Protein deficiency impairs ADCC mechanism against NBL in lungs during Trichinella spiralis infection

LOMBARDO T; PALLARO AN; SARACINO MP; DIAZ M; VILA CC; FALDUTO GH; BALDI PC

Ciudad del Cabo

Congreso; Keystone Symposia Conference T4. Helminths: New Insights from Immunity to Global Health; 2019

Keystone Symposia

On their way to skeletal muscle cells, Trichinella spiralis newborn larvae(NBL) travel along the lungs, among other sites. Our previous studies demonstratedthat lung mucosa leukocytes can kill NBL by ADCC mechanism. In rats fed with aprotein deficient diet (PD), we observed an impaired mucosal immune response inintestine and lungs. The aim of this work was to assess the effect of a PD dietduring T. spiralis infection on ADCC exvivo using lung cell suspensions (LCS). For that purpose, two groups of weaningWistar rats received PD diet (6.5% casein) and other two received control diet(C, 20% casein); 10 days later one group of each diet was orally infected (PDI,CI). Animals were euthanized at 6 and 13 days p.i. to obtain LCS andlung tissue extracts (LTE). Antibodies (Abs) against NBL in LTE, rat cytotoxicsera (RCS, positive control) and non-infected rat sera (NIRS, negative control)were measured by indirect IFA. LCS were concentrated and stained with Giemsa todetermine the leukocyte formula. In ADCC assays, NBL were incubated with LCS frominfected or non-infected rats (PD, C) or peritoneal cells from non-infected C ratsin the presence of LTE, RCS or NIRS, and NBL mortality percentage (%M) wasevaluated. Titers of specific Abs in LTE were lower in PDI than CI.In ADCC assays with peritoneal cells, %M was lower with LTE from PDIcompared to CI at day 13 p.i. (21.2±2.83 vs. 29.66±2.22, P