Our research group has recently described that radiation-induced airborne stress signals can be communicated between Caenorhabditis elegans (C. elegans). This paper addresses the question of whether heat stress can also induce emission of airborne stress signal to alert neighboring C. elegans and elicit their subsequent stress response. Here, we report that heat-stressed C. elegans produces volatile stress signal(s) that trigger an increase in radiation resistance in neighboring unheat-stressed C. elegans. When several loss-of-function mutations affecting the thermosensory neuron (AFD), heat shock factor-1 (HSF-1), and small heat-shock proteins (HSPs) were used as the heat-stressed C. elegans, we found that the production of the volatile stress signal(s) were blocked, demonstrating the heat shock response as a role in controlling the production of the volatile stress signal(s). It can be found that the mutations affecting DNA damage response (DDR) could inhibit the increasing of radiation resistance in neighboring unheat-stressed C. elegans having received the volatile stress signal(s), which indicate that the DDR might contribute to RAR induction by the volatile stress signal(s). Together, this study demonstrates that heat-stressed nematodes could communicate with unheat-stressed nematodes via volatile stress signal. In addition, the regulating pattern of signal production and action are preliminarily clarified.