Rodney W. Johnson, a professor in the department of animal sciences and the interdisciplinary Division of Nutritional Sciences, and colleagues have studied chronic infectious respiratory diseases that affect most swine during their critical growing stage. The researchers have found that the production of inflammatory cytokines by immune cells appear to be responsible for declines of both protein accretion and weight gain in swine infected with Porcine Reproductive and Respiratory Syndrome Virus.
Photo by Kwame Ross
CHAMPAIGN, Ill. - A study looking at chronic infectious respiratory diseases that affect most swine during their critical growing stage has shed new light on the reasons for restricted weight gain and reduced muscle mass.
In the November issue of the Journal of Nutrition, scientists at the University of Illinois at Urbana-Champaign report that the production of inflammatory cytokines by immune cells appears to be responsible for declines of both protein accretion and weight gain in swine infected with Porcine Reproductive and Respiratory Syndrome Virus (PRRSV).
The study also suggests that myostatin, a protein that limits muscle growth, is overproduced during infection, thereby reducing the growth of skeletal muscle, said Rodney W. Johnson, a professor in the department of animal sciences and the interdisciplinary Division of Nutritional Sciences.
Johnson and colleagues isolated pigs in disease-containment chambers and exposed different experimental groups to the bacterium Mycoplasma hyopneumoniae and/or PRRSV.
Almost all U.S. swine are exposed to the bacterium in production facilities, while about 60 percent are exposed to PRRSV. These pathogens open the way for other infectious agents. During the pivotal growing stage, pigs are at the most risk and suffer from cough, fevers and depressed appetite. Reduced market weight or increased time for pigs to reach a desired market weight can be a substantial cost to producers.
Infection from the bacterium alone did not reduce weight gain compared with the control group during the four-week-long experiment, but it did lead to the development of lesions that affected 8 percent of the total lung area in infected pigs. The finding was similar to earlier work in Johnson's laboratory. However, the introduction of PRRSV caused damage to the lungs from the bacterium to jump to 40 percent.
"One thing the virus does is suppress the immune system," Johnson said. "When PRRSV and mycoplasma are together, the PRRSV-induced immunosuppression allows the mycoplasma to spread unchecked. It really takes over the lungs."
PRRSV infection alone resulted in a daily weight gain of just 50 percent of that of the control animals (300 grams per day compared with 600 grams per day) and substantially less protein accretion. The drop in growth began three days after exposure to PRRSV and continued for the remaining two weeks of the trial.
PRRSV infects macrophages, a type of white blood cell that attacks pathogens. The virus is spread from the lungs as the macrophages migrate to other tissues. Before infected macrophages die from the virus, they produce inflammatory cytokines, hormone-like molecules that enable the immune system to influence other parts of the body. One part affected is the brain, which is why animals have reduced appetite when they are sick.
"The cytokine molecules are the key, because they are the messengers used by the immune system to alter other systems that are relevant to growth," Johnson said.
At the suggestion of co-author Jeffery Escobar, a former doctoral student now with the USDA/ARS Children's Research Center at the Baylor College of Medicine in Houston, the researchers examined myostatin gene expression in the infected pigs.
Myostatin's role in muscle development is becoming clear, Johnson said. Mice with the myostatin gene deleted become muscle-bound, and a defective myostatin gene has been linked to double muscling in cattle and to abnormally large muscles in a German child.
Johnson's team found a substantial increase in the amount of myostatin mRNA in the muscles of infected pigs. "We have shown, using an infectious disease model where animals grow slowly, that there is an increase in muscle myostatin mRNA."
In addition to Johnson and Escobar, co-authors were William G. Van Alstine of the Animal Disease and Diagnostic Laboratory at Purdue University and David H. Baker, a professor of animal sciences at Illinois. The Illinois Council for Food and Agricultural Research funded the study.