The Immune System

Immune System Lines of Defense

Ready to read some more technical but simply fascinating information? Sure you are!

Our Immune System army has 3 Lines of Defense:

  1. Physical and Chemical barriers (innate immunity) such as the skin and mucous membranes
  2. Non-specific Resistance (innate immunity) such as phagocytosis and inflammation
  3. Specific defense mechanisms (acquired immunity) that provide protection by stimulating unique antibodies following exposure to specific substances.[1]

Let’s review each of these.

First Line of Defense: Physical and Chemical Barriers

Skin

The epidermis is our very first line of protection.[2] Periodic shedding of the dead cells in the epidermis is a way to remove toxins and microbes. When we exert energy during physical exercise and we perspire, we then flush dead skin and microbes from the surface of our skin.  The use of saunas or hot baths to “flush out toxins” via sweating is an age-old practice.

Our skin actually has its own community of microbes called the skin normal flora. There are literally trillions of bugs (bacteria and fungi) that live on our skin. Itchy yet? 😉 The skin microbiome varies depending on the location, the amount of light and whether the area is moist, dry, hairy, or oily. It also differs with age, gender, place of residence (even differentiating between urban and rural habitation), and cohabitation with other humans or animals.[3] The skin is naturally acidic which can deter hostile microbes. Obviously when we get a cut on our skin, the barrier is damaged, allowing pathogens to enter the body and travel via blood and lymph. This also brings up a poignant point on overuse of anti-bacterial soaps, wipes and hand sanitizers that kill our normal flora, leaving us more susceptible to pathogens.[4]

Did You Know?

We all know handwashing with soap is superior to any other method of cleaning our hands to ward off pathogens. Do you ever think about the type of soap you’re using? Do you reach for products that are labeled “antibacterial”, thinking it will be better to rid yourself of germs? Did you know that in 2014, the FDA in the United States declared that manufacturers had to prove that antibacterial soap was both safe and more effective than simply washing with conventional soap and water in order to sell it, due to health concerns? Canada appears to have had taken a more conservative approach, and puts the onus on the consumer. Canadians are advised to practice “reading labels to avoid buying products with triclosan” and to use soap and water, as “in most cases, antibacterial or antimicrobial soap is not necessary for safe, effective hand hygiene”.[5]

The chemical triclosan is the most common active ingredient used as an antibacterial, and is found not only in soap, but wipes, hand gels, cutting boards, mattress pads, toothpaste, mouthwash, makeup, deodorants and many more household items. However, it appears triclosan is not as benign or beneficial as one might think.

We’ve all heard of antibiotic resistance, which is where strains of bacteria have mutated to resist some types of antibiotics. Several studies have indicated that triclosan may be helping fuel that resistance.[6]

Other research has found that antibacterial soaps could act as endocrine disruptors, specifically with the thyroid hormone, potentially impacting puberty, obesity, cancer and infertility.[7]

Scientists have also hypothesized that children may be more susceptible to allergies due to reduced exposure to bacteria, which is a necessary part of childhood for proper immune system development and functioning.[8]

Evidence is mounting that triclosan persists after treatment at sewage plants and has been detected in bodies of water.[9] It has been shown to disrupt algae’s photosynthesis, and concerning blood levels have been observed in bottlenose dolphins off the coast of Florida, indicating it moves up the food chain.[10] Alarmingly, a survey done by CDC scientists in 2004 detected triclosan in the urine of 75% of the 2517 people who were tested.[11]

So next time you’re buying something that is labeled “anti-bacterial”, perhaps ponder that choice.

 

Mucous Membranes

While just the thought of the word mucus makes some people gag, our mucosal immunity is an imperative part of our first line of defense.

Mucosal surfaces such as the linings of the respiratory, digestive, reproductive, or urinary tracts produce mucus that trap pathogens and debris, allowing them to be expelled from our system without an opportunity to penetrate deeper. Fine hairs in our nostrils filters the air we breathe, as it contains microbes, dust, and pollutants. Sneezing is a protective measure to expel foreign invaders. Cilia (tiny hair-like organelles) lines the upper respiratory tract to trap and propel debris that we may inhale by causing us to cough.

Ever cut your finger and you immediately put it in your mouth to suck it? Licking a wound is an automatic response -especially in animals – but does it actually help our injuries to heal faster?  Our saliva not only contains mucus, but also many compounds that are antibacterial as well as white blood cells.[12]. The mucus helps to trap bacteria.[13]  Let’s be clear, though – our mouth contains a plethora of bacteria, and while they may be harmless while in our mouth, they can cause infection to a wound through our saliva. So really, licking a wound shouldn’t be your go-to 😉

Finally, urine flushes microbes out of the urethra, and gastric juice in the stomach destroys pathogens due to its highly acidic pH of approximately 2-3.[14] In fact, there is much research regarding gastric hypochlorhydria (low stomach acid) and the increased prevalence of gastrointestinal infections and diseases. More on this in the Nutrition section.

Second Line of Defense: Non-Specific Resistance

The second line of defense includes the non-specific processes of inflammation and phagocytosis.

Inflammation is the body’s non-specific response to tissue injury or invasion by a pathogen, resulting in inflammations’ primary signs of redness, swelling, warmth, pain, and loss of function.[15] Inflammation occurs due to damaged cells releasing  chemicals which makes blood vessels dilate (vasodilation) to bring more blood and white blood cells to the area. The chemical mediators in the inflammatory response include numerous chemicals including histamine, cytokines (interleukins and lymphokines), prostaglandins and leukotrienes.[16]  Each of these have major actions that are necessary to understand especially when the immune system overreacts or is “hyperactive”. More on that later.

The capillaries also become increasingly permeable or “leaky” to allow plasma proteins to move into the space, diluting toxic materials at the site. Increased blood flow causes the area to become reddened and swollen due to the increased blood and fluid in the tissues. The area will also become warm to touch due to this extra blood, and painful due to the swelling.

Inflammation, having attracted white blood cells to the area, leads us to the next process, phagocytosis.

Phagocytosis is the process by which some phagocytic cells (primarily macrophages and neutrophils) engulf, ingest and destroy all microbes such as bacteria, cellular debris or foreign matter that pass into body tissues.[17] This ultimately results in prevention of more tissue damage, and healing of the tissue.[18] Macrophages also make protein markers that will assist with T-cell activation, a type of specific resistance.[19]

Third Line of Defense: The Specific Adaptive Immune System

Our adaptive immune system produces antibodies that will kill specific antigens. Antigens are foreign substances that are marked by the cells of the immune system, resulting in an immune response.[20] Antigens don’t have to be just pathogens such as bacteria and viruses, they can also be pollen, foods, drugs and even tissues that the immune system recognizes as a foreign invader or not part of the body.[21] Our body produces antibodies to fight the antigens and tries to eradicate them. This is where our specific leukocytes, namely our B-cells and T-cells, come in.

Cell-mediated immunity is called as such because T-cells become activated and respond to the presence of specific antigens.[22] Cell-mediated immunity is very effective against pathogenic microbes such as fungi, bacteria and viruses, certain types of cancer cells and foreign tissue transplants.[23]

There are 4 major types of T-cells:[24]

  1. Cytotoxic (killer) T-cells eliminate microbes directly or via chemicals.
  2. Memory T-cells fight pathogens that they recognize from previous exposures.
  3. Suppressor T-cells help to slow down all of the destruction the other T-cells are engaged in to prevent harm to normal cells.
  4. Helper T-cells secrete a substance called interleukin 2 that helps increase production of cytotoxic T-cells and B-cells, so more antibodies can be produced. This is called Antibody-mediated Immunity.[25]

B-cells (B lymphocytes) produce antibodies (also called Immunoglobulins or Ig’s) that bind to antigens and neutralize them.[26] The body contains millions of different B-cells that can react to one specific antigen.[27] Memory B-cells remember specific antigens from the past. Having too few immunoglobulins could suggest a bigger chance of getting infections as discussed in the Immune System Deficiencies chapter. Having too many could involve allergies or an overactive immune system, which is reviewed in the Immune System in Overdrive chapter.

There are 5 classes of antibodies:[28]

  1. IgG is the antibody that protects us against infection by “remembering” which antigens we’ve encountered before.[29]
  2. IgM is one of the first antibodies to sound the alarm, so it’s important in the beginning of a potential infection.[30] IgM can also appear when someone is re-exposed to a disease.
  3. IgA is generally found in mucosal areas, such as the intestine, mouth, vagina, saliva, tears, and breast milk.[31] IgA is a , first line of defense against pathogens because it can survive in tough environments such as the GI and respiratory tracts, tackling pathogens, toxins and food antigens.[32] A fecal Secretory IgA (SIgA) test can determine how strong or thin your gut-lining is, which will give an indication of an individual’s capability to win against infections, allergies and food reactions.[33] Decreased levels are most often found in individuals with low immunity, food allergies, bacterial overgrowth of the small intestine (SIBO), chronic candida, celiac disease, and inflammatory bowel diseases such as Crohn’s and ulcerative colitis.[34]
  4. IgE is responsible for the allergic response by starting a histamine response. It is mostly found in the lungs, skin, and mucous membranes, which is indicative of allergic responses such as difficulty breathing, itchiness, hives and swelling of mucous membranes.[35]
  5. IgD is the least understood antibody, but has been found to be important in the early stages of the immune response by sending signals to cells to activate.[36]

Immune system disorders occur when the immune system is either underactive or overactive. The overactive immune system may start attacking harmless substances we might come into contact with. An underactive immune system means the immune system is too weak to fight pathogens, making us susceptible to disease.

You’ve made it this far! Read on to review each of these issues.

  1. Government of Canada. (2019). Triclosan Fact Sheet. Retrieved from: https://www.canada.ca/en/health-canada/services/chemicals-product-safety/triclosan.html ↵
  2. Yazdankhah, S. P., Scheie, A. A., Høiby, E. A., Lunestad, B. T., Heir, E., Fotland, T. Ø., Naterstad, K., & Kruse, H. (2006). Triclosan and antimicrobial resistance in bacteria: an overview. Microbial drug resistance (Larchmont, N.Y.), 12(2), 83–90. https://doi.org/10.1089/mdr.2006.12.83 ↵
  3. Veldhoen, N., Skirrow, R., Osachoff, H., Wigmore, H., Clapson, D., Gunderson, M., Van Aggelen, G., & Helbing, C.(2006). The bactericidal agent triclosan modulates thyroid hormone-associated gene expression and disrupts postembryonic anuran development. (2006). Aquatic Toxicology. 80 (3) 217-227. Retrieved from: https://www.sciencedirect.com/science/article/pii/S0166445X06003407 ↵
  4. Clayton, E. M., Todd, M., Dowd, J. B., & Aiello, A. E. (2011). The impact of bisphenol A and triclosan on immune parameters in the U.S. population, NHANES 2003-2006. Environmental health perspectives, 119(3), 390–396. Retrieved from: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3060004/ ↵
  5. Government of Canada. (2019). Triclosan Fact Sheet. Retrieved from: https://www.canada.ca/en/health-canada/services/chemicals-product-safety/triclosan.html ↵
  6. Yazdankhah, S. P., Scheie, A. A., Høiby, E. A., Lunestad, B. T., Heir, E., Fotland, T. Ø., Naterstad, K., & Kruse, H. (2006). Triclosan and antimicrobial resistance in bacteria: an overview. Microbial drug resistance (Larchmont, N.Y.), 12(2), 83–90. https://doi.org/10.1089/mdr.2006.12.83 ↵
  7. Veldhoen, N., Skirrow, R., Osachoff, H., Wigmore, H., Clapson, D., Gunderson, M., Van Aggelen, G., & Helbing, C.(2006). The bactericidal agent triclosan modulates thyroid hormone-associated gene expression and disrupts postembryonic anuran development. (2006). Aquatic Toxicology. 80 (3) 217-227. Retrieved from: https://www.sciencedirect.com/science/article/pii/S0166445X06003407 ↵
  8. Clayton, E. M., Todd, M., Dowd, J. B., & Aiello, A. E. (2011). The impact of bisphenol A and triclosan on immune parameters in the U.S. population, NHANES 2003-2006. Environmental health perspectives, 119(3), 390–396. Retrieved from: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3060004/ ↵
  9. Sprague, L. & Battaglin, W. (2004). Wastewater chemicals in Colorado's streams and groundwater. USGS Fact Sheet 2004. Retrieved from: https://pubs.usgs.gov/fs/2004/3127/ ↵
  10. Fair, P. A., Lee, H. B., Adams, J., Darling, C., Pacepavicius, G., Alaee, M., Bossart, G. D., Henry, N., & Muir, D. (2009). Occurrence of triclosan in plasma of wild Atlantic bottlenose dolphins (Tursiops truncatus) and in their environment. Environmental pollution (Barking, Essex : 1987), 157(8-9), 2248–2254. Retrieved from: https://pubmed.ncbi.nlm.nih.gov/19410343/ ↵
  11. Centers for Disease Control and Prevention. (2017). Triclosan Factsheet. National Biomonitoring Program. Retrieved from: https://www.cdc.gov/biomonitoring/Triclosan_FactSheet.html  ↵
  12. Sprague, L. & Battaglin, W. (2004). Wastewater chemicals in Colorado's streams and groundwater. USGS Fact Sheet 2004. Retrieved from: https://pubs.usgs.gov/fs/2004/3127/ ↵
  13. Fair, P. A., Lee, H. B., Adams, J., Darling, C., Pacepavicius, G., Alaee, M., Bossart, G. D., Henry, N., & Muir, D. (2009). Occurrence of triclosan in plasma of wild Atlantic bottlenose dolphins (Tursiops truncatus) and in their environment. Environmental pollution (Barking, Essex : 1987), 157(8-9), 2248–2254. Retrieved from: https://pubmed.ncbi.nlm.nih.gov/19410343/ ↵
  14. Centers for Disease Control and Prevention. (2017). Triclosan Factsheet. National Biomonitoring Program. Retrieved from: https://www.cdc.gov/biomonitoring/Triclosan_FactSheet.html ↵
  15. Chen, L., Deng, H., Cui, H., Fang, J., Zuo, Z., Deng, J., Li, Y., Wang, X., & Zhao, L. (2017). Inflammatory responses and inflammation-associated diseases in organs. Oncotarget, 9(6), 7204–7218. Retrieved from: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5805548/ ↵
  16. Chen, L., Deng, H., Cui, H., Fang, J., Zuo, Z., Deng, J., Li, Y., Wang, X., & Zhao, L. (2017). Inflammatory responses and inflammation-associated diseases in organs. Oncotarget, 9(6), 7204–7218. Retrieved from: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5805548/ ↵
  17. Rosales, C., & Uribe-Querol, E. (2017). Phagocytosis: A Fundamental Process in Immunity. BioMed research international, 2017, 9042851. Retrieved from: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5485277/ ↵
  18. Abdulkhaleq, L. A., Assi, M. A., Abdullah, R., Zamri-Saad, M., Taufiq-Yap, Y. H., & Hezmee, M. (2018). The crucial roles of inflammatory mediators in inflammation: A review. Veterinary world, 11(5), 627–635. Retrieved from: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5993766/ ↵
  19. Rosales, C., & Uribe-Querol, E. (2017). Phagocytosis: A Fundamental Process in Immunity. BioMed research international, 2017, 9042851. Retrieved from: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5485277/ ↵
  20. Sela, M. (1998). Antigens. In Encylopedia of Immunology (2nd Edition). Science Direct. Retrieved from: https://www.sciencedirect.com/topics/medicine-and-dentistry/antigen ↵
  21. Sela, M. (1998). Antigens. In Encylopedia of Immunology (2nd Edition). Science Direct. Retrieved from: https://www.sciencedirect.com/topics/medicine-and-dentistry/antigen ↵
  22. Dornell, J. (2022). Humoral vs Cell-Mediated Immunity. Technology Networks. Immunology and Microbiology. Retrieved from: https://www.technologynetworks.com/immunology/articles/humoral-vs-cell-mediated-immunity-344829 ↵
  23. Dornell, J. (2022). Humoral vs Cell-Mediated Immunity. Technology Networks. Immunology and Microbiology. Retrieved from: https://www.technologynetworks.com/immunology/articles/humoral-vs-cell-mediated-immunity-344829 ↵
  24. Sauls, R.S., McCausland, C., Taylor, B.N. (2022). Histology, T-Cell Lymphocyte. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing. Retrieved from: https://www.ncbi.nlm.nih.gov/books/NBK535433/ ↵
  25. Luckheeram, R. V., Zhou, R., Verma, A. D., & Xia, B. (2012). CD4⁺T cells: differentiation and functions. Clinical & developmental immunology, 2012, 925135. Retrieved from: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3312336/ ↵
  26. Alberts, B., Johnson, A., Lewis, J., et al. (2002). Molecular Biology of the Cell. 4th edition. New York: Garland Science. B Cells and Antibodies. Available from: https://www.ncbi.nlm.nih.gov/books/NBK26884/ ↵
  27. Mallick, I. (2022). B-Cells in Your Immune System. Very Well Health. Retrieved from: https://www.verywellhealth.com/b-cells-2252132 ↵
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  29. Vidarsson, G., Dekkers, G., Rispens, T. (2015). IgG subclasses and allotypes: from structure to effector functions. Frontiers Immunol. 5: 520. Retrieved from: https://www.frontiersin.org/articles/10.3389/fimmu.2014.00520/full ↵
  30. Heyman, B., & Shulman, M.J. (2016). Structure, function, and production of immunoglobulin M (IgM). Encyclopedia Immunobiol. 1-14. Retrieved from: https://www.sciencedirect.com/science/article/pii/B9780123742797050013?via=ihub ↵
  31. Bakema, J. E., & van Egmond, M. (2011). Immunoglobulin A: A next generation of therapeutic antibodies?. mAbs, 3(4), 352–361. Retrieved from: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3218532/ ↵
  32. Thomas, H. (2018). Unlocking the secrets of IgA. Nat Rev Gastroenterol Hepatol 15, 389. Retrieved from: https://www.nature.com/articles/s41575-018-0036-3 ↵
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  35. Schroeder HW, Cavacini L. (2010). Structure and function of immunoglobulins. J Allergy Clin Immunol. 2010;125(2 Suppl 2):S41-52. Retrieved from: https://www.jacionline.org/article/S0091-6749(09)01465-1/fulltext ↵
  36. Schroeder HW, Cavacini L. (2010). Structure and function of immunoglobulins. J Allergy Clin Immunol. 2010;125(2 Suppl 2):S41-52. Retrieved from: https://www.jacionline.org/article/S0091-6749(09)01465-1/fulltext ↵
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