Figure 2
Figure 2. Clots formed in HRG-deficient or SIC-treated plasma fail to contain S pyogenes bacteria. Washed S pyogenes (E-H) or phosphate-buffered saline (A-D) was added to plasma, and clot formation was initiated by addition of Thrombomax reagent to wild-type (A,E), HRG-deficient (B,F), HRG-deficient plus purified HRG (C,G), or SIC-treated wild-type plasma (D,H). The fibrin network formed in the absence or presence of bacteria was analyzed using scanning electron microscopy. Scale bar represents 5 μm. Representative images of 4 independent experiments are shown. (I) The amount of bacteria present in the supernatant of clots A to H was quantified. Data are mean ± SEM; n = 4. **P = .001; *P = .02 (Mann-Whitney test). (J-K) The clot formed in wild-type plasma in the presence of S pyogenes was thin-sectioned, immunolabeled with anti-HRG, gold-labeled secondary antibodies (black dots), and subjected to transmission electron microscopy.

Clots formed in HRG-deficient or SIC-treated plasma fail to contain S pyogenes bacteria. Washed S pyogenes (E-H) or phosphate-buffered saline (A-D) was added to plasma, and clot formation was initiated by addition of Thrombomax reagent to wild-type (A,E), HRG-deficient (B,F), HRG-deficient plus purified HRG (C,G), or SIC-treated wild-type plasma (D,H). The fibrin network formed in the absence or presence of bacteria was analyzed using scanning electron microscopy. Scale bar represents 5 μm. Representative images of 4 independent experiments are shown. (I) The amount of bacteria present in the supernatant of clots A to H was quantified. Data are mean ± SEM; n = 4. **P = .001; *P = .02 (Mann-Whitney test). (J-K) The clot formed in wild-type plasma in the presence of S pyogenes was thin-sectioned, immunolabeled with anti-HRG, gold-labeled secondary antibodies (black dots), and subjected to transmission electron microscopy.

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