Possible modulating functions of probiotic Lactiplantibacillus plantarum in particulate matter-associated pulmonary inflammation

Abstract

Pulmonary disease represents a substantial global health burden. Increased air pollution, especially fine particulate matter (PM_2.5) is the most concerned proportion of air pollutants to respiratory health. PM_2.5 may carry or combine with other toxic allergens and heavy metals, resulting in serious respiratory allergies and anaphylactic reactions in the host. Available treatment options such as antihistamines, steroids, and avoiding allergens/dust/pollutants could be limited due to certain side effects and immense exposure to air pollutants, especially in most polluted countries. In this mini-review, we summarized how PM_2.5 triggers respiratory hyperresponsiveness and inflammation, and the probiotic Lactiplantibacillus plantarum supplementation could minimize the risk of the same. L. plantarum may confer beneficial effects in PM_2.5-associated pulmonary inflammation due to significant antioxidant potential. We discussed L. plantarum's effect on PM_2.5-induced reactive oxygen species (ROS), inflammatory cytokines, lipid peroxidation, and DNA damage. Available preclinical evidence shows L. plantarum induces gut-lung axis, SCFA, GABA, and other neurotransmitter signaling via gut microbiota modulation. SCFA signals are important in maintaining lung homeostasis and regulating intracellular defense mechanisms in alveolar cells. However, significant research is needed in this direction to contemplate L. plantarum's therapeutic potential in pulmonary allergies.

Keywords: Nrf2 activation; PM2.5-associated allergies; alveolar cell protection; anti-inflammatory cytokines; gut microbiota dysbiosis; gut-lung axis; probiotics supplementation; pulmonary inflammation.

Figure 1

(A) PM_2.5 derived lung inflammation and disturbed Gut-lung Axis: Inhalation of particulate pollutants (A); Interaction and accumulation PM_2.5 with pulmonary epithelial cells (B); PM_2.5 may contain a variety of pollutants such as heavy metals which absorb in alveolar cells (B1); accumulated pollutant trigger TLR associated inflammation, induced by excess production of ROS, change in mRNA expression and inflammatory cytokines, which facilitate WBCs and IgE recruitment (B2); excess recruitment of immune cells and histamine cause localized inflammation (B3); PM_2.5 can translocate to other organs via pulmonary vein (B4); translocated PM_2.5 may cause inflammation or damage to other organs (C) and altered gut microbiota composition, and disturbed Gut-lung and gut-organ specific (D). (B) Chemokines Response: PM_2.5 and Polycyclic aromatic hydrocarbons (PAHs) triggered IL-8 and neutrophil deposition into lungs cells.

Figure 2

Air pollutant -associated asthma and allergic rhinitis exacerbation (A). Comparative depiction of PM_2.5 associated pulmonary inflammation and probiotics role: PM_2.5 ligands bind with TLR and provoke ROS overproduction and alteration in mRNA expression which produces inflammatory cytokines (1); while probiotic supplementation induces the PM_2.5 ligands and reduces the production of ROS, induce gut-lung axis induces intracellular defense system and activate Nrf2 which regulates mRNA expression and produces anti-inflammatory cytokines (2) (B). Outcomes from recent clinical trials showed a probiotic positive effect on pulmonary function in asthmatic patients (C).