shield as signal lipopolysaccharides and the evolution of immunity to gram-negative bacteria屏蔽信号脂多糖和免疫进化的革兰氏阴性细菌.pdfVIP

Opinions Shield as Signal: Lipopolysaccharides and the Evolution of Immunity to Gram-Negative Bacteria Robert S. Munford*, Alan W. Varley ccording to the innate immunity concept [1], animals antimicrobial peptides (CAMPs) [3]. As noted by Miller [4] A defend themselves from microbes by recognizing and others, increased resistance to CAMPs and other host pathogen-associated molecular patterns. To detect molecules may explain why Gram-negative bacteria that many Gram-negative bacteria, animals use the CD14–MD-2– colonize mucosae usually make LPS with six or more acyl TLR4 receptor mechanism to recognize the lipid A moiety of chains (Figure 1). Although we found no demonstration that the cell wall lipopolysaccharide (LPS). Lipid A is a this lipid A structure enables commensal bacteria to thrive on glucosamine disaccharide that carries phosphates at positions mucosal surfaces, the evidence that it does so for colonizers 1 and 49 and usually has four primary (glucosamine-linked) and pathogens is extensive. Having hexaacyl (rather than hydroxyacyl chains and one or more secondary acyl chains. pentaacyl) lipid A enables Bordetella and Haemophilus species to Gram-negative bacteria produce numerous variations on this persist in the respiratory tract [5–7] and Neisseria gonorrhoeae basic structure, yet sensitive LPS recognition and pro- to survive within epithelial cells [8]. Pseudomonas aeruginosa inflammatory signaling by human TLR4 occur only when lives in water, produces a predominantly pentaacylated LPS, lipid A has both phosphates and is hexaacyl, with two and does not colonize the mucosae of normal humans. When secondary acyl chains.