Merino S, Albertí S, Tomás J M
Departamento de Microbiología, Universidad de Barcelona, Spain.
Infect Immun. 1994 Dec;62(12):5483-90. doi: 10.1128/iai.62.12.5483-5490.1994.
The resistance of Aeromonas salmonicida to complement-mediated killing was investigated by using different strains and their isogenic mutants that had been previously characterized for their surface components. We found that the classical complement pathway is involved in serum killing of susceptible A. salmonicida strains, while the alternative complement pathway seems not to be involved. All of the A. salmonicida strains are able to activate complement, but the smooth strains (with or without the A-layer) are resistant to complement-mediated killing. The reasons for this resistance are that C3b may be bound far from the cell membrane and that it is rapidly degraded; therefore, the lytic final complex C5b-9 (membrane attack complex) is not formed. Isogenic rough mutants are serum sensitive because they bind more C3b than the smooth strains, and if C3b is not completely degraded, then the lytic complex (C5b-9) is formed.
利用先前已对其表面成分进行表征的不同菌株及其同基因突变体，研究了杀鲑气单胞菌对补体介导杀伤的抗性。我们发现，经典补体途径参与了对易感杀鲑气单胞菌菌株的血清杀伤作用，而替代补体途径似乎未参与其中。所有杀鲑气单胞菌菌株均能够激活补体，但光滑菌株（有或没有A层）对补体介导的杀伤具有抗性。这种抗性的原因在于，C3b可能在远离细胞膜的位置结合且迅速降解，因此，不会形成溶细胞终末复合物C5b-9（膜攻击复合物）。同基因粗糙突变体对血清敏感，因为它们比光滑菌株结合更多的C3b，并且如果C3b没有完全降解，那么就会形成溶细胞复合物（C5b-9）。
