Maternal Lactoferrin Reduces Vertically-Acquired Escherichia coli Infection in the Offspring without Modifying Innate Immune Response in a Mouse Model
Presenter Status
Medical Student
Abstract Type
Clinical Research
Primary Mentor or Principal Investigator
Susana Chavez-Bueno
Presentation Type
Poster
Start Date
19-5-2026 11:00 AM
End Date
19-5-2026 12:00 PM
Abstract Text
Background:
Escherichia coli is a leading pathogen in neonatal early-onset sepsis (EOS), a major cause of newborn mortality worldwide. Maternal administration of lactoferrin, an antimicrobial and immunomodulatory glycoprotein, may reduce EOS by protecting the offspring against vertical E. coli infection while modulating associated innate immune responses.
Objectives/Goal:
To determine if maternal vaginal administration of bovine lactoferrin (BLF) ameliorates invasive infection and modifies tissue CXCL2 production in the embryos of pregnant mice pretreated with BLF prior to vaginal E. coli inoculation.
Methods/Design:
Pregnant C57BL/6 mice received BLF (75 mg/mL) or placebo vaginally in a novel oil/aqueous bi-gel on embryonic days (E) days 16 and 17, followed by vaginal inoculation with 105 colony forming units (CFU) of the neonatal E. coli strain RS218 on E17.
Embryos were collected on E18, and liver–spleen tissue homogenates were plated to quantify E. coli CFU per 100 mg tissue. CXCL2 (human IL-8 homolog) concentrations in homogenates were measured by ELISA. Four independent experiments were done, including 35 embryos in the BLF group, and 31 in the placebo group.
Bacterial load was modeled as a function of treatment group and CXCL2 concentrations using a generalized linear mixed model (GLMM) with a negative binomial distribution to address overdispersion and include random mouse effects. Spearman analyses were done to correlate CFU with CXCL2 levels. P < 0.05 was considered significant.
Results:
Placebo treatment was associated with a 12.5-fold increase in bacterial load as compared to BLF treatment (incidence rate ratio (IRR) = 12.5; 95% CI 3.9-39.7, p < 0.001), supporting a substantial protective effect of BLF on infection severity (Fig. 1). In addition, bacterial load was associated with CXCL2 concentration (IRR = 4.3; 95% CI 2.6– 7.2; p < 0.001), indicating a strong positive relationship between bacterial infection and CXCL2 production. This was further supported by Spearman correlation analysis, which found positive correlations for both treatment groups (BLF: r = 0.49, p < 0.001; placebo: r = 0.61, p < 0.001) (Fig. 2). While increased bacterial loads correlated strongly with increased CXCL2 levels, we did not observe a significant difference in CXCL concentrations between treatment groups (Fig. 3).
Conclusions:
Maternal vaginally administered BLF significantly reduced neonatal E. coli burden. CXCL2 levels positively correlated with bacterial loads but were not significantly modulated by treatment. Further studies are needed to elucidate lactoferrin’s effects on innate host responses to neonatal E. coli infection.
Maternal Lactoferrin Reduces Vertically-Acquired Escherichia coli Infection in the Offspring without Modifying Innate Immune Response in a Mouse Model
Background:
Escherichia coli is a leading pathogen in neonatal early-onset sepsis (EOS), a major cause of newborn mortality worldwide. Maternal administration of lactoferrin, an antimicrobial and immunomodulatory glycoprotein, may reduce EOS by protecting the offspring against vertical E. coli infection while modulating associated innate immune responses.
Objectives/Goal:
To determine if maternal vaginal administration of bovine lactoferrin (BLF) ameliorates invasive infection and modifies tissue CXCL2 production in the embryos of pregnant mice pretreated with BLF prior to vaginal E. coli inoculation.
Methods/Design:
Pregnant C57BL/6 mice received BLF (75 mg/mL) or placebo vaginally in a novel oil/aqueous bi-gel on embryonic days (E) days 16 and 17, followed by vaginal inoculation with 105 colony forming units (CFU) of the neonatal E. coli strain RS218 on E17.
Embryos were collected on E18, and liver–spleen tissue homogenates were plated to quantify E. coli CFU per 100 mg tissue. CXCL2 (human IL-8 homolog) concentrations in homogenates were measured by ELISA. Four independent experiments were done, including 35 embryos in the BLF group, and 31 in the placebo group.
Bacterial load was modeled as a function of treatment group and CXCL2 concentrations using a generalized linear mixed model (GLMM) with a negative binomial distribution to address overdispersion and include random mouse effects. Spearman analyses were done to correlate CFU with CXCL2 levels. P < 0.05 was considered significant.
Results:
Placebo treatment was associated with a 12.5-fold increase in bacterial load as compared to BLF treatment (incidence rate ratio (IRR) = 12.5; 95% CI 3.9-39.7, p < 0.001), supporting a substantial protective effect of BLF on infection severity (Fig. 1). In addition, bacterial load was associated with CXCL2 concentration (IRR = 4.3; 95% CI 2.6– 7.2; p < 0.001), indicating a strong positive relationship between bacterial infection and CXCL2 production. This was further supported by Spearman correlation analysis, which found positive correlations for both treatment groups (BLF: r = 0.49, p < 0.001; placebo: r = 0.61, p < 0.001) (Fig. 2). While increased bacterial loads correlated strongly with increased CXCL2 levels, we did not observe a significant difference in CXCL concentrations between treatment groups (Fig. 3).
Conclusions:
Maternal vaginally administered BLF significantly reduced neonatal E. coli burden. CXCL2 levels positively correlated with bacterial loads but were not significantly modulated by treatment. Further studies are needed to elucidate lactoferrin’s effects on innate host responses to neonatal E. coli infection.
Comments
Full text not provided by primary author
Poster Board Number: 21