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Effect of Influenza Virus Infection in a Murine Model of Asthma
Hwan Soo Kim1, Huisu Lee1, Hyun Sook Kim1
1Department of Pediatrics, College of Medicine, The Catholic University of Korea, Seoul, Republic of Korea.
Abstract:
Respiratory virus infection is a major cause of asthma exacerbation. However, the underlying mechanisms of this exacerbation are unknown. Therefore, to determine the mechanisms, we examined the effect of influenza infection in a murine model of asthma. Mice were divided into four groups: the phosphate-buffered saline (PBS), house dust mite(HDM), influenza, and HDM/influenza groups. The influenza group and the HDM/influenza group were infected with influenza A virus. We measured airway resistance (Penh value), examined the lung tissue for pathology, and analyzed the cells and cytokines in bronchoalveolar lavage fluid (BALF) by ELISA. At 50 mg/mL methacholine, the HDM/influenza group showed a significantly higher Penh value than the PBS, HDM, and influenza groups. The number of neutrophils in BALF was higher in the HDM/influenza group than in the HDM group. A significantly greater number of lymphocytes and macrophages were detected in the HDM/influenza group than in the HDM group. IFN-γ and IL-1β levels were higher in the HDM/influenza group than in the HDM group. IL-5 levels did not vary between the HDM and HDM/influenza groups, IL-10 was significantly lower in the HDM/influenza than in the HDM group. Chemokine (C-X-C motif) ligand 1 (CXCL1) and regulated upon activation, normal T cell expressed and secreted (RANTES) were higher in the HDM/influenza group than in the HDM group. In a murine model of asthma, influenza-induced airway inflammation appeared to be caused by simultaneous activation of neutrophilic and eosinophilic inflammation.
Insights
Influenza infection worsens asthma exacerbations by increasing airway inflammation. This study in mice reveals that influenza combined with house dust mite exposure causes significant airway hyperresponsiveness and neutrophilic inflammation.
Area of Science:
- Immunology
- Pulmonology
- Virology
Background:
- Respiratory virus infections are a primary trigger for asthma exacerbations.
- The precise mechanisms underlying virus-induced asthma exacerbations remain unclear.
- Understanding these mechanisms is crucial for developing effective therapeutic strategies.
Purpose of the Study:
- To investigate the mechanisms by which influenza infection exacerbates asthma.
- To analyze the impact of influenza A virus infection on airway inflammation in a murine model of asthma.
Main Methods:
- A murine model of asthma was established using house dust mite (HDM) exposure.
- Mice were infected with influenza A virus, with separate groups for HDM and influenza exposure.
- Airway resistance, lung pathology, and bronchoalveolar lavage fluid (BALF) cell counts and cytokine levels were analyzed.
Main Results:
- Combined HDM and influenza exposure significantly increased airway hyperresponsiveness (measured by Penh value).
- Influenza infection led to increased neutrophils, lymphocytes, and macrophages in BALF.
- Elevated levels of IFN-γ, IL-1β, CXCL1, and RANTES were observed, while IL-10 decreased in the combined exposure group.
Conclusions:
- Influenza infection exacerbates asthma in a murine model.
- The exacerbation appears to be driven by the simultaneous activation of neutrophilic and eosinophilic inflammation.
- These findings elucidate key inflammatory pathways involved in virus-induced asthma exacerbations.
