Mechanism of Metarhizium rileyi evading cellular immune responses in Helicoverpa armigera.

Abstract

Upon entry into the hemocoel of host insects, entomopathogenic fungi switch to yeast-like hyphal bodies that are not recognized by host hemocytes and replicate extensively in the hemolymph. The mechanism by which hyphal bodies evade host cellular immunity is not well understood. This study compares Metarhizium rileyi conidia and hyphal bodies with respect to elicitation of the immune response of Helicoverpa armigera and recognition by host pattern recognition receptors (PRRs). We found that the ability of host hemocytes to phagocytize and nodulate hyphal bodies was weaker than those responses against conidia, suggesting that hyphal bodies are more able to evade host cellular immunity. Additionally, we found that the binding affinity of H. armigera β-1,3-glucan recognition proteins was much lower for hyphal bodies than for conidia. We observed no agglutination response of H. armigera C-type lectin 3 (HaCTL3) against hyphal bodies, and HaCTL3 bound significantly less to hyphal bodies than to conidia, indicating that host PRRs have a lower affinity for hyphal bodies than for conidia. This study provides direct evidence that the mechanism whereby entomopathogenic fungi escape host cellular immunity involves the inability of host PRRs to sufficiently recognize hyphal bodies to elicit the cellular immune response.