Role of immunodeficiency in Acinetobacter baumannii associated pneumonia in mice.
10.1097/CM9.0000000000001027
- Author:
Ai-Ran LIU
1
;
Wen-Jing DU
2
;
Jian-Feng XIE
1
;
Jing-Yuan XU
1
;
Ying-Zi HUANG
1
;
Hai-Bo QIU
1
;
Yi YANG
1
Author Information
1. Department of Critical Care Medicine, Zhong-Da Hospital, School of Medicine, Southeast University, Nanjing, Jiangsu 210009, China.
2. Department of Critical Care Medicine, Xuzhou Central Hospital, Xuzhou, Jiangsu 221009, China.
- Publication Type:Journal Article
- From:
Chinese Medical Journal
2020;133(18):2161-2169
- CountryChina
- Language:English
-
Abstract:
BACKGROUND:Acinetobacter baumannii (A. baumannii) has become one of the most important opportunistic pathogens inducing nosocomial pneumonia and increasing mortality in critically ill patients recently. The interaction between A. baumannii infection and immune response can influence the prognosis of A. baumannii related pneumonia. The target of the present study was to investigate the role of immunodeficiency in A. baumannii induced pneumonia.
METHODS:Male BALB/c mice were randomly divided into the normal immunity control (NIC) group, normal immunity infection (NIA) group, immune compromised control (CIC) group, and immune compromised infection (CIA) group (n = 15 for each group). Intraperitoneal injection of cyclophosphamide and intranasal instillation of A. baumannii solution were used to induce compromised immunity and murine pneumonia, respectively. The mice were sacrificed at 6 and 24 h later and the specimens were collected for further tests. Seven-day mortality of mice was also assessed.
RESULTS:After A. baumannii stimulation, the recruitment of neutrophils in mice with normal immunity increased sharply (P = 0.030 at 6 h), while there was no significant raise of neutrophil counts in mice with compromised immune condition (P = 0.092 at 6 h, P = 0.772 at 24 h). The Th cell polarization presented with pulmonary interleukin (IL)-4 and interferon (IFN)-γ level in response to the A. baumannii in CIA group were significantly depressed in comparison with in NIA group (IFN-γ: P = 0.003 at 6 h; P = 0.001 at 24 h; IL-4: P < 0.001 at 6 h; P < 0.001 at 24 h). The pulmonary conventional dendritic cell accumulation was even found to be inhibited after A. baumannii infection in immunocompromised mice (P = 0.033). Correspondingly, A. baumannii associated pneumonia in mice with compromised immunity caused more early stage death, more severe histopathological impairment in lung.
CONCLUSION:A. baumannii could frustrate the immune response in immunocompromised conditions, and this reduced immune response is related to more severe lung injury and worse outcome in A. baumannii induced pneumonia.
