Despite formidable immune and mechanical defense systems, the human body harbors an extensive, well-adapted population of microorganisms on the skin and in the gastrointestinal, vaginal, and upper respiratory tracts. The organisms maintain their foothold on these epithelial surfaces chiefly by adherence, and they indirectly benefit the host by excluding pathogenic bacterial colonization and by priming the immune system. If anti-microbial agents alter this host–microbe interplay by eliminating the normal flora, the host’s susceptibility to normally excluded pathogenic microorganisms is increased. When the mechanical defenses of the epithelial layers are breached and normally sterile areas are exposed, or if a critical component of the immune system that usually prevents microbial invasion fails, severe infections can result from the normal microbial flora.
The components of the immune system of multicellular organisms are sorted into 2 categories. The first, innate immunity, is present in nearly all multicellular organisms and includes humoral and cellular immune receptors that have broad specificity. The innate immune response is usually immediate; there is no immune memory of prior exposure.
The second category, adaptive immunity, is found only in vertebrates and does involve immune memory of prior exposure. Pathogens are recognized by many randomly generated B-lymphocyte and T-lymphocyte receptors, each of which has a very narrow specificity, that can recognize a particular antigen (epitope). Adaptive immune response is initially slower (days), because the clones of responding immune cells take time to proliferate. After the first encounter, the adaptive immune response is faster and stronger, because of immunologic memory.
However, even when both the mechanical and immune defense systems are intact, pathogenic microbes can cause infections by means of specific virulent characteristics that allow the microbes to invade and multiply. These virulent traits vary among different species and include attachment, polysaccharide encapsulation, blocking of lysosomal fusion, antigenic surface variation, immunoglobulin A protease, endotoxins, exotoxins, and biofilm formation.
The immune system, which makes possible the host’s adaptive response to colonization and infection, is classically divided into the humoral and cellular immune systems. The humoral immune system, composed of cells derived from the B lymphocytes, is responsible for antibody-mediated opsonization, complement-mediated bacterial killing, antitoxin, and mediation of intracellular infections. The cellular immune system, determined by the T lymphocytes, is responsible for interaction with and stimulation of the humoral immune system, direct cytotoxicity, release of chemical messengers, and control of chronic infections. The successful interplay between the humoral and cellular immune systems mitigates and usually eradicates infections, allowing for repair and healing. Also see BCSC Section 9, Uveitis and Ocular Inflammation.
Excerpted from BCSC 2020-2021 series: Section 1 - Update on General Medicine. For more information and to purchase the entire series, please visit https://www.aao.org/bcsc.