6.7, 6.11 - Barriers and non-specific defences

Routes into the body

The route by which a pathogen arrives determines which protective surfaces it encounters first.

Transmission is movement of an infectious agent between sources and hosts. Its entry route is where it gains access to the new host. For example, a contaminated hand can transmit a pathogen to the mouth; the entry route is then through the digestive tract. A pathogen must reach a suitable site and overcome defences to establish an infection. Exposure alone does not prove infection.

Some pathogens can also pass from mother to baby across the placenta or during birth. This is another route; it does not mean every pathogen can cross the placenta. Different pathogens have different suitable entry routes: HIV does not spread by ordinary inhalation, and intact skin is an effective barrier to many agents that could cause infection if introduced through a puncture.

The respiratory and digestive tracts have surfaces connected to the outside through body openings. Pathogens in a gut lumen have not automatically crossed its epithelium into body tissues. This distinction explains why protection is needed at both the surface and within tissues.

Skin and stomach acid as barriers

A barrier reduces the chance that a pathogen reaches a site where it can survive and multiply.

The outer epidermis of the skin contains closely packed cells, with a tough outer layer of dead, keratinised cells. This continuous physical barrier is difficult for many pathogens to cross. Surface cells are shed, removing attached microorganisms. A cut disrupts continuity and gives pathogens access to underlying living tissue. Clotting and scab formation help seal that breach while the tissue repairs; a scab does not sterilise the wound.

Skin also provides chemical protection. Sweat and sebum contribute to conditions that inhibit the growth of some microorganisms. The skin's resident flora adds biological protection, which we consider next. These mechanisms work together: a physical barrier need not kill an organism to stop it entering.

Hydrochloric acid secreted into the stomach creates a strongly acidic environment. Low pH disrupts the function of many microbial proteins and enzymes, reducing survival of many swallowed pathogens before they reach the intestine. This is chemical protection, whereas the skin's continuous outer layer is physical protection. Acid does not kill every pathogen: some survive acid exposure or are protected by the material swallowed with them.

For example, if stomach contents become less acidic, one protective condition has weakened. It is reasonable to predict that more acid-sensitive pathogens could survive passage through the stomach. It is not reasonable to conclude that infection is certain, because other barriers and defences remain.

Protection by gut and skin flora

Many microorganisms normally live on skin and in the gut without causing disease at those sites.

Established gut flora and skin flora can protect against invading pathogens by competing for nutrients and attachment sites. A pathogen that cannot obtain enough resources or attach successfully is less likely to establish a population. Some resident microorganisms also produce substances that inhibit other microbes. Flora therefore form a living biological barrier alongside physical and chemical barriers.

This does not mean all resident microorganisms are always harmless. The effect depends on species, strain, site and host conditions. A normally tolerated skin microbe may cause infection if it enters deep tissue. Broad antimicrobial exposure can disturb resident communities as well as affect pathogens, so removing more microbes does not always improve protection.

Consider this original, simplified gut-community model. The surfaces, nutrients and introduced pathogen are otherwise the same; these are illustrative observations, not patient data.

Depletion is associated with more attachment than in the community-present condition. Restoration is associated with less attachment than in the depleted condition. Together these comparisons support a protective role for the resident community, consistent with competition. They do not identify which species or inhibitory molecule is responsible, and they do not show that attachment or infection is impossible when flora are present. Read a comparison and its evidence together, rather than turning “protective” into “complete immunity”.

Inflammation brings defences to infected tissue

If pathogens pass the surface barriers, local cells can initiate a rapid response in the affected tissue.

Innate, or non-specific, defences are ready to respond without previous exposure to that particular pathogen. Here “non-specific” means that they act against broad groups of invaders, rather than recognising one unique antigen through a selected B- or T-cell response. Innate cells still have receptors that recognise common microbial features or signs of tissue damage; they do not attack everything indiscriminately.

Damaged cells and activated tissue immune cells release signalling molecules. Mast cells, for example, release histamine. Other signals from immune cells help attract additional phagocytes. These coordinated events produce familiar changes:

1. Local arterioles dilate, increasing blood flow through the area. This contributes to redness and warmth.
2. Small blood vessels become more permeable, so fluid and plasma proteins pass into the tissue. The extra tissue fluid contributes to swelling; inflammatory mediators and pressure can contribute to pain.
3. Circulating phagocytes adhere to vessel walls and move between endothelial cells into the tissue. They follow chemical signals towards the affected site. This directed movement is chemotaxis.