It is well known that stress can elicit hypothalamic-pituitary-adrenal axis (HPA) axis activation and promote the following cortisol release, which finally contributes to oxidative, inflammatory, physiological, and mental stress [1]. As described precedingly, under the stimulation of stress, corticotropin-releasing hormone (CRH) can be released from the paraventricular nucleus (PVN) of the hypothalamus (Chap. 1 ). Over the past few decades, CRH and other corticotropin-releasing hormone (factor) family peptides (CRF peptides, CRFp) have been shown to play important roles both centrally and peripherally, balancing the interplay of hormonal, behavioral, and immune systems in response to stress [2]. Up to this point, our comprehension of the intricate interactions between CRFp and immune-mediated inflammatory responses has undergone remarkable advancement.