Lactobacillus casei modulates the inflammation-coagulation interaction in a pneumococcal pneumonia experimental model

Area of Science:

• Microbiology
• Immunology
• Hematology

Background:

• Previous studies demonstrated Lactobacillus casei CRL 431 enhances resistance to pneumococcal infection in mice.
• Streptococcus pneumoniae infection triggers significant inflammatory and coagulation responses.

Purpose of the Study:

• To investigate the impact of Lactobacillus casei CRL 431 (L. casei) on coagulation and fibrinolysis during Streptococcus pneumoniae infection.
• To evaluate the modulation of inflammatory cytokines and their role in the protective effects of L. casei.

Main Methods:

• Oral administration of L. casei to a mouse model of Streptococcus pneumoniae infection.
• Assessment of coagulation parameters (PT, APTT, TATc, factors), fibrinolytic activity (PAI-1), and cytokine levels (TNF-α, IL-1β, IL-6, IL-4, IL-10) in plasma and bronchoalveolar lavage (BAL).

Main Results:

• Infection activated coagulation, leading to fibrin deposition in lungs, increased thrombin-antithrombin complex (TATc), and altered coagulation factor levels.
• Reduced fibrinolytic activity was observed, with increased plasminogen activation inhibitor-1 (PAI-1).
• L. casei treatment improved lung tissue integrity, reduced fibrin deposition, normalized coagulation tests, decreased PAI-1 levels, and increased anti-inflammatory cytokines IL-4 and IL-10.

Conclusions:

• L. casei effectively regulates coagulation and fibrinolysis during pneumococcal infection, mitigating lung fibrin deposition.
• The protective effects of L. casei are associated with the induction of IL-4 and IL-10, which may counterbalance pro-inflammatory and pro-coagulant responses.