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Fish Oil-Fed Mice Have Impaired Resistance to Influenza Infection - Article Example

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From the paper "Fish Oil-Fed Mice Have Impaired Resistance to Influenza Infection" it is clear that the modern view of the way in which PUFA-polyunsaturated fatty acids have effects on the immune system is focused on their capabilities to alter the production of cytokine and biosynthesis diminishing…
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Fish Oil-Fed Mice Have Impaired Resistance to Influenza Infection
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The critique and analysis focus on feeding animal trials which include in vivo problems of the host with a live agent of infection. Pathogen clearance and host survival are the typical endpoints analyzed in the studies.

Data shows that (n-3) PUFA can both impair and improve the resistance of the host to a certain pathogens number. Nevertheless, the information is still limited in depth and breadth. For the pathogens with existing data, published studies numbers generally do not surpass three or two. Emphasis is on defining crucial immunological and microbiological differences in pathogen-host interactions that assist to explain the published findings' incongruity. Researchers believe that a straight examination of (n-3) PUFA on the infectious disease of human resistance is warranted.

From the oils of fish, Omega-3 fatty acids are considered inflammation modulators. This is the action mode for their efficiency and effectiveness against the illness of modernity. The diseases include arthritis and rheumatoid. However, there is a downside, because inflammation is a section of response by the immune system, fish oil decreases immunity. The other side of inflammation decreases. For instance, mice fed with the oil of fish, have impaired opposition to the infection of influenza.

In regard to the dietary long-chain PUFA derived from fish oil has been shown to have beneficial effects on chronic inflammatory and autoimmune disorders (1,2) and long-chain PUFA such as eicosapentaenoic acid appear to be most beneficial. A number of studies report that the immunosuppressive effects of PUFA are a result of decreased cytokine production and reductions in T cell proliferation, activation, and signaling Studies of rodents fed fish oil-enriched diets have shown a reduction in natural killer (NK)4 cell activity (8), decreased lymphocyte proliferation (9,10), and decreased antigen presentation functions. In addition, decreases in ex vivo production of tumor necrosis factor.

Whereas the anti-inflammatory properties of PUFA may be beneficial for some chronic inflammatory illnesses, these same anti-inflammatory properties may be detrimental to response to infection when an intact immune system is needed to eradicate an invading pathogen. For example, diets supplemented with fish oils have been shown to lower host resistance to Mycobacterium tuberculosis (19), reduce the survival of mice against infection with Listeria monocytogenes, and decrease the resistance of mice infected with Salmonella typhimurium. Similarly, fish oil feeding can diminish host defense against influenza virus due to delays in viral clearance.

Despite the availability of vaccines and antiviral agents, the influenza virus continues to be a major cause of morbidity and mortality worldwide Influenza virus infects cells of the respiratory system, resulting in acute and diffuse inflammation of the bronchoalveolar tract. Following infection, a coordinated immune response consisting of both innate and adaptive mechanisms results in an accumulation of immune cells and secretion of immunomodulatory proteins designed to limit viral spread. In the mouse model of influenza virus infection, NK cells, neutrophils, and T lymphocytes increase in the lung post-infection and contribute to host protection. The secretion of both inflammatory and antiviral cytokines helps to eliminate the virus and reduce further spread. Whereas this inflammatory response is necessary for viral clearance, it also contributes to lung pathology. Although there are many studies documenting the anti-inflammatory properties of fish oil, there are few studies that have examined the effects of fish oil on viral infection.

Because of the known health benefits, fish oil supplementation is on the rise. A survey conducted among health care professionals in the US reported an increase in fish oil supplementation from 24 to 30% from 2006 to 2007 Additionally, in 2007, 37.4% of the U.S. population reported using fish oil or fish oil supplements for health reasons (30). With the anticipated increase in fish consumption and the increase in the usage of fish oil supplements, there is a growing concern that the beneficial anti-inflammatory properties of (n-3) fatty acids may have adverse effects when inflammation is necessary to combat infection (1,28,31). This study was undertaken to investigate the effects of fish oil feeding on the immune response to influenza virus infection in mice.

Six-week-old male C57BL/6J mice were purchased from Jackson Laboratories. All mice were housed at the University of North Carolina Animal Facility, which is fully accredited by the American Association for Accreditation of Laboratory Animal Care. Animals were maintained under protocols approved by the Institutional Animal Care and Use Committee. All mice were housed under a 12-h-light/-dark schedule with free access to food and water. Mice consumed ad libitum a control semipurified diet containing
Virus and infection.

Previous studies from our laboratory determined that this dose of virus is sufficient to effectively elicit an immune response with normal mortality in mice (32). Mice were weighed daily following infection and percent weight loss compared with starting weight at the time of infection was calculated.
Pathology.

As previously described, lung viral titers were determined by a modified tissue culture infectious dose 50 (TCID50) using hemagglutination as an endpoint (32). Briefly, supernates from lung homogenates were serially diluted and used to infect Madin-Darby canine kidney cells. Virus titers were determined based on the presence or absence of hemagglutination of human O RBC and TCID50 was determined by the method of Reed and Muench (34).
Determination of NK cell cytotoxicity.

Total lung and spleen cells were analyzed using a standard chromium-51 release assay in triplicate following a previously published method Read More
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