External morphology and abundance of mouthpart sensilla in Australian Gryllacrididae,Stenopelmatidae, and Tettigoniidae

Sensilla diversity and abundance were extremely high on the apex of the maxillary and labial palpi of two species of Gryllacrididae. The terminal segment of the maxillary palpi of these species had 9 and 15 sensilla types, respectively, and up to 2,834 sensilla. The labial palpi had 7 and 12 types, respectively, and up to 5,195 sensilla. Several types of multiporous smooth and ridged olfactory basiconic sensilla, and coeloconic, coelosphaeric, placoid, and multipapilliform sensilla occurred, as well as many trichoid sensilla and the more typical uniporous basiconic contact receptors. Two species of the closely related Stenopelmatidae were compared to the gryllacridids and found to have similar sensillar diversity and abundance, but three species of the more distantly related Tettigoniidae had only 4 or 5 sensilla types and a total number ranging from 320 to 960 on their maxillary palpi.     

Influence of parasite encoded inhibitors of serine peptidases in early infection of macrophages with Leishmania major

Ecotin is a potent inhibitor of family S1A serine peptidases, enzymes lacking in the protozoan parasite Leishmania major . Nevertheless, L. major has three ecotin-like genes, termed inhibitor of serine peptidase (ISP). ISP1 is expressed in vector-borne procyclic and metacyclic promastigotes, whereas ISP2 is also expressed in the mammalian amastigote stage. Recombinant ISP2 inhibited neutrophil elastase, trypsin and chymotrypsin with K _is between 7.7 and 83 nM. L. major ISP2–ISP3 double null mutants (Δ isp 2/3) were created. These grew normally as promastigotes, but were internalized by macrophages more efficiently than wild-type parasites due to the upregulation of phagocytosis by a mechanism dependent on serine peptidase activity. Δ isp 2/3 promastigotes transformed to amastigotes, but failed to divide for 48 h. Intracellular multiplication of Δ isp 2/3 was similar to wild-type parasites when serine peptidase inhibitors were present, suggesting that defective intracellular growth results from the lack of serine peptidase inhibition during promastigote uptake. Δ isp 2/3 mutants were more infective than wild-type parasites to BALB/c mice at the early stages of infection, but became equivalent as the infection progressed. These data support the hypothesis that ISPs of L. major target host serine peptidases and influence the early stages of infection of the mammalian host.