Assessment of mechanisms of infectious pneumonia based on expression of fibrinogen, procalcitonin, high-sensitivity C-reactive protein expression, T helper 17 cells, regulatory T cells interleukin-10, and interleukin-17.

Abstract

BackgroundInfectious pneumonia is one of the important causes of neonatal death that can lead to the imbalance of T helper 17 cells (Th17) and T regulatory T cells (Treg) cells. The correlation between plasma fibrinogen (FIB), procalcitonin (PCT), C-reactive protein (CRP) and Th17/Treg-IL-10/IL-17 axis balance and their specific role in the occurrence and development of infectious pneumonia are not completely clear.MethodsThirty specific-pathogen free Sprague Dawley (SD) rats were randomly divided into a control group for comparison and IPN model group. After the establishment of infectious pneumonia model, levels of FIB, PCT, hs-CRP, IL-10, and IL-17 in the serum of the two groups were measured using enzyme linked immunosorbent assay (ELISA), the pathological changes of lung tissue were observed using hematoxylin and eosin (HE) staining, the number of Treg and Th17 cells and the ratio of Th17/Treg in serum were detected using flow cytometry, and the levels of retinoic acid-related orphan receptor γt and forkhead box P3 (FOXP3) in lung tissue were detected using reverse transcription polymerase chain reaction (RT-PCR) and western blot.ResultsThe results showed that the serum levels of FIB, PCT, hs-CRP, Th17 cell number, Th17/Treg ratio, left lung dry and wet weight, lung tissue wet/dry ratio, lung pathology score and IL-17 level in the model group were significantly higher than those in the control group, while the number of Treg cells and the level of IL-10 in the model group were significantly lower than those in the control group. In addition, the expression of Foxp3mRNA and protein in lung tissue of model group decreased significantly, while the expression level of ROR- γ t mRNA and protein increased.ConclusionsIn infectious pneumonia, the expression levels of FIB, PCT and hs-CRP are up-regulated, and Th17 cells are activated, Treg cells are inhibited, proinflammatory cytokine IL-17 expression is up-regulated, anti-inflammatory cytokine IL-10 expression is down-regulated, resulting in increased inflammatory response, thus promoting the occurrence and development of infectious pneumonia.