Lactobacilli inhibit Shigella dysenteriae 1 induced pro-inflammatory response and cytotoxicity in host cells via impediment of Shigella-host interactions.
OBJECTIVE
Shigella dysenteriae Type 1 dysentery is a major cause of morbidity and mortality in children from less developed and developing countries. The present study explores the hypothesis that lactobacilli protect the host cell during S. dysenteriae Type 1 infection and its mechanism of action.


METHODS
Caco-2 cells incubated for 1h with Lactobacillus rhamnosus or Lactobacillus acidophilus at the multiplicity of infection of 100, either alone or in combination followed by addition of Shigella at the same multiplicity of infection for 5h served as treatment groups. Cells incubated with Shigella without lactobacilli addition served as infected cells. At the end of experimental period, cells were processed suitably to enumerate adherent and internalized Shigella. Reverse transcription-polymerase chain reaction was performed to assess mRNA expression of interleukin-8 and tumour necrosis factor-alpha. Immunoblot for heat shock protein-70 and cytotoxicity assay were performed.


RESULTS
Pretreatment with the combination of lactobacilli significantly (p<0.05) prevented adherence and internalization of Shigella coupled with reduced expression of tumour necrosis factor-alpha and interleukin-8 in host cells.


CONCLUSIONS
L. rhamnosus and L. acidophilus, synergistically offered better protection during S. dysenteriae Type 1 infection by efficiently inhibiting adherence and internalization of Shigella coupled with inhibition of pro-inflammatory response.
Moorthy
G
G
Department of Biochemistry, University of Madras, Guindy Campus, Sardar Patel Road, Chennai 600 025, Tamil Nadu, India.
Murali
M R
MR
Niranjali Devaraj
S
S
D001422:Bacterial Adhesion; D018938:Caco-2 Cells; D018920:Coculture Techniques; D004405:Dysentery, Bacillary / Q000276:immunology / Q000382:microbiology*; D018840:HSP70 Heat-Shock Proteins / Q000378:metabolism; D054884:Host-Pathogen Interactions / Q000502:physiology*; D006801:Humans; D007113:Immunity, Innate; D016209:Interleukin-8 / Q000378:metabolism; D007779:Lactobacillus acidophilus / Q000502:physiology*; D052201:Lacticaseibacillus rhamnosus / Q000502:physiology*; D012762:Shigella dysenteriae / Q000276:immunology / Q000502:physiology*; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
C508606:CXCL8 protein, human; D018840:HSP70 Heat-Shock Proteins; D016209:Interleukin-8; D014409:Tumor Necrosis Factor-alpha