No abstract

Antimicrobial peptides (AMPs), major innate immune effectors, are induced to protect hosts against invading microorganisms. AMPs are also induced under non-infectious stress; however, the signaling pathways of non-infectious stress-induced AMP expression are yet unclear. We demonstrated that growth-blocking peptide (GBP) is a potent cytokine that regulates stressor-induced AMP expression in insects. GBP overexpression in Drosophila elevated expression of AMPs. GBP-induced AMP expression did not require Toll and immune deficiency (Imd) pathway-related genes, but imd and basket were essential, indicating that GBP signaling in Drosophila did not use the orthodox Toll or Imd pathway but used the JNK pathway after association with the adaptor protein Imd. The enhancement of AMP expression by non-infectious physical or environmental stressors was apparent in controls but not in GBP-knockdown larvae. These results indicate that the Drosophila GBP signaling pathway mediates acute innate immune reactions under various stresses, regardless of whether they are infectious or non-infectious.

Insects combat infection through carefully measured cellular (for example, phagocytosis) and humoral (for example, secretion of antimicrobial peptides (AMPs)) innate immune responses. Little is known concerning how these different defense mechanisms are coordinated. Here, we use insect plasmatocytes and hemocyte-like Drosophila S2 cells to characterize mechanisms of immunity that operate in the haemocoel. We demonstrate that a Drosophila cytokine, growth-blocking peptides (GBP), acts through the phospholipase C (PLC)/Ca2+ signalling cascade to mediate the secretion of Pvf, a ligand for platelet-derived growth factor- and vascular endothelial growth factor-receptor (Pvr) homologue. Activated Pvr recruits extracellular signal-regulated protein kinase to inhibit humoral immune responses, while stimulating cell ‘spreading’, an initiating event in cellular immunity. The double-stranded RNA (dsRNA)-targeted knockdown of either Pvf2 or Pvr inhibits GBP-mediated cell spreading and activates AMP expression. Conversely, Pvf2 overexpression enhances cell spreading but inhibits AMP expression. Thus, we describe mechanisms to initiate immune programs that are either humoral or cellular in nature, but not both; such immunophysiological polarization may minimize homeostatic imbalance during infection.

No abstract

ABSTRACT-The bamboo borer, Omphisa fuscidentalis, is a moth found in northern Thailand, Lao and Myanmar and its larvae feed on the inner pulp of bamboo shoots. In a tropical highland (about 500 m sea level) forest at 19°N near Chiang Mai, Thailand, the larvae feed on at least 5 bamboo species. Nucleotide sequence analysis of the region of mitochondrial cytochrome C oxidase subunit 1 gene amplified by the polymerase chain reaction (PCR) verified that larvae collected from different bamboos belong to the same species. Adults appeared in early August and laid clusters of eggs on the newly grown bamboo shoot. The newly hatched larvae bore a hole in the shoot, enter an internode of the shoot and feed on the inner pulp. After maturation in September, the larvae remain in an internodal cavity of bamboo for up to 9 months, from September to the following June. Number of larval instars was estimated by measuring the width of head capsules remained in internodes of bamboo shoots. The growth curve of the width fitted to Dyar's law and the mature larvae were estimated to be 5th instar. Mature larvae were collected in the field each month and their body weight, head capsule width, protein and fat contents and hemolymph ecdysteroid titer were measured. Body weight continuously decreased during the 9 months whereas head capsule width remained constant. Fat content fluctuated during this period while protein level remained at a similar level until March, after which it significantly increased. During this period, hemolymph ecdysteroid concentrations remained low. Current results show that the bamboo borer larvae enter diapause at the end of feeding period of the fifth (last) larval instar and the larval diapause lasts until June.