Wormser G P, Nunez M, Horn D
Clin Dermatol. 1987 Apr-Jun;5(2):112-22. doi: 10.1016/0738-081x(87)90013-7.
The skin and mucous membranes are the principal barriers to invasion of the body by microorganisms. Besides functioning as a mechanical barrier, the mucosae are endowed with an array of still poorly characterized specific and nonspecific host defense capabilities. These include the production of mucus, secretory immunoglobulin (IgA), lysozyme, lactoferrin, and alpha-antitrypsin, in conjunction with a low-grade exudation of leukocytes. In addition, the mucosal surfaces of the upper respiratory, gastrointestinal, and lower vaginal and urinary tracts support a large number of “nonpathogenic” microorganisms that comprise the so-called “normal flora.” This commensal flora plays an important and complex role in protecting the host from microbial invasion. Mechanisms for this protection likely include the following: (1) competition for the same nutrients (interference); (2) competition for the same receptors on host cells (tropism); (3) production of bacteriocins, that is, bacterial products that are toxic to other organisms, usually of the same species; and (4) stimulation of crossprotective immune factors such as the “natural antibodies.” The “normal” flora is inconstant and may be altered by dietary factors, debilitation, hormonal events (such as menstruation, pregnancy, and possibly use of oral contraceptives), personal hygiene, medications, intercurrent infection, and probably many others. Antibiotic therapy and menstruation can have a profound effect on the composition of this group of microorganisms. Disturbance of the delicate host-commensal relationship may cause a clinically significant infection due to these “nonpathogens.” This may occur in response to the aforementioned factors (eg, pregnancy predisposing to vaginal candidiasis) or because of disruption of the anatomic barrier (eg, local mucosal infection at a site of trauma, or injury from cytotoxic drugs) or in association with exogenous infection (eg, rhinoviral infection leading to secondary bacterial otitis media). Invasion by “normal flora” may result in serious systemic illness. A clear example of the latter is the development of infective endocarditis caused by viridans streptococci following a dental procedure.
皮肤和黏膜是微生物侵入人体的主要屏障。除了作为机械屏障发挥作用外，黏膜还具有一系列特性仍未完全明确的特异性和非特异性宿主防御能力。这些能力包括产生黏液、分泌性免疫球蛋白（IgA）、溶菌酶、乳铁蛋白和α-抗胰蛋白酶，同时伴有白细胞的轻度渗出。此外，上呼吸道、胃肠道以及下阴道和尿道的黏膜表面存在大量“非致病性”微生物，它们构成了所谓的“正常菌群”。这种共生菌群在保护宿主免受微生物入侵方面发挥着重要而复杂的作用。这种保护机制可能包括以下几点：（1）争夺相同的营养物质（干扰）；（2）争夺宿主细胞上相同的受体（嗜性）；（3）产生细菌素，即对其他生物体（通常是同一物种）有毒的细菌产物；（4）刺激交叉保护免疫因子，如“天然抗体”。“正常”菌群并非一成不变，可能会因饮食因素、身体虚弱、激素变化（如月经、怀孕以及可能使用口服避孕药）、个人卫生、药物治疗、并发感染以及可能的许多其他因素而改变。抗生素治疗和月经对这组微生物的组成可能会产生深远影响。这种微妙的宿主-共生关系的紊乱可能会导致这些“非病原体”引发具有临床意义的感染。这可能是对上述因素（如怀孕易引发阴道念珠菌病）的反应，或者是由于解剖屏障的破坏（如创伤部位的局部黏膜感染或细胞毒性药物造成的损伤），或者与外源性感染相关（如鼻病毒感染导致继发性细菌性中耳炎）。“正常菌群”的侵入可能导致严重的全身性疾病。后者的一个明显例子是牙科手术后由草绿色链球菌引起的感染性心内膜炎。
