Correlation of adhesion molecules and non-typeable haemophilus influenzae growth in a mice coinfected model of acute inflammation

Primary influenza virus (IV) infection can predispose hosts to secondary infection with Haemophilus influenzae (H. influenzae), which further increases the severity and mortality of the disease. While adhesion molecules play a key role in the host inflammatory response and H. influenzae colonization, it remains to be clarified which types of adhesion molecules are associated with H. influenzae colonization and invasion following IV infection. In this study, we established a mouse model of co-infection with influenza A virus (A/Puerto Rico/8/34, H1N1) (PR8) and non-typeable H. influenzae (NTHi) and found that sequential infection with PR8 and NTHi induced a lethal synergy in mice. This outcome may be possibly due to increased NTHi loads, greater lung damage and higher levels of cytokines. Furthermore, the protein levels of intracellular adhesion molecules-1 (ICAM-1) and Fibronectin (Fn) were significantly increased in the lungs of coinfected mice, but the levels of carcinoembryonic adhesion molecule (CEA-CAM)-1, CEACAM-5 and platelet-activating factor receptor (PAFr) were unaffected. Both the protein levels of ICAM-1 and Fn were positively correlated with NTHi growth. These results indicate the correlation between adhesion molecules, including ICAM-1 and Fn, and NTHi growth in secondary NTHi pneumonia following primary IV infection. (C) 2021 Institut Pasteur. Published by Elsevier Masson SAS. All rights reserved.

Automated summary

Primary influenza virus infection can predispose hosts to secondary infection with Haemophilus influenzae, which increases disease severity and mortality. Sequential infection with influenza A virus and Haemophilus influenzae induced lethal synergy in a mouse model, possibly due to increased bacterial loads and lung damage. Analysis showed a correlation between specific adhesion molecules and bacterial growth in secondary pneumonia following primary viral infection.