Clinical significance of cellular immunity function and inflammatory factors assays in alveolar lavage fluid for severe COVID‐19 pneumonia

Abstract

In this study, we aimed to investigate the changes of lymphocyte subsets (CD3 + , CD4 + , CD8 + ) and inflammatory factors , hypersensitive C-reactive protein [HS-CRP], and procalcitonin [PCT]) of alveolar lavage fluid in patients with severe corona virus-2019 (COVID-19) pneumonia and their clinical impact on the assessment of disease severity and prognosis. Twenty-four patients with severe COVID-19 pneumonia were admitted to the intensive care unit (ICU) of the Ezhou Central Hospital from February 1 to March 22, 2020. According to the 28-day prognosis, they were assigned to a death group and a survival group. On the 3rd day of ICU admission, peripheral blood and alveolar lavage fluid were collected for examination of lymphocyte subsets and inflammatory factors by flow cytometry and immunoturbidimetry, respectively. The CD3 + , CD4 + , and CD8 + cell counts in alveolar lavage fluid and serum were significantly higher in the survival group than those of the death group (p < .05). The levels of IL-6, HS-CRP, and PCT in the alveolar lavage fluid and serum of the death group were statistically higher than those of the survival group (p < .05); The CD3 + , CD4 + cell count, and IL-6 level were negatively correlated with Sequential Organ Failure Assessment (SOFA) and Acute Physiology and Chronic Health Evaluation II scores, respectively (p < .05). The CD4 + cell and SOFA score have a regression relationship for the prognosis of COVID-19 severe patients. The CD3 + , CD4 + , CD8 + cells, and IL-6 levels are valuable in determining the prognosis of severe COVID-19 pneumonia and are strongly correlated with the severity of the disease; the CD4 + cell is an independent risk factor affecting the prognosis of COVID-19 pneumonia.

Inflammatory factors in alveolar lavage fluid from severe COVID-19 pneumonia: PCT and IL-6 in epithelial lining fluid

“…Our results are different from the results of the paper by Liao and Yang [ 1 ]. Concentrations of PCT and IL-6 were not statistically different between survivors and non-survivors, and only PCT in BALF ( p = 0.0759) and IL-6 in serum ( i = 0.0630) tended to be higher in non-survivors [ 3 ].…”

“…The research article “Clinical Significance of Cellular Immunity and Inflammatory Factors Assays in Alveolar Lavage Fluid for Severe COVID-19 Pneumonia” by Liao and Yang [ 1 ] reported that the concentrations of interleukin-6 (IL-6), C-reactive protein (CRP), and procalcitonin (PCT) in the alveolar lavage fluid and in the serum of survivors were lower compared to those of non-survivors. Levels of IL-6, CRP, and PCT were higher in samples of alveolar lavage than in the serum, indicating that viral infections lead to abnormal oxygen and carbon dioxide exchange in the alveoli and to a secondary inflammation-mediated immune response disorder.…”

The Robustness of Cellular Immunity Determines the Fate of SARS-CoV-2 Infection

“…The severity of the disease also correlates with cytokine levels and these patients secrete higher levels of IL-6 and IL-10 ( 175 ). Thus, in ICU patients a further increase in IL-6 and IL-10 plus TNF-α ( 165 ) has been observed and has also been found to be higher in the bronchoalveolar lavage fluid of deceased patients than in those who survive IL-6 ( 120 ). The increase in TNF-α may explain why antibody levels correlate with disease severity, since this cytokine secreted by CD4+ T cells serves as a co-stimulatory signal for B cells.…”

“…In addition, symptomatic SARS-CoV-2 infection tends to elicit a higher peripheral blood T cell response with respect to asymptomatic infection (117,118).The reduced frequencies of peripheral T cells during acute infection are likely to be associated with decreased CD4+ T cell proliferation and CD8+ T cell hyperactivation with T cell migration into the lungs (119). However, Liao L. et al (120) have observed an increase of T cells in bronchoalveolar lavage fluids in mild patients but not in severe patients, suggesting a difference in T cell migration into the lungs in severe patients (120)(121)(122).…”