Roles of neutrophil @entity8042 integrins in kinetics of @entity2259 , extravasation, and tick acquisition of @entity4210 in XXXX .

@entity32 @entity8042 @entity548 @entity776 @entity19 @entity8116 @entity12213 @entity281 @entity4459 @entity3804 @entity2259 @entity4210
Tick saliva contains anti-inflammatory and immunosuppressive substances that facilitate blood feeding and enhance tick-vectored pathogen transmission, including @entity4210 an etiologic agent of @entity8116 . As such, @entity32 at a tick-feeding site is strikingly different than that typically observed at other sites of @entity32 . Up-regulation of @entity3804 / @entity12213 occurs in host granulocytes following interaction or @entity281 with A phagocytophila, and the absence of @entity3804 / @entity12213 results in early @entity2259 . We hypothesized that @entity8042 integrin-dependent @entity281 kinetics and leukocyte extravasation are important determinants of neutrophil trafficking to, and pathogen acquisition at, tick-feeding sites. A phagocytophila @entity281 kinetics were evaluated in @entity4459 / @entity12213 , @entity3804 / @entity12213 , and @entity12213 knock-out @entity19 using quantitative polymerase chain reaction (PCR) of blood, ticks, and skin biopsies in conjunction with histopathology. A marked increase in the rate of A phagocytophila @entity281 of neutrophils and pathogen burden in blood followed tick feeding. Infection kinetics were modified by @entity8042 integrin expression and systemic neutrophil counts. Significant neutrophil-pathogen trafficking was observed to both suture and tick sites. Despite the prominent role for @entity8042 integrins in neutrophil arrest in flowing blood, successful pathogen acquisition by ticks occurred in the absence of @entity8042 integrins. Establishment of feeding pools that rely less on leukocyte trafficking and more on small @entity548 may explain the ready amplification of A phagocytophila DNA from ticks infested on @entity776 / @entity12213 -deficient @entity19 strains.
