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Expression of chemokine receptor CX 3 CR1 in infants with respiratory syncytial virus bronchiolitis
Author(s) -
Cepika AlmaMartina,
Gagro Alenka,
Bace Ana,
TjesicDrinkovic Dorian,
Kelecic Jadranka,
BaricicVoskresensky Tamara,
Matic Mladen,
Drazenovic Vladimir,
Marinic Igor,
MlinaricGalinovic Gordana,
TjesicDrinkovic Duska,
Vrtar Zvonimir,
Rabatic Sabina
Publication year - 2008
Publication title -
pediatric allergy and immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.269
H-Index - 89
eISSN - 1399-3038
pISSN - 0905-6157
DOI - 10.1111/j.1399-3038.2007.00611.x
Subject(s) - perforin , bronchiolitis , immunology , medicine , chemokine , convalescence , cd8 , virus , mononegavirales , paramyxoviridae , inflammation , immune system , viral disease
Respiratory syncytial virus (RSV) glycoprotein G mimics fractalkine, a CX 3 C chemokine, which mediates chemotaxis of leukocytes expressing its receptor, CX 3 CR1. The aim of this study was to examine the relationship between RSV infection and expression of perforin and IFN‐ γ in CX 3 CR1‐expressing peripheral blood CD8 + T cells. Samples were collected from infants with RSV bronchiolitis, both in the acute and convalescence phase (n = 12), and from their age‐ and sex‐matched healthy controls (n = 15). Perforin expression and IFN‐ γ secretion in CX 3 CR1 + CD8 + T cells were assessed by four‐color flow cytometry. The NF‐ κ B p50 and p65 subunit levels were also determined as markers of RSV‐induced inflammation. Study results showed perforin and CX 3 CR1 expression to be significantly lower in the convalescent phase of infected infants than in healthy controls. There was no significant difference in IFN‐ γ secretion and NF‐ κ B binding activity between two time‐points in RSV‐infected infants, or when compared with healthy controls. Infants with prolonged wheezing had lower acute‐phase CX 3 CR1 levels in peripheral blood. These data indicate existence of an event persisting after acute RSV infection that is able to modulate effector functions of cytotoxic T cells, and also link disease severity with CX 3 CR1 expression.