This recent paper caught my eye, as as some of my recent research has related to the regulation of antimicrobial defence in Drosophila. Insects have a two ways of coping with microbial infection. Firstly, microbes may be dealt with by circulating blood cells (haemocytes) of which there are several classes. Haemocytes to no play any role in respiration in insects. A second means of controlling microbes involves several peptides that kill bacteria or fungi: these are usually expressed in response to the presence of microbes in the haemolymph. Interestingly, this induced system has a counterpart in vertebrates. It’s generally thought that the important system in clearing pathogenic microbes in insects is the induced antimicrobial peptides. This paper investigates the roles of both systems.
The authors have evaluated the relative use of these two mechanisms of infection control in Tenebrio molitorI, the mealworm (picture above). Their hypothesis is that the haemocytes represent the first line of defence, with the induced response of antimicrobial peptides mopping up microbes remaining from the first round defence. In this model, the induced antimicrobial response largely functions to eliminate suviving pathogens that may be refractory to the first line of defence.
Three predictions follow: that most infecting bacteria will be eliminated before the induced antimicrobial response occurs; that some bacterial will escape the haemocyte response; and that these surviving bacteria will be more resistant to haemocytes of a naive host than the original pathogen strain. To investigate these predictions, several experiments were conducted that involved direct inoculation of beetles with known quantities of stationary phase Staphylococcus aureus cultures. In the first experiment, haemolymph samples were recovered at different time points following infection with 4 x 106 cfu of bacteria, and surviving cfu measured. This revealed almost total clearance within one hour. In parallel, induced anti-S. aureus activity was measured in haemolymph samples, and found to rise well after 99.5% of bacteria were cleared, rising to a maximum after 24h, and maintained for 28 days. To test whether the rare bacteria surviving the beetles’s efforts to eliminate them were more resistant that the original strain, surviving bacteria were collected from beetles, cultured and tested by inoculating naive beetles, and found to be more resistant to elimination by host defences than were the original bacterial strain.
This paper is interesting in that it takes an organismal level view of insect immunity, and concludes that pathogen clearance always leaves a residual level of infection, though small, and that the main mechanism for pathogen clearance is the initial haemocyte mediated system. A few weeks ao, I blogged about another paper on the immune response in insects – in that case, the system was tripartite, involving viral pathogens and Wolbachia in the fruit fly Drosophila, the findings being that the presence of intracellular Wolbachia impacts significantly on survival of viral infection. It may well be that complex interaction may exist between host, pathogen andintracellular bacteria. Aside from the blue-sky biological interest, what other implications are there? One aspect that springs to mind is the application of insect immunity strategies to meadical treatment of infections, while the second is perhaps more interesting to me as a biologist. If the presence of Wolbachia within an insect modulates its resistance to pathogens, then routine prophylactic treatment of insects such as honey bees with antbiotics might well have unexpected side effects, potentially exacerbating the spread of bee diseases. And don’t forget the commercial and ecological importance of bee colonies.
E. R. Haine, Y. Moret, M. T. Siva-Jothy, J. Rolff (2008). Antimicrobial Defense and Persistent Infection in Insects Science, 322 (5905), 1257-1259 DOI: 10.1126/science.1165265
See also the accompanying Perspectives article:
D. S. Schneider, M. C. Chambers (2008). MICROBIOLOGY: Rogue Insect Immunity Science, 322 (5905), 1199-1200 DOI: 10.1126/science.1167450