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. Author manuscript; available in PMC: 2017 Sep 28.
Published in final edited form as: Int J Dev Biol. 2014;58(10-12):757–766. doi: 10.1387/ijdb.140271jr

Fig. 7. The rXlCSF1R abrogates heat-killed E. coli and Frog Virus 3 elicited recruitment of tadpole peritoneal leukocytes and reduces FV3 dissemination.

Fig. 7

(A) Tadpoles were injected with vector control, heat-killed (hk) E. coli, FV3 (104 PFU), a combination of hk E. coli and rXlCSF1 (1µg) or a combination of FV3 (104 PFU) and rXlCSF1R (1µg). After 24hrs peritoneal phagocytes were lavaged and enumerated. Results are means ± SEM, N=4. (*) denotes statistical difference from the vector control and the (*) above lines denotes significant difference between treatment groups indicated by the lines, P<0.05. (B) Tadpoles were injected with 1×104 PFU of FV3 alone, or in combination with 1µg of rXlCSF1R. Following 24 hrs, tadpoles were sacrificed; their tissues were isolated and examined for infectious FV3 burdens by plaque assays. Results are means ± SEM, N=3. (*) above lines denotes significant difference between treatment groups indicated by the lines, P<0.05.