|Title:||Adenovirus replication and host innate response in primary human airway epithelial cells||Authors:||Yang T.-I.
|Issue Date:||2019||Publisher:||Elsevier Ltd||Journal Volume:||52||Journal Issue:||2||Start page/Pages:||207-214||Source:||Journal of Microbiology, Immunology and Infection||Abstract:||
Background: Adenovirus infections are very common in children and sometimes fatal. Immune responses and hypercytokinemia are related to disease severity in patients with adenovirus infection. Understanding of viral replication and immune responses could help elucidate the immunopathogenesis of severe adenovirus infections. Methods: Polarized human airway epithelial cells (hAECs) were set up to mimic human airway, and we conducted high (1 the multiplicity of infection, MOI) and low dosage (0.5 MOI) of wild-type adenovirus serotype 3 infection in hAECs from both apical (AP) and basolateral (BL) compartments, compared the viral replication kinetics and measured 25 cytokine and 9 chemokine levels by multiplex immunoassay to evaluate the host immune response. Results: Virus titer was the highest in the apical compartment in low dose apical infection. BL infection showed a relative steady viral titer in different doses and infection sites. Responses of several cytokines such as IL-1RA, IL-21 and all of the chemokines were found after adenovirus infection. Besides, the responses detected in the BL compartment were generally higher than those in the apical compartment, especially IL-1RA, IL-21, GM-CSF, GRO-α, SDF-1α and IL-8. Conclusion: During the infections of hAECs by adenovirus, higher viral replication was found in the apical compartment but cytokine and chemokine responses were higher in the basolateral compartment. This indicated viral entrance and replication occurred more in the apical part and major innate response took place in the basolateral part, which may make adenovirus infect human airway efficiently and cause different degree of severity. ? 2018
|ISSN:||1684-1182||DOI:||10.1016/j.jmii.2018.08.010||metadata.dc.subject.other:||alpha interferon; eotaxin; gamma interferon; gamma interferon inducible protein 10; granulocyte macrophage colony stimulating factor; interleukin 1 receptor blocking agent; interleukin 10; interleukin 12p70; interleukin 13; interleukin 15; interleukin 17; interleukin 18; interleukin 2; interleukin 21; interleukin 22; interleukin 23; interleukin 27; interleukin 31; interleukin 4; interleukin 5; interleukin 6; interleukin 7; interleukin 8; interleukin 9; macrophage inflammatory protein 1alpha; macrophage inflammatory protein 1beta; monocyte chemotactic protein 1; RANTES; stromal cell derived factor 1alpha; chemokine; cytokine; Adenoviridae; adenovirus infection; airway epithelium cell; Article; cell differentiation; cell structure; human; human cell; immunoassay; immunopathogenesis; innate immunity; lung cancer; nonhuman; virus load; virus replication; adenovirus infection; cell culture; cytology; epithelium cell; host pathogen interaction; immunology; innate immunity; metabolism; pathogenicity; respiratory mucosa; virology; virus entry; virus replication; Adenoviridae; Adenoviridae Infections; Cell Differentiation; Cells, Cultured; Chemokines; Cytokines; Epithelial Cells; Host-Pathogen Interactions; Humans; Immunity, Innate; Respiratory Mucosa; Viral Load; Virus Internalization; Virus Replication
|Appears in Collections:||醫學系|
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