Commensal Bacteria: An Emerging Player in Defense Against Respiratory Pathogens

Abstract

A diverse community of trillions of commensal bacteria inhabits mucosal and epidermal surfaces in humans and plays an important role in defense against pathogens, including respiratory pathogens. Commensal bacteria act on the host's immune system to induce protective responses that prevent colonization and invasion by pathogens. On the other hand, these bacteria can directly inhibit the growth of respiratory pathogens by producing antimicrobial products/signals and competing for nutrients and adhesion sites. Such mechanisms preserve the niche for commensal bacteria and support the host in containing respiratory infections. Herein, we discuss current evidence on the role of commensal bacteria in conferring protection against respiratory pathogens and the underlying mechanisms by which these bacteria do so. A deeper knowledge of how commensal bacteria interact with the host and pathogens might provide new insights that are poised to aid in the development of vaccines and therapeutics that target infectious diseases.

Keywords: commensal; host; lungs; pathogen; vaccine.

Figure 1

Commensal bacteria mediated innate immunity to respiratory pathogens. Commensal bacteria stimulate various innate immune cells, particularly alveolar macrophages (Mϕ), mucosa-associated invariant T (MAIT) cells, group 3 innate lymphoid cells (ILC3), and natural killer (NK) cells, to induce early protection. These bacteria promote pathogen killing via granulocyte–macrophage colony-stimulating factor (GM-CSF), which stimulates pathogen killing and clearance by alveolar macrophages (Mϕ) through phagocytosis, reduced reactive oxygen species (RO), and extracellular signal regulated kinase (ERK) signaling. Intrapulmonary GM-CSF production in response to infection is regulated by the microbiota via interleukin-17A (IL-17A). Pattern recognition receptor (PRR) expressed by Mϕ recognizes PRR ligands, such as nod-like receptor ligands (NOD RL), leading to the activation of Mϕ. NK and MAIT cells when activated by commensal bacteria produce large quantities of IL-17A, whereas ILC3 cells secrete IL-22, aiding in inhibition/killing of various respiratory pathogens.