Contribution of Streptococcus pseudopneumoniae and Streptococcus salivarius to vocal fold mucosal integrity and function

Dis Model Mech. 2024 Jul 1;17(7):dmm050670. doi: 10.1242/dmm.050670. Epub 2024 Jul 16.

Abstract

Structural changes to the vocal fold (VF) epithelium, namely, loosened intercellular junctions, have been reported in VF benign lesions. The potential mechanisms responsible for the disruption of cell junctions do not address the contribution of resident microbial communities to this pathological phenomenon. In this study, we focused on determining the relationship between Streptococcus pseudopneumoniae (SP), a dominant bacterial species associated with benign lesions, and Streptococcus salivarius (SS), a commensal bacterium, with human VF epithelial cells in our three-dimensional model of the human VF mucosa. This experimental system enabled direct deposition of bacteria onto constructs at the air/liquid interface, allowing for the assessment of bacterium-host interactions at the cellular, molecular and ultrastructural levels. Our findings demonstrate that SP disrupts VF epithelial integrity and initiates inflammation via the exported products HtrA1 and pneumolysin. In contrast, SS attaches to the VF epithelium, reduces inflammation and induces Mmp2-mediated apical desquamation of infected cells to mitigate the impact of pathogens. In conclusion, this study highlights the complexity of microbial involvement in VF pathology and potential VF mucosal restoration in the presence of laryngeal commensals.

Keywords: Commensals; Epithelial integrity; Pathogenic bacteria; Remodeling; Vocal fold mucosa.

MeSH terms

  • Epithelial Cells / microbiology
  • Epithelial Cells / pathology
  • Humans
  • Inflammation / microbiology
  • Inflammation / pathology
  • Mucous Membrane / microbiology
  • Mucous Membrane / pathology
  • Streptococcus pneumoniae / physiology
  • Streptococcus salivarius* / physiology
  • Vocal Cords* / microbiology
  • Vocal Cords* / pathology