CD44 deficiency leads to decreased proinflammatory cytokine production in lung induced by PCV2 in mice

- PCV2 infection leads to increased CD44 expression in lung.
- CD44 could facilitate PCV2 outgrowth and dissemination in mice.
- CD44 deficiency resulted in reduced lymphocytes recruitment to BALF.
- CD44 deficiency decreased proinflammatory cytokine production in lung.

Porcine circovirus type 2 (PCV2) is the primary etiological agent of postweaning multisystemic wasting syndrome (PMWS). CD44 is a widely expressed class I transmembrane glycoprotein implicated in immunological and inflammatory responses. In previous studies, the role of CD44 in host defense against microorganism infection remains controversial. The role of CD44 in host defense against PCV2 infection has never been studied before. In this study, we investigated the role of CD44 in the development of pneumonia induced by PCV2 in mice model. Upon infection, CD44 mRNA level in lung tissue was upregulated, and we confirmed a detrimental role of CD44 in host defense against PCV2 infection. The results demonstrated that CD44 deficiency could result in decreased proinflammatory cytokine production in lung induced by PCV2 in mice, suggesting a previously unrecognized role for CD44 in the development of pneumonia response to PCV2 infection.