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.

原发性流感病毒 (IV) 感染可使宿主易于继发感染流感嗜血杆菌 (H.fluxene)，这进一步增加了疾病的严重性和死亡率。虽然粘附分子在宿主炎症反应和流感嗜血杆菌定植中起关键作用，但仍有待澄清哪些类型的粘附分子与IV 感染后流感嗜血杆菌的定植和侵袭有关。在本研究中，我们建立了甲型流感病毒 (A/Puerto Rico/8/34, H1N1) (PR8) 和不可分型流感嗜血杆菌共同感染的小鼠模型(NTHi) 并发现 PR8 和 NTHi 的连续感染在小鼠中诱导了致命的协同作用。这一结果可能是由于 NTHi 负荷增加、肺损伤更大和细胞因子水平更高。此外，共感染小鼠肺部细胞内粘附分子-1（ICAM-1）和纤连蛋白（Fn）的蛋白水平显着升高，但癌胚粘附分子（CEACAM）-1、CEACAM-5和血小板-激活因子受体（PAFr）不受影响。ICAM-1 和Fn 的蛋白质水平均与NTHi 生长呈正相关。这些结果表明粘附分子（包括 ICAM-1 和 Fn）与原发性 IV 感染后继发性 NTHi 肺炎中 NTHi 生长之间的相关性。