Host resistance to intranasal Acinetobacter baumannii reinfection in mice. Issue 5 (17th May 2016)

• Record Type: Journal Article
• Authors: Qiu, Hongyu; Li, Zack; KuoLee, Rhonda; Harris, Greg; Gao, Xiaoling; Yan, Hongbin; Xu, H. Howard; Chen, Wangxue
• Is Part Of: Pathogens and disease. Volume 74:Issue 5(2016:Jul.)
• Publication Date: 2016-05-17
• Subjects: Acinetobacter baumannii -- reinfection -- host defense -- pneumonia; Medical microbiology -- Periodicals; Pathogenic microorganisms -- Periodicals; Communicable diseases -- Microbiology -- Periodicals; Communicable diseases -- Pathogenesis -- Periodicals; Host-parasite relationships -- Periodicals; Systems biology -- Periodicals; 616.904105
• DOI: 10.1093/femspd/ftw048
• Languages: English
• ISSNs: 2049-632X

Abstract

Abstract : Acinetobacter baumannii is a major causative agent of healthcare-associated infection and develops multidrug resistance rapidly. However, little is known in the host defense mechanisms against this infection. In this study, we examined if mice recovered from a previous intranasal A. baumannii infection (recovered mice) are fully protected against a subsequent reinfection. We found that, despite the presence of specific serum IgG and mucosal IgA responses prior to the reinfection, the recovered mice were only marginally better protected against intranasal challenge with low doses of homologous or heterologous A. baumannii strains than the naïve mice. Post-challenge immune and inflammatory (cells and cytokines) responses were generally comparable between recovered and naïve mice although the recovered mice produced significantly higher amounts of IFN-γ and IL-17 and had higher percentages and numbers of resident lung CD44 hi CD62L – CD4 + and CD19 + B lymphocytes. Taken together, our results suggest that mice recovered from a previous A. baumannii infection remain susceptible to reinfection, indicating the complexity of immune protection mechanism for this Gram-negative, multidrug-resistant emerging pathogen. Abstract : Mice that recovered from an intranasal Acinetobacter infection are only marginally more resistant to a reinfection than naive mice, indicating the complexity of immune protection for this multidrug-resistant emerging pathogen.