Characterization of Stress and Innate Immunity Resistance of Wild-Type and Δ.

is a causative agent of Lyme disease, the most common arthropod-borne disease in the United States.evades host immune defenses to establish a persistent, disseminated infection. Previous work showed that P66-deficient(Δ) is cleared quickly after inoculation in mice. We demonstrate that the Δstrain is rapidly cleared from the skin inoculation site prior to dissemination. The rapid clearance of Δbacteria 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 Δwas 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 ofinfection. Δmutants 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 WTbacterial burdens in the skin (inoculation site), ear, heart, or tibiotarsal joint at early time points postinoculation. This was unexpected given that priorstudies demonstrated neutrophils phagocytose and killThese data, together with our previous work, suggest that despite theability of host innate defenses to kill, individual innate immune mechanisms have limited contributions to controlling earlyinfection in the laboratory model used.