Fig. 5
Anti-O1 and anti-O2 mAbs are protective in vivo. a Therapeutic activity of the mAbs was tested in C57BL/6 mice infected intranasally with a K. pneumoniae O1 (Kp1131115, 6 × 107 CFU) or O2 (Kp961842, 2 × 108 CFU) strain. KPE33 (anti-O1), KPN42 (anti-O2) and KPN70 (anti-O1/O2) mAbs were administered intravascular 1 h post infection at the doses indicated. An isotype-matched mAb (c-IgG) was used as a negative control. b Prophylactic activity of the mAbs was tested in C57BL/6 mice infected intraperitoneal with the O1 strain Kp1131115 (3 × 106 CFU) or the O2 strain Kp961842 (1 × 107 CFU). mAbs were administered IP 24 h prior to infection at the doses indicated; survival was monitored for 5 days post infection. c CF1 mice received a dorsal burn followed by K. pneumoniae O1 (Kp1131115, 5 × 106) bacterial inoculation subcutaneously at the burn site. KPE33 (45 or 15 mpk) or isotype-matched control mAb (c-IgG, 45 mpk) were administered IP 24 h post infection, and organs were harvested 48 h post infection to determine bacterial CFU. All graphs are representative of at least three separate experiments. Mantel-Cox analysis was done to assess significant survival benefit compared to the control mAb. For thermal injury CFU comparison, Kruskal Wallace one way Anova analysis was done to compare differences in CFU between KPE33 treated vs. control IgG treated groups, ****p < 0.0001, ***p < 0.001, **p < 0.01
