The nutritional and pharmaceutical values of long-chain polyunsaturated fatty acids (LC-PUFAs) such as arachidonic, eicosapentaenoic and docosahexaenoic acids have been well recognized. These LC-PUFAs are physiologically important compounds in bacteria and eukaryotes. Although little is known about the biosynthetic mechanisms and functions of LC-PUFAs in bacteria compared to those in higher organisms, a combination of genetic, bioinformatic, and molecular biological approaches to LC-PUFA-producing bacteria and some eukaryotes have revealed the notably diverse organization of the pfa genes encoding a polyunsaturated fatty acid synthase complex (PUFA synthase), the LC-PUFA biosynthetic processes, and tertiary structures of the domains of this enzyme. In bacteria, LC-PUFAs appear to take part in specific functions facilitating individual membrane proteins rather than in the adjustment of the physical fluidity of the whole cell membrane. Very long chain polyunsaturated hydrocarbons (LC-HCs) such as hentriacontanonaene are considered to be closely related to LC-PUFAs in their biosynthesis and function. The possible role of LC-HCs in strictly anaerobic bacteria under aerobic and anaerobic environments and the evolutionary relationships of anaerobic and aerobic bacteria carrying pfa-like genes are also discussed.

Poly(quinoxaline-2,3-diyl) copolymers bearing various "sergeant" chiral units with common "soldier" achiral units have been synthesized to investigate the efficiency of screw-sense induction and its dependence on the nature of the solvents. Optically active 2-alkoxymethyl side chains located at the 6- and 7-positions of the quinoxaline ring induced a single-handed helical conformation more efficiently than 3-methylpentyl or 2-methylbutoxy chiral side chains. Among the 2-alkoxymethyl side chains, those bearing higher 2-alkoxy groups induced a single-handed screw sense more efficiently. For instance, a monomer unit bearing (R)-2-octyloxymethyl groups stabilized the P-helix by 1.01 kJ/mol, whereas the monomer bearing (S)-2-butoxymethyl groups stabilized the M-helix by 0.59 kJ/mol. The effect of the position of the sergeant units in the polymer main chain on the screw-sense induction was also investigated using copolymers in which the positions of the sergeant units were carefully controlled by their synthesis via living polymerization. Chiral units placed sparsely could induce single-handed helical structure efficiently. Chiral units bearing 2-alkoxymethyl, 3-methylpentyl, and 2-methylbutoxy groups showed solvent-dependent helix inversion in CHCl3 and 1,1,2-trichloroethane. No helix inversion was observed in those solvents with chiral units bearing 2-butoxy or (2-methylbutoxy)methyl side chains. The 40-mer of the (R)-2-octyloxymethyl units showed P-helical structures in THF, t-BuOMe, and c-C5H11OMe, toluene, pyridine, Et3N, 1-BuOH, CHCl3, CH2Cl2, 1,4-dichlorobutane, 1,1,-dichloroethane, and 1,1,1-trichloroethane, whereas M-helical structures were induced in 1-BuCN, 1-PrCN, 1,2-dichloroethane, 1,3-dichloropropane, and 2-BuOH.

The immune responses against helminths have been investigated individually, and it is well-established that infected hosts develop an immunological memory to resist reinfection by the same pathogen. In contrast, it is poorly understood how the host immune system responds to subsequent infection by unrelated parasites after elimination of the first infection. We previously reported that infection of mice with Strongyloides venezuelensis induces the accumulation of group 2 innate lymphoid cells (ILC2s) in the lung. Here, we demonstrated that S. venezuelensis-experienced (Sv-exp) mice became significantly resistant against infection by Nippostrongylus brasiliensis. N. brasiliensis infection induced enhanced accumulation of ILC2s and eosinophils with increased expressions of mRNA for Th2 cytokines in the lungs of Sv-exp mice. The resistance was dependent on ILC2s, and eosinophils but not on CD4+ T cells. Furthermore, pulmonary ILC2s in Sv-exp mice acquired a highly responsive “trained” phenotype; in response to N. brasiliensis infection, they rapidly increased and produced IL-5 and IL-13, which in turn induced the early accumulation of eosinophils in the lungs. IL-33 was required for the accumulation of ILC2s and the resistance of mice against N. brasiliensis infection but insufficient for the induction of trained ILC2s. In conclusion, animals infected with one type of lung-migratory nematodes acquire a specific-antigen-independent resistance to another type of lung-migrating nematodes, providing animals with the capacity to protect against sequential infections with various lung-migratory nematodes.

Human cystatin SN suppresses AR symptoms through inhibiting allergen protease activities and protecting the nasal TJ barrier in an allergen-specific manner. We propose that upregulation of nasal endogenous protease inhibitors, including cystatin SN, is a novel therapeutic strategy for protease allergen-induced AR.