Lactobacillus pentosus strain b240 suppresses pneumonia induced by Streptococcus pneumoniae in mice

Lett Appl Microbiol. 2011 Jul;53(1):35-43. doi: 10.1111/j.1472-765X.2011.03079.x. Epub 2011 May 31.


Aims: Oral administration of probiotics has been known to improve inflammatory responses against infectious diseases. Here, we describe the inhibitory effect of oral intake of heat-killed Lactobacillus pentosus strain b240 (b240) on pneumococcal pneumonia in a murine experimental model.

Method and results: The mice treated with oral b240 for 21 days before Streptococcus pneumoniae infection exhibited prolonged survival time and less body weight loss, compared with saline-treated control mice. Mild pneumonia with significantly reduced secretion of inflammatory cytokines/chemokines according to related mitogen-activated protein kinase signalling molecules (phosphorylated c-Jun N-terminal kinase) was found in b240-treated mice, whereas severe pneumonia with hypercytokinemia was evident in control mice. Prominent reduction in the number of pneumococci and elevated expression of Toll-like receptor 2 and 4 in the lung tissues was concomitantly noted in b240-treated mice.

Conclusions: These findings indicate that b240 has inhibitory effects on pneumococcal pneumonia induced by Strep. pneumoniae infection and improves inflammatory tissue responses, resulting in reduced damages to the respiratory tissues.

Significance and impact of the study: These results demonstrate that oral administration of b240 might protect host animals from Strep. pneumoniae infection by augmentation of innate immune response.

MeSH terms

  • Animals
  • Cytokines / immunology
  • Cytokines / metabolism
  • Lactobacillus* / classification
  • Lung / immunology
  • Lung / microbiology
  • MAP Kinase Signaling System
  • Male
  • Mice
  • Mice, Inbred BALB C
  • Pneumonia, Pneumococcal / immunology*
  • Pneumonia, Pneumococcal / microbiology
  • Probiotics / administration & dosage*
  • Specific Pathogen-Free Organisms
  • Streptococcus pneumoniae*
  • Toll-Like Receptors / immunology


  • Cytokines
  • Toll-Like Receptors