{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,6,20]],"date-time":"2026-06-20T07:06:37Z","timestamp":1781939197789,"version":"3.54.5"},"reference-count":45,"publisher":"American Society for Microbiology","issue":"2","license":[{"start":{"date-parts":[[2007,2,1]],"date-time":"2007-02-01T00:00:00Z","timestamp":1170288000000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.asm.org\/non-commercial-tdm-license"}],"content-domain":{"domain":["journals.asm.org"],"crossmark-restriction":true},"short-container-title":["Infect Immun"],"published-print":{"date-parts":[[2007,2]]},"abstract":"<jats:title>ABSTRACT<\/jats:title><jats:p>Lyme arthritis, caused by the spirochete<jats:italic>Borrelia burgdorferi<\/jats:italic>, can be recurrent or prolonged, whereas Lyme carditis is mostly nonrecurring. A prominent difference between arthritis and carditis is the differential representation of phagocytes in these lesions: polymorphonuclear leukocytes (PMN) are more prevalent in the joint, and macrophages predominate in the heart lesion. We have previously shown differential efficiency of<jats:italic>B. burgdorferi<\/jats:italic>clearance by PMN and macrophages, and we now investigate whether these functional differences at the cellular level may contribute to the observed differences in organ-specific pathogenesis. When we infected mice lacking the neutrophil chemokine receptor (CXCR2<jats:sup>\u2212\/\u2212<\/jats:sup>mice) with spirochetes, we detected fewer PMN in joints and less-severe arthritis. Here we have investigated the effects of the absence of the macrophage chemokine receptor CCR2 on the development and resolution of Lyme carditis in resistant (C57BL\/6J [B6]) and sensitive (C3H\/HeJ [C3H]) strains of mice. In B6 CCR2<jats:sup>\u2212\/\u2212<\/jats:sup>mice, although inflammation in hearts is mild, we detected an increased burden of<jats:italic>B. burgdorferi<\/jats:italic>compared to that in wild-type (WT) mice, suggesting reduced clearance in the absence of macrophages. In contrast, C3H CCR2<jats:sup>\u2212\/\u2212<\/jats:sup>mice have severe inflammation but a decreased<jats:italic>B. burgdorferi<\/jats:italic>burden compared to that in WT C3H mice both at peak disease and during resolution. Histopathologic examination of infected hearts revealed that infected C3H CCR2<jats:sup>\u2212\/\u2212<\/jats:sup>animals have an increased presence of PMN, suggesting compensatory mechanisms of<jats:italic>B. burgdorferi<\/jats:italic>clearance in the hearts of infected C3H CCR2<jats:sup>\u2212\/\u2212<\/jats:sup>mice. The more efficient clearance of<jats:italic>B. burgdorferi<\/jats:italic>from hearts by CCR2<jats:sup>\u2212\/\u2212<\/jats:sup>versus WT C3H mice suggests a natural defect in the recruitment or function of macrophages in C3H mice, which may contribute to the sensitivity of this strain to<jats:italic>B. burgdorferi<\/jats:italic>infection.<\/jats:p>","DOI":"10.1128\/iai.00685-06","type":"journal-article","created":{"date-parts":[[2006,11,14]],"date-time":"2006-11-14T02:33:56Z","timestamp":1163471636000},"page":"613-620","update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":59,"title":["Recruitment of Macrophages and Polymorphonuclear Leukocytes in Lyme Carditis"],"prefix":"10.1128","volume":"75","author":[{"given":"Ruth R.","family":"Montgomery","sequence":"first","affiliation":[{"name":"Department of Internal Medicine"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Carmen J.","family":"Booth","sequence":"additional","affiliation":[{"name":"Section of Comparative Medicine, Yale University School of Medicine, New Haven, Connecticut 06510"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Xiaomei","family":"Wang","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Victoria A.","family":"Blaho","sequence":"additional","affiliation":[{"name":"Departments of Veterinary Pathobiology and Molecular Microbiology and Immunology, University of Missouri, Columbia, Missouri"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Stephen E.","family":"Malawista","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Charles R.","family":"Brown","sequence":"additional","affiliation":[{"name":"Departments of Veterinary Pathobiology and Molecular Microbiology and Immunology, University of Missouri, Columbia, Missouri"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"235","reference":[{"key":"e_1_3_2_2_2","doi-asserted-by":"publisher","DOI":"10.1126\/science.285.5428.736"},{"key":"e_1_3_2_3_2","doi-asserted-by":"publisher","DOI":"10.4269\/ajtmh.1992.47.249"},{"key":"e_1_3_2_4_2","doi-asserted-by":"publisher","DOI":"10.1093\/infdis\/163.2.419"},{"key":"e_1_3_2_5_2","doi-asserted-by":"publisher","DOI":"10.1093\/infdis\/172.3.778"},{"key":"e_1_3_2_6_2","first-page":"223","year":"1992","unstructured":"Barthold, S. 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