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Obesity Impairs Immune Response, Boosts Death Risk Ofinfluenza: Study

Posted on: Wednesday, 6 April 2005, 09:00 CDT

Obesity impairs immune response, boosts death risk of influenza: study

LOS ANGELES, April 4 (Xinhua)-- Obesity apparently reduces laboratory mice's ability to turn on immune systems necessary for controlling influenza infection, US researchers reported Monday.

The findings indicate that obesity in humans has a similar effect, said scientists at the University of North Carolina at Chapel Hill School of Medicine.

Compared to mice of normal weight, which were otherwise identical, obese mice were 10 times as likely to die when infected with the flu virus. Four percent of lean mice died during the experiments, compared with 40 percent of the extra fat ones, the study showed.

Presented at an American Society of Nutritional Sciences meeting this weekend in San Diego, California, the study is the first of its kind to examine the effects of obesity on the immune response to infection with influenza.

Numerous marked alterations seen in the mice's immune response suggest that the growing obese population is at increased risk for immune dysfunction during influenza infection, which may lead in humans to increased mortality as it did in the mice, according to Melinda A. Beck, an associate professor who led the study.

Influenza virus currently is responsible for 36,000 deaths and 114,000 hospitalizations in the United States each year. Scientists have warned an influenza prevalence can kill millions worldwide.

In this research, 35 mice fed a high-fat, high-sugar diet for five months grew 37 percent heavier than 35 mice fed a regular rodent diet high in carbohydrates. The obese mice had a body fat percentage of 31 percent, compared to 21 percent in the lean mice.

Following influenza infection at five months, which is adulthood for mice, the obese mice demonstrated significantly decreased capacity in every step of the inflammatory immune response in the lungs necessary to stop spread of the virus, Beck said.

The immune response after infection with influenza virus begins with the production of cytokines whose function is to control the spread of infection and turn on various immune system components, she said. This step is followed by activation of T cells that circulate into the lungs to further limit viral spread.

There were considerable differences between the obese and lean animals in both gene expression and protein expression of several antiviral and pro-inflammatory cytokines, the researchers said.

Antiviral cytokines, important in the control of initial viral spread, were significantly lower in obese animals. Similarly, some of the pro-inflammatory cytokines, which induce fever, swelling, and recruitment of immune cells, were also significantly lower in obese animals in the early days of infection when they were most needed.

Another important finding in the obese animals was the reduced ability of natural killer cells, which limit viral replication by killing infected cells and play a central role in the early immune response.

Natural killer cells in the obese animals had a 50 percent reduction in their killing capacity compared to lean animals, Beck said.

Source: Xinhua News Agency - CEIS

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