Lack of an adaptive strategy to combat infection creates opportunities for the innate immune system to guide invertebrate defense mechanisms. The innate immunity signaling cascades in invertebrates are elaborate, complex, and pathogen‐specific. Among invertebrates, the most extended repertoire of molecules that function in the regulatory signaling pathways has been observed in insects. This is highlighted by the fact that antimicrobial peptide (AMP) production against pathogens is orchestrated through diverse immune pathways, either independently or through cross‐talk mechanisms. The Janus kinase/signal transducer and activator of transcription (JAK/STAT) pathway coordinates immune responses from cytokines and regulates multiple homeostasis mechanisms in the host. That pathway has been implicated in the regulation of cell growth, differentiation, apoptosis, and inflammatory reactions. Many novel therapeutic interventions for tumors have been aimed at inhibitors of the JAK/STAT cascade. The regulatory pathway has much fewer components in Drosophila, and human homologs of almost all the critical pathway components and negative regulators have been identified. Loss‐of‐function mutation analysis and RNA interference‐based gene silencing modeling have produced functional characterization of the core components and negative regulators in Drosophila melanogaster, Aedes aegypti, and Anopheles gambiae, and in some hymenopteran and lepidopteran species. The genome‐wide analysis of the coleopteran species, Tribolium castaneum and Tenebrio molitor have been explored for elucidation of their JAK/STAT pathway regulatory components. Considering the promise of the JAK/STAT pathway in the mammalian model, the regulatory pathway in insects seems interesting especially for understanding pathogen surveillance mechanisms.

Although it is known that the Drosophila Toll-7 receptor plays a critical role in antiviral autophagy, its function in other insects has not yet been reported. Here, we have identified a Toll-like receptor 7 gene, TmToll-7, in the coleopteran insect T. molitor and examined its potential role in antibacterial and antifungal immunity. We showed that TmToll-7 expression was significantly induced in larvae 6 h after infection with Escherichia coli and Staphylococcus aureus and 9 h after infection with Candida albicans. However, even though TmToll-7 was induced by all three pathogens, we found that TmToll-7 knockdown significantly reduced larval survival to E. coli, but not to S. aureus, and C. albicans infections. To understand the reasons for this difference, we examined the effects of TmToll-7 knockdown on antimicrobial peptide (AMP) gene expression and found a significant reduction of E. coli-induced expression of AMP genes such as TmTenecin-1, TmDefensin-1, TmDefensin-2, TmColeoptericin-1, and TmAttacin-2. Furthermore, TmToll-7 knockdown larvae infected with E. coli showed significantly higher bacterial growth in the hemolymph compared to control larvae treated with Vermilion dsRNA. Taken together, our results suggest that TmToll-7 plays an important role in regulating the immune response of T. molitor to E. coli.

Carbon nanotubes (CNTs) have specific properties, including electrical and thermal conductivity, great strength, and rigidity, that allow them to be used in many fields. However, this increasing contact with humans and the environment is also raising health and safety concerns. Thus, research on the safety of CNTs has attracted much interest, including a comparison of the toxic effects of asbestos and carbon nanotubes, due to their physical similarity of a high aspect ratio (length/diameter). Nonetheless, there has not yet been a toxicogenomic comparison. Therefore, to examine toxicogenomic effects, the 50% growth inhibition (GI(50)) concentration was determined for multi-wall carbon nanotubes (MWCNTs) and asbestos (crocidolite) and found to be approximately 0.0135 and 0.066%, respectively, in the case of 24-h treatment of normal human bronchial epithelia (NHBE) cells. Using these GI(50) concentrations, NHBE cells were then treated with MWCNTs and asbestos for 6 and 24 h, followed by a DNA microarray analysis. Among 31,647 genes, 1,201 and 1,252 were up-regulated by both asbestos and MWCNTs after 6 and 24 h of exposure, respectively. Meanwhile, 1,977 and 1,542 genes were down-regulated by both asbestos and MWNCTs after 6 and 24 h of exposure, respectively. In particular, the asbestos and MWCNTs both induced an over twofold up- and down-regulated expression of 12 mesothelioma-related genes and 22 lung cancer-related genes when compared with the negative control. Plus, the genes induced by the MWCNT exposure were expressed in the brain, lungs, epithelium, liver, and colon.