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ARS Home » Midwest Area » Columbia, Missouri » Biological Control of Insects Research » Research » Publications at this Location » Publication #395864

Research Project: Biologically-Based Products for Insect Pest Control and Emerging Needs in Agriculture

Location: Biological Control of Insects Research

Title: Thromboxane mobilizes insect blood cells to infection foci

item ROY, MILTAN CHANDRA - Andong National University
item NAM, KIWOONG - University Of Montpellier
item KIM, JAESU - Jeonbuk National University
item Stanley, David
item KIM, YONGGYUN - Andong National University

Submitted to: Frontiers in Immunology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 11/18/2021
Publication Date: 12/20/2021
Citation: Roy, M., Nam, K., Kim, J., Stanley, D.W., Kim, Y. 2021. Thromboxane mobilizes insect blood cells to infection foci. Frontiers in Immunology. 12:791319.

Interpretive Summary: Insects protect themselves from bacterial and fungal infections via effective immune systems. Some insect biological control programs are based on deploying bacteria and fungi that are lethal to some pest insects, but not to other animals or plants. Insect immune systems can reduce the ability of some of these biological control agents to control pest insects. The broad mechanisms of insect immune responses to infections are generally understood, however, the biochemical signals responsible for coordinating insect immune responses to infections are not. This is a serious shortcoming because a more thorough understanding of these biochemical signals may be developed into new mechanisms of weakening pest insect immunity. In this paper, we report on identification of a previously unknown biochemical signal that directs insect blood cells to the site of an infection. This is a necessary step in insect immune responses to infection. This new knowledge will be used by scientists working to improve application of insect-specific bacteria and fungi to pest insect management. Such improvements will contribute to production of abundant and healthy foods needed to support a growing human population.

Technical Abstract: Innate immune responses are effective for insect survival to defend against entomopathogens including a fungal pathogen, Metarhizium rileyi, that infects a lepidopteran Spodoptera exigua. In particular, the fungal virulence was attenuated by cellular immune responses, in which the conidia were phagocytosed by hemocytes (insect blood cells) and hyphal growth was inhibited by hemocyte encapsulation. However, the chemokine signal to drive hemocytes to the infection foci was little understood. The hemocyte behaviors appeared to be guided by a Ca2+ signal stimulating cell aggregation to the infection foci. The induction of the Ca2+ signal was significantly inhibited by the cyclooxygenase (COX) inhibitor. Under the inhibitory condition, the addition of thromboxane A2 or B2 (TXA2 or TXB2) among COX products was the most effective to recover the Ca2+ signal and hemocyte aggregation. TXB2 alone induced a microaggregation behavior of hemocytes under in vitro conditions. Indeed, TXB2 titer was significantly increased in the plasma of the infected larvae. The elevated TXB2 level was further supported by the induction of phospholipase A2 (PLA2) activity in the hemocytes and subsequent up-regulation of COX-like peroxinectins (SePOX-F and SePOX-H) in response to the fungal infection. Finally, the expression of a thromboxane synthase (Se-TXAS) gene was highly expressed in the hemocytes. RNA interference (RNAi) of Se-TXAS expression inhibited the Ca2+ signal and hemocyte aggregation around fungal hyphae, which were rescued by the addition of TXB2. Without any ortholog to mammalian thromboxane receptors, a prostaglandin receptor was essential to mediate TXB2 signal to elevate the Ca2+ signal and mediate hemocyte aggregation behavior. Specific inhibitor assays suggest that the downstream signal after binding TXB2 to the receptor follows the Ca2+-induced Ca2+ release pathway from the endoplasmic reticulum of the hemocytes. These results suggest that hemocyte aggregation induced by the fungal infection is triggered by TXB2 via a Ca2+ signal through a PG receptor.