omega-3 fatty acids. Polyunsaturated fatty acids (PUFA) such as arachidonic acid contribute to the phospholipid bilayer of cells. Ester-linked arachidonic acid is potentially biologically active and can be mobilized by phospholipase A2 to generate the free arachidonic acid during stress, infection or when exposed to environmental challenges (dust, ammonia) producing proinflammatory LTB4 through lipooxygenase. Omega-3 fatty acids compete with omega-6 fatty acid in the lipoxygenase pathway producing less proinflammatory LTB5. Thus the current broiler diet rich in n-6 fatty acids shift the physiological state to one that is proinflammatory, leading to metabolic diseases. Given the fact that omega-3 fatty acids are known to manifest a significant positive effect in reducing inflammatory disorders and cardiovascular diseases in humans, it would be important to evaluate the extent to which supplementation of omega-3 fatty acids during growth would influence eicosanoid metabolism and reduce mortality associated with metabolic diseases in broiler birds. The objective of the current study was to determine the effect of yolk omega-3 fatty acids on immune cell fatty acid status and leukotriene production in broiler chicks. We hypothesized that the chicks hatched from eggs containing high omega-3 fatty acids will incorporate higher levels of omega-3 fatty acids in heterophils and decrease the production of proinflammatory leukotrienes during growth. Our results demonstrated that chicks hatched from omega-3 rich eggs retained higher level of n-3 fatty acids in immune tissues and produced less pro-inflammatory eicosanoids during growth.

Impacts
Metabolic diseases cost the U.S. poultry industry over $100 million annually. Our findings will generate new knowledge about the fundamental relationship between maternal diet, fatty acid metabolism and inflammation mediators in the etiology of metabolic diseases. This will have important practical implications for improving bird health, productivity and will bring increased economic returns to the U.S. poultry industry. Positive findings could be rapidly incorporated into the poultry industry simply by changing feed formulation.

Publications

  • S. Jha., J.A. Hall., G. Cherian, and J.W. Schlipf. 2004. Optimization of Conditions for Leukotriene B4 Synthesis by Neutrophils or Heterophils Isolated from Peripheral Blood of Monogastric Animals. Proc. Western Section of Am. Soc. Anim. Sci. 55: 233-236.