The primary role of the immune system is to prevent or restrict infections caused by pathogenic microorganisms such as bacteria, viruses, parasites, and fungi. The identification of microorganisms and foreign substances is the first occurrence in a host’s immune response. The body’s defense mechanisms are classified as (a) innate (natural) immunity and (b) acquired (adaptive) immunity.
Innate immunity is the resistance that a person is born with. Individual immunity, racial immunity, and species immunity are three types of innate immunity.
Individual immunity refers to resistance to infection that differs among individuals of the same race and species and is genetically determined. For example, if one homozygous twin develops tuberculosis, the other twin is more likely to develop tuberculosis as well. However, in heterozygous twins, the other twin has a very low chance of contracting tuberculosis.
Racial immunity: A difference in susceptibility or resistance to infection among different races within the same species is referred to as racial immunity. For example, races with sickle cell anemia, which is common along the Mediterranean coast, are resistant to malaria parasite Plasmodium falciparum infection. This is due to an erythrocyte genetic abnormality that results in sickle-shaped erythrocytes that resist parasitization by P. falciparum. Individuals with an inherited deficiency of glucose6-phosphatase dehydrogenase are therefore less prone to P. falciparum infection.
Species immunity: Species immunity refers to the absolute or relative resistance to a pathogen shown by all members of a specific species. Chickens, for example, are immune to Bacillus anthracis, while rats are resistant to Corynebacterium diphtheriae and humans are susceptible to these bacteria. The exact cause of this form of immunity is unknown.
Factors influencing innate immunity
Factors that could have an effect on the host’s innate immunity include the host’s age and nutritional status
Extremes of age make a person highly susceptible to various infections. This is clarified in part by a young child’s immature immune system and waning immunity in older people. The placental barrier normally protects the fetus-in-utero from maternal infections. Human immunodeficiency virus (HIV), rubella virus, cytomegalovirus, and Toxoplasma gondii, on the other hand, cross the placental barrier and cause congenital infections.
Very old people are more likely than young people to suffer more from a disease (e.g., pneumonia) and have a higher mortality rate. Measles, mumps, poliomyelitis, and chicken pox are a few diseases that cause more serious clinical illness in adults than in infants. This may be attributed to an adult’s more aggressive immune response, which causes more tissue damage.
The host’s nutritional status is critical in innate immunity. Malnutrition reduces both humoral and cell-mediated immunity. Here are some examples:
- In protein–calorie malnutrition, neutrophil activity is reduced, interferon response is reduced, and C3 and factor B of the complement are reduced.
- A lack of vitamins A, C, and folic acid makes a person highly susceptible to infection by a variety of microbial pathogens.
People who suffer from such hormonal disorders are more vulnerable to infection. Individuals with diabetes, hypothyroidism, and adrenal dysfunction, for example, are particularly vulnerable to staphylococcal infection, streptococcal infection, candidiasis, aspergillosis, zygomycosis, and a variety of other microbial infections. Similarly, due to a higher level of steroid during pregnancy, pregnant women are more vulnerable to certain infections.
Mechanisms of innate immunity
The host’s innate immunity serves two essential functions: it destroys invading microbes and stimulates acquired (adaptive) immune processes. In contrast to adaptive immunity, innate immunity has no memory and does not recover after re-exposure to the same microorganism. Innate immunity relies on four types of protective barriers: (a) anatomic barriers, (b) physiologic barriers, (c) phagocytosis, and (d) inflammatory responses.
Skin and mucous membranes are examples of anatomic barriers. They are the most crucial elements of innate immunity. They serve as mechanical barriers, preventing microorganisms from entering the body. The intact skin prevents microorganisms from entering. Breaks in the skin, such as those caused by cuts, wounds, or abrasion, may lead to infection. Insect bites that include pathogenic species (e.g., mosquitoes, mites, ticks, fleas, and sandflies) introduce the pathogens into the body and spread the infection. Skin produces sebum, which inhibits the growth of many microorganisms. The sebum is composed of lactic acid and fatty acids that keep the skin’s pH between 3 and 5, which prevents the growth of most microorganisms.
Mucous membranes cover a considerable portion of the human host’s gastrointestinal, respiratory, genitourinary, and other tracts. A variety of nonspecific defense mechanisms work to prevent microorganisms from entering the body via the mucous membrane.
- Saliva, tears, and mucous secretions wash away possible invading microorganisms, preventing them from attaching to the site of infection. These secretions also contain antibacterial or antiviral agents that destroy the pathogens.
- Mucus is a viscous fluid secreted by mucous membrane epithelial cells that entraps invading microorganisms.
- Cilia, the hair-like protrusions of epithelial cell membranes, shield the mucous membrane in the lower respiratory tract. The synchronous movement of cilia propels microorganisms caught in mucus from these tracts.
- Furthermore, nonpathogenic species have a tendency to colonize the epithelial cells of mucosal surfaces. In general, these natural flora compete with pathogens for attachment sites on the epithelial cell surface as well as nutrients.
The following are examples of physiologic barriers that lead to innate immunity:
- Since very few ingested microorganisms can withstand the low pH of stomach contents, gastric acidity is an intrinsic physiologic barrier to infection.
- Some of the soluble mediators of innate immunity are lysozyme, interferon, and complement. Because of its action on the bacterial cell wall, lysozyme has an antibacterial impact. Interferons are secreted by cells in reaction to virally infected cells’ products. These substances have a wide antiviral effect by inhibiting viral structural protein synthesis. Complement is a class of serum-soluble substances that, when activated, cause cell membrane damage.
- Certain types of molecules are only present in bacteria and are never found in multicellular species. The host’s ability to identify and resist invaders exhibiting such molecules is a key feature of innate immunity.
Another essential innate immunity defense mechanism is phagocytosis. Phagocytosis is the mechanism by which some specialized cells, such as blood monocytes, neutrophils, and tissue macrophages, consume extracellular particulate content. It is a form of endocytosis in which phagocytic cells consume invading microorganisms from the environment. During this phase, the cell’s plasma membrane extends around the particulate material, which may include whole pathogenic microorganisms, to form large vesicles known as phagosomes.
Tissue damage caused by a wound or an invading pathogenic microorganism triggers a complex chain of events known as the inflammatory responses. The end result of inflammation may be the activation of a particular immune response to the invasion or the clearance of the invader by innate immune system components. Rubor (redness), calor (temperature rise), dolor (pain), and tumor are the four cardinal features of inflammatory responses (swelling).
Mediators of inflammatory reactions
Inflammatory reactions are mediated by histamine, kinins, acutephase proteins, and defensin.
It is a chemical substance that is formed by various cells in response to tissue damage. It is a primary mediator of the inflammatory response. It binds to receptors on capillaries and venules nearby, causing vasodilation and increased permeability.
These are some of the other essential mediators of the inflammatory response. They are usually found in inactive form in blood plasma. Tissue damage stimulates these small peptides, resulting in vasodilation and increased capillary permeability. Bradykinin activates pain receptors in the skin as well. Since pain usually causes a person to protect the injured region, this effect most likely serves a protective function.
C-reactive proteins and mannose-binding proteins are examples of innate immunity proteins. As a nonspecific response to microorganisms and other types of tissue injury, these proteins are released at a higher concentration in plasma during the acute-phase reaction. They are produced in the liver in response to proinflammatory cytokines such as interleukin-1 (IL-1) and interleukin-6 (IL-6) and tissue necrosis factor (TNF) (TNF). They are known as proinflammatory cytokines since they boost inflammatory responses.
They are also another crucial component of innate immunity. They are cationic peptides that cause pores in the bacteria’s membrane and thus destroy them. These can be found mostly in the lower respiratory tract and the gastrointestinal tract. β-defensins are found in the respiratory tract, while β-defensins are found in the gastrointestinal tract. Antiviral activity is also shown by β-defensins. They bind to the CXCR4 receptors and prevent the HIV virus from entering the cell. It is unknown how these defensins distinguish microbes from other cells.