Respiratory syncytial virus may be a pathogen in allergic conjunctivitis.

Abstract

The host response to allergens appears to be regulated by T helper type 2 cell patterns of local cytokine production. We hypothesized that respiratory syncytial virus (RSV) infects the normal conjunctival epithelium and produces interleukin (IL)-4, causing a local allergic reaction. Giemsa staining, immunocytochemical study, flow cytometric analysis, and reverse-transcriptase polymerase chain reaction (RT-PCR) were performed on tear and cytology samples from individuals with allergic and postoperative conjunctivitis. Histamine was assayed by radioimmunoassay, and IL-4 by enzyme-linked immunosorbent assay. The total number of cells collected by brush cytology did not differ between allergic and postoperative conjunctivitis. The levels of IL-4 and histamine in the specimens and mean IL-4 tear level were significantly increased in patients with allergic conjunctivitis. Cytocentrifuge preparations contained conjunctival epithelial cells with lymphocytes (a few CD3- and CD4-bearing cells), mast cells, eosinophils, and higher human leukocyte antigen (HLA)-DR expression in allergic patients. RT-PCR analysis showed that samples from allergic conjunctivitis expressed increased transcripts of IL-4 and IL-13. A higher percentage of RSV sequences were detected in allergic patient samples. Immunocytochemical study and RT-PCR showed that epithelial cells were infected with RSV. Average concentrations of IL-4 in culture supernatants were higher than levels in uninfected cells. These results suggest that the clinical features of human allergic conjunctivitis are associated with T helper type 2 cytokine expression. RSV in conjunctival epithelial cells may be an environmental pathogen in allergic conjunctivitis.