American journal of reproductive immunology (New York, N.Y. : 1989) · 2009
Pregnancy does not deter the development of a potent maternal protective CD8+ T-cell acquired immune response against Listeria monocytogenes despite preferential placental colonization.
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Krishnan Lakshmi, Pejcic-Karapetrovic Branka, Gurnani Komal, Zafer Ahmed, Sad Subash
Аннотация
PROBLEM: Listeria monocytogenes (LM) preferentially colonizes the placenta and causes fetal loss and systemic disease during pregnancy. As systemic CD8+ T-cell memory is critical in controlling LM infection, we addressed the issue as to whether it is modulated during pregnancy.
METHOD OF STUDY: Pregnant mice were infected with LM and their immune response was quantified relative to the non-pregnant cohort using advanced immunological techniques.
RESULTS: Pregnant mice exhibited progressive and massive placental LM infection leading to fetal resorptions. In contrast, they harbored significantly lower bacteria in spleen and liver relative to non-pregnant controls, and rapidly cleared systemic infection. Both pregnant and non-pregnant mice exhibited similar activation of systemic innate immunity. Moreover, LM infection in pregnant and non-pregnant hosts evoked strong antigen-specific cytolytic CD8+ T cells that produced IFN-gamma. Consequently, LM infection initiated during pregnancy afforded long-term protective memory to secondary infection.
CONCLUSION: Maternal hosts generate a normal Listeria-specific adaptive immunity in particular CD8+ T-cell memory response suggesting that systemic listeriosis during pregnancy may be an immunopathology associated with placental infection.
METHOD OF STUDY: Pregnant mice were infected with LM and their immune response was quantified relative to the non-pregnant cohort using advanced immunological techniques.
RESULTS: Pregnant mice exhibited progressive and massive placental LM infection leading to fetal resorptions. In contrast, they harbored significantly lower bacteria in spleen and liver relative to non-pregnant controls, and rapidly cleared systemic infection. Both pregnant and non-pregnant mice exhibited similar activation of systemic innate immunity. Moreover, LM infection in pregnant and non-pregnant hosts evoked strong antigen-specific cytolytic CD8+ T cells that produced IFN-gamma. Consequently, LM infection initiated during pregnancy afforded long-term protective memory to secondary infection.
CONCLUSION: Maternal hosts generate a normal Listeria-specific adaptive immunity in particular CD8+ T-cell memory response suggesting that systemic listeriosis during pregnancy may be an immunopathology associated with placental infection.