Correlation of adhesion molecules and non-typeable haemophilus influenzae growth in a mice coinfected model of acute inflammation |
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| Institution: | 1. State Key Laboratory of Respiratory Disease, National Clinical Research Center for Respiratory Disease, Guangzhou Institute of Respiratory Health, The First Affiliated Hospital of Guangzhou Medical University, Guangzhou, Guangdong, 510000, PR China;2. State Key Laboratory of Quality Research in Chinese Medicine, Macau Institute for Applied Research in Medicine and Health, Macau University of Science and Technology, Taipa, Macau SAR, 999078, PR China;3. Guangdong-Hong Kong-Macao Joint Laboratory of Infectious Respiratory Disease, Guangzhou, 510000, PR China;4. School of Pharmaceutical Science and Yunnan Key Laboratory of Pharmacology for Natural Products, Kunming Medical University, Kunming, 650500, PR China;5. Dongguan People''s Hospital, Dongguan, 523000, China;6. Kunming University of Science and Technology, Kunming, 650000, PR China;7. Department of Dermatology, Guangdong Provincial People''s Hospital, Guangdong Academy of Medical Sciences, Guangzhou, 510000, PR China;1. Institute of Cytology, RAS, St Petersburg, Russia;2. Institute of Molecular Genetics of National Research Center “Kurchatov Institute”, RAS, Moscow, Russia;3. Demidov Yaroslavl State University, Yaroslavl, Russia |
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| Abstract: | 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 (CEACAM)-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. |
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| Keywords: | Influenza A virus Co-infection Adhesion molecule |
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