Abstract
Circulating immune cells, which are recruited to the site of injury/disease, secrete various inflammatory mediators that are critical to nociception and pain. The role of tissue-resident immune cells, however, remains poorly characterized. One of the first cells to be activated in peripheral tissues following injury are γδT cells, which serve important roles in infection, disease, and wound healing. Using a mouse line lacking these cells, we sought to identify their contribution to inflammatory pain. Three distinct models of peripheral inflammatory pain were used: intraplantar injection of formalin (spontaneous inflammatory pain), incisional wound (acute inflammatory pain), and intraplantar injection of complete Freund's adjuvant (chronic inflammatory pain). Our results show that absence of γδT cells does not alter baseline sensitivity, nor does it result in changes to mechanical or thermal hypersensitivity after tissue injury. Myeloid cell recruitment did show differential changes between models of acute and chronic inflammatory pain. These results were consistent in both male and female mice, suggesting that there are no sex differences in these outcomes. This comprehensive characterization suggests that γδT cells do not contribute to basal sensitivity or the development and maintenance of inflammatory pain.
Highlights
The immune and nervous systems are intimately connected, during inflammatory pain
Our work started by showing that loss of γδT cells did not have an effect on basal sensitivity, an important finding given that these cells are known to interact with sensory fibers during inflammation [46]
Using three models of peripheral inflammatory pain, including intraplantar injection of formalin/CFA and incisional wound, we found that γδT cells do not alter mechanical or thermal sensitivity during inflammation
Summary
The immune and nervous systems are intimately connected, during inflammatory pain. Peripheral inflammation is brought on by the wellorchestrated recruitment and activation of circulatory and tissue-resident immune cells, including mast cells, neutrophils, and macrophages [4, 5] These cells and their secreted mediators can alter nociceptor function/activity to induce nociceptor activation and/or peripheral sensitization, triggering increased responsiveness to noxious stimuli and pain hypersensitivity [1,2,3,4,5,6,7]. Recent work suggests skin-resident mast cells have no effect on inflammatory pain hypersensitivity [12], surprising given that these cells are known producers of inflammatory mediators that alter hypersensitivity [20,21,22] This brings about the question whether other tissue-resident immune cells play a role in inflammatory pain
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