It's happened to us all; you work your socks off for that big deadline and when it's over, you're felled by a bug. Why? Because a window of vulnerability has opened. Stress hormones pounding through your system interfere with your immune system, leaving you prone to infection. And we're not the only ones. According to Shelley Adamo, most creatures' immune systems take a tumble after stress. However, why immune systems fail when you are vulnerable wasn't clear. Could the immune system fail because of a physiological constraint,such as competition between key survival systems for a shared component? Adamo explains that one of the insect's key lipid transport proteins (lipophorin III) also plays a major role in immunity by detecting bacterial infection. Could lipophorin III, which supplies fuel during periods of high energy demand, be the lynch pin that lets the immune system down? Teaming up with colleagues Janet Ross, Russell Easy and Neil Ross, Adamo needed to prove that losing lipophorin III to the energy transport system compromised the insect's resistance ().
First the team measured the insects' free lipophoprin III level after allowing the crickets to fly for 5 min and found that they plummeted by 46%. And when the team measured the crickets' free lipophorin III after exposure to infection, it fell even further. Both situations reduced the amount of free lipophorin in the insects' haemolymph.
But was the energy delivery system hijack of the immune system's protein leading to compromised resistance? If so, the insect's immunity would suffer when it activated the lipid delivery system to fuel flight. Knowing that adipokinetic hormone activates fuel delivery and reduces the amount of lipophorin III in the haemolymph, the team tested the cricket's resistance to infection after a dose of adipokinetic hormone. The cricket's resistance dropped by 20%. The insects needed free lipophorin III to fight infection, but Adamo still needed convincing that the fuel delivery system was depleting the insect's lipophorin III supplies.
The team decided to offer the flying insects an alternative fuel source. The team reasoned that the flying insects wouldn't resort to lipids if supplied with an alternative fuel (trehalose), so could maintain their haemolymph lipophorin III levels and reduce their susceptibility to infection. Dosing crickets with trehalose, the team exposed them to infection after flying, and recorded their resistance. The trehalose-dosed insect's survival rate was much better than untreated crickets. Amazingly, increased free lipophorin III levels had protected the insects from infection.
That left one test to try before Adamo was sure that lipophorin III was the key to the cricket's immunosuppression. Could a dose of the free protein restore a stressed insect's failing resistance? The team administered lipophorin III to crickets, and tested their postflight resistance: it was restored. Finally Adamo was convinced that the insect's fuel delivery system was kidnapping free lipophorin III from the immune system, leaving it vulnerable to infection.
Adamo is very excited about this discovery, and says that `this result could have interesting ramifications'. According to Amano, stress induced immunosuppression is widespread across all phyla, and competition between the immune system and other key physiological systems could prove to be wide spread and `explain the paradox of stress induced immunosuppression' she says.
