In experiment I (Fig. 1), 4 animals had been infected with dbpAB/dbpAB

Tissue samples from ear, bladder and hind tibiotarsal joint were Procyanidin B2 dose collected for culture. In experiment II, 20 animals had been infected with dbpAB/dbpAB (groups 7, 9 and 11) and 20 animals with dbpAB (groups eight, ten and 12). Two uninfected animals (group six) were damaging controls. Sixteen animals (groups 9 and 10) have been treated with ceftriaxone and 16 animals (groups 11 and 12) with ceftriaxone and anti-TNF-alpha. In Experiment III, mice have been killed at two weeks to study infection kinetics and bacterial load in joints. In Experiment IV, eight infected animals were treated with ceftriaxone at six we.In experiment I (Fig. 1), 4 animals were infected with dbpAB/dbpAB (group 2), eight with dbpAB/dbpA (group three), eight with dbpAB/dbpB (group 4), and two with dbpAB (group five). Two uninfected animals (group 1) had been damaging controls. The development of joint manifestations was monitored by measuring the medio-lateral diameter with the hind tibiotarsal joints when per week. The measurer was blinded for the group's identity. The mice have been killed at seven weeks of infection. Tissue samples from ear, bladder and hind tibiotarsal joint had been collected for culture. In experiment II, 20 animals have been infected with dbpAB/dbpAB (groups 7, 9 and 11) and 20 animals with dbpAB (groups 8, 10 and 12). Two uninfected animals (group 6) had been damaging controls. Sixteen animals (groups 9 and ten) were treated with ceftriaxone and 16 animals (groups 11 and 12) with ceftriaxone and anti-TNF-alpha. The ceftriaxone treatment was started at two weeks title= 10253890.2011.586446 along with the anti-TNF-alpha therapy at seven weeks of infection. Ceftriaxone (Rocephalin1, Roche, Mannheim, Germany) was administered twice a day 25 mg/kg intraperitoneally for five days. Rat murine chimeric TNF-alpha antibody of IgG2ak isotype (Centocor, Malvern, PA, USA) was administered after a week ten mg/kg intraperitoneally for four weeks. The development of joint manifestations was monitored as described above. The mice have been killed at 15 weeks of infection. Tissue samples from ear, bladder and hind tibiotarsal joint were collected for culture and PCR analyses. Blood was collected for serology, and one tibiotarsal joint for histology. In experiment III, eight dbpAB/dbpAB (group 14), eight dbpAB (group 15) infected animals, and 4 uninfected control (group 13) animals have been killed at two weeks of infection. Samples from ear, bladder and hind tibiotarsal joint had been collected for culture. One particular hind tibiotarsal joint was collected for PCR analysis of B. burgdorferi title= j.bmc.2011.07.043 tissue load, and blood was title= 2042098611406160 collected for serology. In experiment IV, eight animals we infected with dbpAB/dbpAB (groups 17 and 19) and eight animals with dbpAB (groups 18 and 20). 4 uninfected animals (group 16) had been adverse controls. Eight animals (groups 19 and 20) were treated with ceftriaxone at six weeks. The development of joint manifestations was monitored as explained above. The mice have been killed at 15 weeks of infection. Tissue samples from ear, bladder and hind tibiotarsal joint had been collected for culture and PCR analyses. Blood was collected for serology.PLOS A single | DOI:ten.1371/journal.pone.0121512 March 27,3 /DbpA and B Market Arthritis and Post-Treatment Persistence in MiceFig 1.