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CME Credit Offered
CME Credit Offered
Abstract Award
Abstract Award
Recording available 2/16-5/2
Recording available 2/16-5/2
AIUM Credit
AIUM Credit
Foundation Awardee
Foundation Awardee
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Abstract Award
Abstract Award
Foundation Awardee
Foundation Awardee

Poster Session 3

Category: Prematurity

Poster Session 3

(937) Is Interleukin-1 Alpha a Key Mediator of Perinatal Neuroinflammation Associated With Preterm Birth?

Thursday, February 12, 2026
10:30 AM - 12:00 PM  
Objective:
Perinatal white matter injury results from neuroinflammation mediated primarily by interleukin 1 (IL-1) signaling via the cytokines IL-1a and IL-1B. The role of IL-1B in brain injury is extensively characterized yet treatments targeting IL-1B have proven ineffective. Little is known regarding the function and therapeutic potential of IL-1a. We aimed to examine the role of IL-1a in an established modality of perinatal neuroinflammation using a mouse model where Il1a is deleted.

Study Design:
Il1a knockout (KO) and wild type (wt) dams received an intrauterine injection of bacterial endotoxin (LPS) to induce fetal neuroinflammation or the vehicle (PBS) as a control, at embryonic day 15 of the 19-21 days gestation. Fetal brains and placentas were isolated at the peak of inflammation, 6-hours following intrauterine injections (Figure 1A) and analyzed for the expression of inflammatory receptors and cytokines; Tlr4, Il1r1, Il1a, Il1b, Il6 and Tnf.

Results:
Inflammatory receptors were upregulated by LPS exposure mainly in placentas, with exception to Tlr4 which varied in feta brains by condition and genotype (Figure 1B). Cytokines were significantly upregulated in wild type embryo brains that received LPS vs. PBS (Figure 2). In KO brains, Il1b and Il6 were also upregulated with LPS. With LPS exposure the expression of Tnf in KO brains was significantly lower than wild type and similar to PBS controls. In placentas, cytokines were equally upregulated with LPS in both KO and wild type. No Il1a transcript was detected in KO tissues.

Conclusion:
Similarities in Il1r1 between genotypes suggest that interleukin-1 receptor signaling was not altered by absence of Il1a in KO animals. Results suggest that in fetal brains IL-1a plays a significant role in Tnf production, a mediator of tissue injury and cell death. This appears specific to neuroinflammation being no differences were observed in placentas. Further research is needed to fully characterize the role and therapeutic potential of targeting IL-1a within the setting of perinatal neuroinflammation.