# Serial Expression of Pro-Inflammatory Biomarkers in Acute Lung Injury During the Post-Resuscitation Periods in Rats with Cardiac Arrest

## TL;DR

This study examines how the TLR4 signaling pathway contributes to lung inflammation in rats after cardiac arrest and resuscitation.

## Contribution

The study reveals the rapid activation of the MyD88-dependent pathway and changes in immune cells after cardiac arrest.

## Key findings

- MyD88 expression increased in lung tissues 2 hours after cardiac arrest and CPR.
- Inflammatory cytokines like IL-1β and IL-6 were elevated in bronchoalveolar lavage fluid.
- Regulatory B cells decreased, while regulatory T cells showed a transient increase after resuscitation.

## Abstract

Acute lung injury may occur after cardiac arrest (CA), with innate immunity likely playing an important role in lung inflammation after CA. This study aimed to survey serial changes in the toll-like receptor (TLR) 4 signaling pathway in post-resuscitation lung injury in CA rats. A randomized animal study was conducted in rats with CA followed by successful cardiopulmonary resuscitation (CPR). The expression of TLR4 pathway biomarkers was analyzed and compared to the sham controls at different time points after CA with CPR. Lung tissues were collected for histological analysis to assess structural damage. Bronchoalveolar lavage fluid (BALF) was analyzed to quantify inflammatory cytokines and to assess changes in regulatory B cells (Bregs) and regulatory T cells (Tregs). Histological examination revealed marked pulmonary hemorrhage and structural injury shortly after CA. CA with CPR increased myeloid differentiation factor 88 (MyD88) mRNA and protein expression compared to controls at 2 h after CA. Cytokine analysis of BALF showed elevated IFN-γ, interleukin (IL)-1α, IL-1β, IL-2, IL-6, and IL-10 at 2 h after CA. A reduction in Bregs was noted at 2 h, whereas Tregs transiently increased between 2 and 4 h but declined at 6 h after CA. The MyD88-dependent signaling pathway appears to be rapidly activated in rats with CA after CPR, which may contribute to the early pulmonary inflammation observed as soon as 2 h after CA.