Premium
Heat shock enhances innate immune response to PG‐PS and M. tuberculosis in C. elegans
Author(s) -
Kannan Krishnaswamy,
Wan Xiaoxiao,
Kannan Aarthi,
Fang Deyu,
Ortmann Robert
Publication year - 2008
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.22.1_supplement.675.21
Subject(s) - tlr2 , innate immune system , immune system , microbiology and biotechnology , biology , antimicrobial peptides , beta defensin , pattern recognition receptor , tlr4 , immunity , acquired immune system , immunology , antimicrobial
C. elegans is a soil nematode with a functioning immune system. It shares many similarities with mammals in their immune response to various pathogens and serves as a simple in vivo model to study innate immunity, including responses made via the toll‐like receptor (TLR) pathway. We investigated the expression of nlp‐29, a candidate antimicrobial gene, to study the host immune response to two gram positive bacterial isolates: (1) peptidoglycan‐polysaccharide (PG‐PS, an extract from streptococcal cell wall) and (2) the soluble fraction of pulverized heat‐killed M. tuberculosis strain H37ra (M. tb). Neither antigen is pathogenic to C. elegans and the worms do not exhibit any avoidance behavior. Our results showed a differential response to PG‐PS and M. tb, both rich in TLR2 agonists. As compared to OP50 E. Coli fed control, PG‐PS treated worms evoked a robust response by both DAF‐16 nuclear translocation and nlp‐29 expression. In comparison, M. tb treated worms exhibited less robust DAF‐16 translocation and no detectable nlp‐29 expression. However, mild heat‐shock at 37°C for an hour enhanced nlp‐29 expression significantly in PG‐PS treated worms and reached detectable levels in the M. tb treated group suggesting a differential response. Our results demonstrate the presence of an inducible innate immune response in C. elegans to PG‐PS and M. tb, both gram positive bacterial preparations rich in TLR2 ligands.