The Skin and the Mucosal Surfaces Provide Protective Barriers Against Infection

Physical and anatomic barriers that tend to prevent the entry of pathogens are an organism's first line of defense against infection. The skin and the surface of mucous membranes are included in this category because they are effective barriers to the entry of most microorganisms. The skin consists of two distinct layers: a thinner outer layer—the epidermis—and a thicker layer—the dermis. The epidermis contains several layers of tightly packed epithelial cells. The outer epidermal layer consists of dead cells and is filled with a waterproofing protein called keratin. The dermis, which is composed of connective tissue, contains blood vessels, hair follicles, sebaceous glands, and sweat glands. The sebaceous glands are associated with the hair follicles and produce an oily secretion called sebum. Sebum consists of lactic acid and fatty acids, which maintain the pH of the skin between 3 and 5; this pH inhibits the growth of most microorganisms. A few bacteria that metabolize sebum live as commensals on the skin and sometimes cause a severe form of acne. One acne drug, isotretinoin (Accutane), is a vitamin A derivative that prevents the formation of sebum.

Breaks in the skin resulting from scratches, wounds, or abrasion are obvious routes of infection. The skin may also be penetrated by biting insects (e.g., mosquitoes, mites, ticks, fleas, and sandflies); if these harbor pathogenic organisms, they can introduce the pathogen into the body as they feed. The protozoan that causes malaria, for example, is deposited in humans by mosquitoes when they take a blood meal. Similarly, bubonic plague is spread by the bite of fleas, and Lyme disease is spread by the bite of ticks.

The conjunctivae and the alimentary, respiratory, and urogenital tracts are lined by mucous membranes, not by the dry, protective skin that covers the exterior of the body. These

TABLE 1-2

Summary of nonspecific host defenses

Type

Mechanism

Anatomic barriers Skin

Mucous membranes

Physiologic barriers Temperature

Low pH

Chemical mediators

Phagocytic/endocytic barriers

Inflammatory barriers

Mechanical barrier retards entry of microbes.

Acidic environment (pH 3-5) retards growth of microbes.

Normal flora compete with microbes for attachment sites and nutrients. Mucus entraps foreign microorganisms. Cilia propel microorganisms out of body.

Normal body temperature inhibits growth of some pathogens. Fever response inhibits growth of some pathogens.

Acidity of stomach contents kills most ingested microorganisms.

Lysozyme cleaves bacterial cell wall.

Interferon induces antiviral state in uninfected cells.

Complement lyses microorganisms or facilitates phagocytosis.

Toll-like receptors recognize microbial molecules, signal cell to secrete immunostimulatory cytokines. Collectins disrupt cell wall of pathogen.

Various cells internalize (endocytose) and break down foreign macromolecules. Specialized cells (blood monocytes, neutrophils, tissue macrophages) internalize (phagocytose), kill, and digest whole microorganisms.

Tissue damage and infection induce leakage of vascular fluid, containing serum proteins with antibacterial activity, and influx of phagocytic cells into the affected area.

membranes consist of an outer epithelial layer and an underlying layer of connective tissue. Although many pathogens enter the body by binding to and penetrating mucous membranes, a number of nonspecific defense mechanisms tend to prevent this entry. For example, saliva, tears, and mucous secretions act to wash away potential invaders and also contain antibacterial or antiviral substances. The viscous fluid called mucus, which is secreted by epithelial cells of mucous membranes, entraps foreign microorganisms. In the lower respiratory tract, the mucous membrane is covered by cilia, hairlike protrusions of the epithelial-cell membranes. The synchronous movement of cilia propels mucus-entrapped microorganisms from these tracts. In addition, nonpatho-genic organisms tend to colonize the epithelial cells of mucosal surfaces. These normal flora generally outcompete pathogens for attachment sites on the epithelial cell surface and for necessary nutrients.

Some organisms have evolved ways of escaping these defense mechanisms and thus are able to invade the body through mucous membranes. For example, influenza virus (the agent that causes flu) has a surface molecule that enables it to attach firmly to cells in mucous membranes of the respiratory tract, preventing the virus from being swept out by the ciliated epithelial cells. Similarly, the organism that causes gonorrhea has surface projections that allow it to bind to epithelial cells in the mucous membrane of the urogenital tract. Adherence of bacteria to mucous membranes is due to interactions between hairlike protrusions on a bacterium, called fimbriae or pili, and certain glycoproteins or glycolipids that are expressed only by epithelial cells of the mucous membrane of particular tissues (Figure 1-2). For this reason, some

Epithelium Pili Surface

FIGURE 1-2

Electron micrograph of rod-shaped Escherichia coli bacteria adhering to surface of epithelial cells of the urinary tract. [From N. Sharon and H. Lis, 1993, Sci. Am. 268(1):85; photograph courtesy of K. Fujita.]

FIGURE 1-2

Electron micrograph of rod-shaped Escherichia coli bacteria adhering to surface of epithelial cells of the urinary tract. [From N. Sharon and H. Lis, 1993, Sci. Am. 268(1):85; photograph courtesy of K. Fujita.]

tissues are susceptible to bacterial invasion, whereas others are not.

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  • Stephen Tanner
    Is skin a mucosal surface?
    7 years ago

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