Clinically Relevant Preclinical Model Of CFA-Induced Inflammatory Pain

Inflammatory pain is a complex perception and affective response to noxious stimuli during an inflammatory or immune response, often triggered by injury or infection. The inflammatory response involves coordinated physiological processes aimed at reversing injury-induced pathology. Acute inflammation leads to pain through the direct activation of sensory neurons, which transmit pain signals to the brain. The onset of inflammatory pain is initiated by the activation of nociceptive sensory neurons via thermal, mechanical stimulation, or inflammatory mediators, followed by the depolarization of sensory nerve endings and the transmission of noxious information through the spinal cord. Key mediators involved in this process include glutamate, ATP, bradykinin, serotonin, prostaglandins, lysophosphatidic acids, nerve growth factor, and sphingosine 1-phosphate.

Preclinical animal models are vital in elucidating the mechanisms of inflammatory pain and in facilitating the development of effective therapies. This report focuses on the design and pharmacological validation of the Complete Freund’s Adjuvant (CFA)-induced inflammatory pain model, which involves the use of an antigen emulsified in mineral oil to enhance immune response. CFA contains inactivated mycobacteria (typically M. tuberculosis), whereas the incomplete form (IFA) lacks these mycobacterial components. These models play a critical role in screening potential analgesic candidates, helping to identify promising therapies for managing inflammatory pain.