MyD88 controls human metapneumovirus-induced pulmonary immune responses and disease pathogenesis

Junping Ren, Deepthi Kolli, Junfang Deng, Rong Fang, Bin Gong, Megan Xue, Antonella Casola, Roberto P. Garafalo, Tian Wang, Xiaoyong Bao

Research output: Contribution to journalArticlepeer-review

10 Scopus citations

Abstract

Human metapneumovirus (hMPV) is a common cause of lung and airway infections in infants and young children. Recently, we and others have shown that hMPV infection induces Toll-like receptor (TLR)-dependent cellular signaling. However, the contribution of TLR-mediated signaling in host defenses against pulmonary hMPV infection and associated disease pathogenesis has not been elucidated. In this study, mice deficient in MyD88, a common adaptor of TLRs, was used to investigate the contribution of TLRs to in vivo pulmonary response to hMPV infection. MyD88-/- mice have significantly reduced pulmonary inflammation and associated disease compared with wild-type (WT) C57BL/6 mice after intranasal infection with hMPV. hMPV-induced cytokines and chemokines in bronchoalveolar lavage fluid (BALF) and isolated lung conventional dendritic cells (cDC) are also significantly impaired by MyD88 deletion. In addition, we found that MyD88 is required for the recruitment of DC, T cells, and other immune cells to the lungs, and for the functional regulation of DC and T cells in response to hMPV infection. Taken together, our data indicate that MyD88-mediated pathways are essential for the pulmonary immune and pathogenic responses to this viral pathogen.

Original languageEnglish (US)
Pages (from-to)241-250
Number of pages10
JournalVirus Research
Volume176
Issue number1-2
DOIs
StatePublished - Sep 1 2013

Keywords

  • Cytokines/chemokines
  • HMPV
  • MyD88
  • Pulmonary immune response

ASJC Scopus subject areas

  • Cancer Research
  • Virology
  • Infectious Diseases

Fingerprint Dive into the research topics of 'MyD88 controls human metapneumovirus-induced pulmonary immune responses and disease pathogenesis'. Together they form a unique fingerprint.

Cite this