Related Experiment Video
Updated: Dec 11, 2025

A Non-invasive and Technically Non-intensive Method for Induction and Phenotyping of Experimental Bacterial Pneumonia in Mice
Published on: September 28, 2016
Role of immunodeficiency in Acinetobacter baumannii associated pneumonia in mice
Ai-Ran Liu1, Wen-Jing Du2, Jian-Feng Xie1
1Department of Critical Care Medicine, Zhong-Da Hospital, School of Medicine, Southeast University, Nanjing, Jiangsu 210009, China.
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.
Insights
Immunodeficiency impairs the immune response to Acinetobacter baumannii pneumonia, leading to increased mortality and lung injury. This highlights the critical role of a robust immune system in combating this severe nosocomial infection.
Area of Science:
- Immunology
- Infectious Diseases
- Pulmonology
Background:
- Acinetobacter baumannii is a significant cause of hospital-acquired pneumonia, particularly in critically ill patients.
- The interplay between A. baumannii infection and the host immune response critically affects patient outcomes.
- Understanding the impact of immunodeficiency on A. baumannii pneumonia is crucial for improving patient prognosis.
Purpose of the Study:
- To investigate the role of compromised immunity in the pathogenesis of Acinetobacter baumannii-induced pneumonia.
- To elucidate how immune deficiency influences the host's response to A. baumannii infection in the lungs.
Main Methods:
- Male BALB/c mice were divided into normal and immune-compromised groups, with and without A. baumannii infection.
- Immunocompromise was induced using cyclophosphamide; pneumonia was induced via intranasal A. baumannii instillation.
- Lung tissues and mortality were assessed at 6 and 24 hours post-infection.
Main Results:
- Immune-compromised mice showed significantly reduced neutrophil recruitment to the lungs following A. baumannii infection compared to normal immunity groups.
- Pulmonary levels of key cytokines, including IL-4 and IFN-γ, were significantly depressed in infected, immune-compromised mice.
- A. baumannii infection in immune-compromised mice resulted in increased early mortality and more severe lung histopathology.
Conclusions:
- Acinetobacter baumannii infection is associated with frustrated immune responses in immunocompromised individuals.
- Reduced immune response in the context of immunodeficiency correlates with exacerbated lung injury and poorer outcomes in A. baumannii pneumonia.
- Maintaining immune competence is vital for effective host defense against A. baumannii pneumonia.
More Related Videos
11:32Following in Real Time the Impact of Pneumococcal Virulence Factors in an Acute Mouse Pneumonia Model Using Bioluminescent Bacteria
Published on: February 23, 2014
12:21A Mouse Model for the Transition of Streptococcus pneumoniae from Colonizer to Pathogen upon Viral Co-Infection Recapitulates Age-Exacerbated Illness
Published on: September 28, 2022