Innate immunity in the context of COVID-19  

This post is an adapted excerpt from our recent paper published in Frontiers in Public Health. Download the full article freely here:  

Mammals have complex immune systems.  Survival depends on the ability to integrate and coordinate adaptive and innate responses to microbial threats.  Adaptive immune responses take days to weeks to produce antibodies to new bacteria and viruses.  In the mean time, the body has to fight off the infection.  Innate immunity is that first line of defense.  Also, it is the entire defense against a novel pathogen before the slower adaptive immune system has an opportunity to respond. This is the reality and challenge that we face in COVID-19.

Humans have multiple layers of innate protection.  Skin on the outside of the body and mucosal epithelial cells, like those found in the respiratory and digestve tracts, provide barrier protection.  Many cell types are sensitive to the presence of microbes, providing cellular surveillance and communications between cells found at mucosal surfaces with other parts of the immune system.  As part of this system of defense, virtually all metazoan animals, including humans, release antimicrobial peptides (AMPs) that both kill invading microbes and act as immune signaling mediators.  Most immune communications are complex but subtle. Under optimal conditions, regulators of immune responses maintain balanced responses, neither too strong nor too weak. An example of an immune system regulator is vitamin D.  Many people world wide are vitamin D deficient.  Without adequate vitamin D, the body’s immune system cannot maintain optimal balance to protect against microbes.

Because of innate immunity, most microbes are not dangerous to other life forms, including humans.  The antimicrobial peptides, AMPs that we mention above,  are key element in successfully maintaining boundaries between the mammalian host and the ever present microbial flora to which all life forms are exposed.   An example of antimicrobial innate protection is cathelicidin and a smaller fragment of it  known as LL37. LL37 is a broad-spectrum antibacterial and antiviral AMP best known for its role in protecting against the organism that causes tuberculosis. Interestingly, LL37 can also destroy envelope viruses, similar to the virus that causes COVID-19.

Our publication in Frontiers in Public Health tells more of the story.  We explain how Vitamin D regulates the production of LL37 and how carbon particles in air pollution can interfere.

This post is an adapted excerpt from our recent paper published in Frontiers in Public Health. Download the full article freely here: 

Citation: Crane-Godreau MA, Clem KJ, Payne P and Fiering S (2020) Vitamin D Deficiency and Air Pollution Exacerbate COVID-19 Through Suppression of Antiviral Peptide LL37. Front. Public Health 8:232. doi: 10.3389/fpubh.2020.00232

Keywords: COVID-19, Vitamin D deficiency, cathelicidin/LL37, air pollution, citrullination of peptide, carbon nanoparticles, African American, tobacco smoke