EXPRESSION AND FUNCTION OF BACTERIAL CELL SURFACE COMPONENTS

细菌细胞表面在细胞的生理学中起作用，但 在细胞与环境的相互作用中也是如此。对于人类来说 病原体，包括粘连、寄主入侵和随后的逃避 宿主防御机制，如血清杀伤、吞噬和 与特定抗体的相互作用。其数量和具体结构 单个细菌细胞表面的成分决定了这些特性。 例如，在革兰氏阴性细菌表面发现的两种结构 脂多糖(LPS)和荚膜多糖。包含以下内容的LP 在细菌上发现了0抗原多糖长侧链 抵抗血清的杀菌作用。类似地，囊膜 多糖可能起到保护细菌细胞免受杀戮的作用 血清的影响。这种保护归功于这些 多糖类干扰药物的沉积速度和/或程度 细菌细胞表面的补体成分C3b。这份证词 是后续事件的先决条件，导致 细菌细胞。伤寒沙门氏菌是导致伤寒的病原体。 人类的发烧，这些细胞的表面覆盖着两层 多糖、脂多糖和被膜多糖称为 VI抗原。我们已经研究了Vi抗原和Vi抗原的相对作用 内毒素0-抗原多糖侧链与异源Vi+/-耐药性的关系 确定伤寒沙门氏菌的相对贡献率 表面结构在保护细胞免受血清杀伤和 吞噬作用。我们发现病毒抗原对抗药性没有影响。 血清杀伤作用，但降低Vi+细胞的相对吞噬速率。 我们认为Vi抗原可能干扰补体的识别。 细菌细胞表面通过吞噬细胞受体。我们还检查了 阿司匹林对细菌抗生素敏感性的影响，发现 在1-5 mM阿司匹林(或泰诺)中生长的细胞会产生抵抗力。 达到治疗过程中通常达到的抗生素水平。这种抵抗力 是由于抑制了细胞表面蛋白OmpF porin的表达， 这对抗生素的吸收起到了作用。这表明 阿司匹林或泰诺与常用抗生素联合使用 会被避开。

The bacterial cell surface functions both in the physiology of the cell but also in the interaction of the cell with its environment. For human pathogens, these include adhesion, host invasion and subsequent evasion of host defense mechanisms such as killing by serum, phagocytosis, and interactions with specific antibodies. The amount and specific structure of individual bacterial cell surface components determine these properties. For example, two structures found on the surface of Gram-negative bacteria are lipopolysaccharide (LPS) and capsular polysaccharide. LPS that contain long side chains of 0-antigen polysaccharide are found on bacteria that resist bacteriocidal effects of serum. Similarly, the capsular polysaccharide may serve to protect the bacterial cell against the killing effects of serum. This protection is due to the ability of these polysaccharides to interfere with the rate and/or extent of deposition of the complement component C3b on the bacterial cell surface. This deposition is a prerequisite for subsequent events leading to the death of the bacterial cell. Salmonellae typhi is the agent responsible for typhoid fever in man and the surface of these cells is coated with two polysaccharides, LPS and the capsular poly- saccharide called the Vi-antigen. We have examined the relative roles of the Vi-antigen and the 0-antigen polysaccharide side chains of LPS in resistance of iogenic Vi+/- strains of Salmonellae typhi to determine the relative contributions of surface structures in the protection of the cell against serum killing and phagocytosis. We found the Viantigen had no influence on resistance to serum killing but decreases the relative rate of phagocytosis of Vi+ cells. We suggest Vi-antigen may interfere with the recognition of complement on the bacterial cell surface by phagocyte receptors. We also examined the effect of aspirin on antibiotic sensitivity of bacteria, and find that cells grown in the presence of 1-5 mM aspirin (or tylenol) become resistent to levels of antibiotics commonly achieved during therapy. This resistance is due to inhibition of expression of cell surface protein, the OmpF porin, that functions the uptake of the antibiotic. This suggests that administration of aspirin or tylenol with commonly prescribed antibiotics be avoided.