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Previous work showed that P66-deficient<jats:named-content content-type=\"genus-species\">B. burgdorferi<\/jats:named-content>(\u0394<jats:italic>p66<\/jats:italic>) is cleared quickly after inoculation in mice. We demonstrate that the \u0394<jats:italic>p66<\/jats:italic>strain is rapidly cleared from the skin inoculation site prior to dissemination. The rapid clearance of \u0394<jats:italic>p66<\/jats:italic>bacteria is not due to inherent defects in multiple properties that might affect infectivity: bacterial outer membrane integrity, motility, chemotactic response, or nutrient acquisition. This led us to the hypothesis that P66 has a role in mouse cathelicidin-related antimicrobial peptide (mCRAMP; a major skin antimicrobial peptide) and\/or neutrophil evasion. Neither wild-type (WT) nor \u0394<jats:italic>p66 B. burgdorferi<\/jats:italic>was susceptible to mCRAMP. To examine the role of neutrophil evasion, we administered neutrophil-depleting antibody anti-Ly6G (1A8) to C3H\/HeN mice and subsequently monitored the course of<jats:named-content content-type=\"genus-species\">B. burgdorferi<\/jats:named-content>infection. \u0394<jats:italic>p66<\/jats:italic>mutants were unable to establish infection in neutrophil-depleted mice, suggesting that the important role of P66 during early infection is through another mechanism. Neutrophil depletion did not affect WT<jats:named-content content-type=\"genus-species\">B. burgdorferi<\/jats:named-content>bacterial burdens in the skin (inoculation site), ear, heart, or tibiotarsal joint at early time points postinoculation. This was unexpected given that prior<jats:italic>in vitro<\/jats:italic>studies demonstrated neutrophils phagocytose and kill<jats:named-content content-type=\"genus-species\">B. burgdorferi<\/jats:named-content>. These data, together with our previous work, suggest that despite the<jats:italic>in vitro<\/jats:italic>ability of host innate defenses to kill<jats:named-content content-type=\"genus-species\">B. burgdorferi<\/jats:named-content>, individual innate immune mechanisms have limited contributions to controlling early<jats:named-content content-type=\"genus-species\">B. burgdorferi<\/jats:named-content>infection in the laboratory model used.<\/jats:p>","DOI":"10.1128\/iai.00186-17","type":"journal-article","created":{"date-parts":[[2017,11,20]],"date-time":"2017-11-20T16:30:18Z","timestamp":1511195418000},"update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":15,"title":["Characterization of Stress and Innate Immunity Resistance of Wild-Type and \u0394<i>p66 Borrelia burgdorferi<\/i>"],"prefix":"10.1128","volume":"86","author":[{"given":"Michael W.","family":"Curtis","sequence":"first","affiliation":[{"name":"Graduate Program in Microbiology, Immunology, and Molecular Genetics, Medical College of Wisconsin, Milwaukee, Wisconsin, USA"},{"name":"Department of Microbiology and Immunology, Medical College of Wisconsin, Milwaukee, Wisconsin, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Beth L.","family":"Hahn","sequence":"additional","affiliation":[{"name":"Department of Medicine, Division of Infectious Diseases, Medical College of Wisconsin, Milwaukee, Wisconsin, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kai","family":"Zhang","sequence":"additional","affiliation":[{"name":"Department of Oral Biology, State University of New York at Buffalo, Buffalo, New York, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Chunhao","family":"Li","sequence":"additional","affiliation":[{"name":"Department of Oral Biology, State University of New York at Buffalo, Buffalo, New York, USA"},{"name":"Department of Microbiology and Immunology, State University of New York at Buffalo, Buffalo, New York, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Richard T.","family":"Robinson","sequence":"additional","affiliation":[{"name":"Department of Microbiology and Immunology, Medical College of Wisconsin, Milwaukee, Wisconsin, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-6460-2017","authenticated-orcid":false,"given":"Jenifer","family":"Coburn","sequence":"additional","affiliation":[{"name":"Department of Microbiology and Immunology, Medical College of Wisconsin, Milwaukee, Wisconsin, USA"},{"name":"Department of Medicine, Division of Infectious Diseases, Medical College of Wisconsin, Milwaukee, Wisconsin, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"235","reference":[{"key":"e_1_3_3_2_2","doi-asserted-by":"publisher","DOI":"10.1126\/science.7043737"},{"key":"e_1_3_3_3_2","doi-asserted-by":"publisher","DOI":"10.1038\/nrmicro2714"},{"key":"e_1_3_3_4_2","first-page":"251","volume-title":"Borrelia: molecular biology, host interaction and pathogenesis","author":"Piesman J","year":"2010","unstructured":"Piesman J, Schwan TG. 2010. 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