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Resident bone cells are capable of recognizing\n                    <jats:italic>Staphylococcus aureus<\/jats:italic>\n                    and initiating an inflammatory immune response that recruits leukocytes and alters bone homeostasis. Importantly, bone tissue is richly innervated with substance P containing nerve fibers and we have previously shown that this neuropeptide can augment the inflammatory responses of both osteoblasts and osteoclasts to\n                    <jats:italic>S. aureus<\/jats:italic>\n                    infection via neurokinin-1 receptors (NK-1R). Here, we have extended these studies by demonstrating that pharmacological inhibition of NK-1R ameliorates disease severity in a mouse model of staphylococcal osteomyelitis. This effect was associated with a significant reduction in leukocyte-attracting chemokine production following infection and reduced local levels of osteoclast and neutrophil activity. We then assessed the effect of\n                    <jats:italic>S. aureus<\/jats:italic>\n                    infection on bone-marrow derived osteoclast gene expression in the absence or presence of substance P. We determined that infection upregulates osteoclast expression of mRNAs encoding inflammatory mediators that include the neutrophil-attracting chemokines identified in vivo. Importantly, we found that, while substance P has no effect on chemokine mRNA expression in infected cells, this neuropeptide significantly increases the release of these chemokines by\n                    <jats:italic>S. aureus<\/jats:italic>\n                    challenged osteoclasts but not osteoblasts. Together, these data further support the ability of substance P to exacerbate inflammatory damage in staphylococcal osteomyelitis and indicate that this effect may be due, in part, to an augmentation of osteoclast immune responses that promote leukocyte recruitment.\n                  <\/jats:p>","DOI":"10.1007\/s10753-025-02280-x","type":"journal-article","created":{"date-parts":[[2025,3,8]],"date-time":"2025-03-08T08:01:47Z","timestamp":1741420907000},"page":"3506-3518","update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":5,"title":["Substance P Augments Chemokine Production by Staphylococcus aureus Infected Murine Osteoclasts"],"prefix":"10.1007","volume":"48","author":[{"given":"Sophie E.","family":"Sipprell","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Quinton A.","family":"Krueger","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Erin L.","family":"Mills","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ian","family":"Marriott","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"M. 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