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

Front Cell Infect Microbiol. 2024 Jan 9:13:1290914. doi: 10.3389/fcimb.2023.1290914. eCollection 2023.

Abstract

Pulmonary disease represents a substantial global health burden. Increased air pollution, especially fine particulate matter (PM2.5) is the most concerned proportion of air pollutants to respiratory health. PM2.5 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 PM2.5 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 PM2.5-associated pulmonary inflammation due to significant antioxidant potential. We discussed L. plantarum's effect on PM2.5-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.

Publication types

  • Review
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Air Pollutants*
  • Anaphylaxis*
  • Humans
  • Inflammation
  • Particulate Matter
  • Pneumonia*

Substances

  • Particulate Matter
  • Air Pollutants

Grants and funding

The author(s) declare financial support was received for the research, authorship, and/or publication of this article. The current work was assisted financially to the Dean of Science and research at King Khalid University via the Group Project under grant number RGP. 1/137/44.