R., Carbonell-Estrany X., Rieger C. wheezing ailments, but the converse is not true. Some evidence of virus specificity is present, in that allergic sensitization NSC-23766 HCl specifically improved the risk of wheezing in individuals infected with HRV, but not RSV. Administration of Palivizumab, a humanized monoclonal antibody that focuses on the A antigenic site of the Fusion-protein of RSV, decreases the risk of hospitalization in high-risk babies and the risk of recurrent of wheezing. However, palivizumab did not possess any effect on subsequent recurrent wheezing in children with a family history of atopy. These findings suggest that illness with RSV and illness with HRV might predispose individuals to recurrent wheezing through an atopy-independent and an atopy-dependent mechanism, respectively. Respiratory virus-induced wheezing ailments may encompass multiple sub-phenotypes that relate to asthma in different ways. (vitamin D receptor), were significantly associated with severe RSV-induced bronchiolitis at both the allele and genotype levels (Janssen et al., 2007). Genetic polymorphisms of (surfactant protein A), (surfactant protein D), (toll like receptor) 4, (tumor necrosis element), IL4 (interleukin Rabbit Polyclonal to GPR142 4), and have been reportedly associated with a susceptibility NSC-23766 HCl to RSV-induced bronchiolitis (Huckabee and Peebles, 2009). Very recently, a significant connection between the 17q21 genotype and human being RSV-induced wheezing illness was shown in two birth cohorts of children: the child years origins of asthma (COAST), and the Copenhagen Prospective Study on Asthma in Child years (COPSAC; Caliskan et al., 2013). The effects of 17q21 variants on an increased susceptibility to asthma are restricted to individuals with a history of HRV-induced wheezing illness during early existence (Caliskan et al., 2013). These studies highlight the important connection between virus-induced illness and genetic variants in individuals with asthma. CELLULAR IMMUNITY OF VIRUS-INDUCED ASTHMA (1) Is definitely RSV- and/or HRV-induced severe bronchiolitis in children associated with a T helper type 2 (Th2)-predominant immune response? RSV-induced severe bronchiolitis in children is associated with a Th2-predominant immune response (Renzi et al., 1997; Roman et al., 1997; Bendelja et al., 2000; Pala et al., 2002; vehicle der Sande et al., 2002; Joshi et al., 2003; Legge and Braciale, 2003) or a decreased Th1 immune response (Joshi et al., 2003; Legge and Braciale, 2003). The concentration of Th2 cytokines was higher than that of interferon (IFN)- in nasopharyngeal secretions (NSP; Bermejo-Martin et al., 2007), particularly in infants less than three months aged (Kristjansson et al., 2005). On the other hand, undetectable or very low Th2 cytokine concentrations have also been reported (Bont et al., 2001; Garofalo et al., 2001; Bennett et al., 2007; Garcia et al., 2012). The majority of virus-infected mouse studies have been performed using RSV because the major group of HRV (88% of known HRV serotypes) uses human being intercellular adhesion molecule-1 (ICAM-1) like a cellular receptor and cannot bind to mouse ICAM-1. Concerning NSC-23766 HCl HRV-induced asthma mouse models, three novel mouse models of HRV illness have been recently developed: illness having a minor-group HRV (the receptor is the low-density lipoprotein receptor family) in BALB/c mice, illness having a major-group HRV in transgenic BALB/c expressing a mouse-human ICAM-1 chimera, and HRV-induced exacerbation of allergic airway swelling (Bartlett et al., 2008). These models are likely to be useful for the future development of therapies for asthma exacerbation. In the majority of NSC-23766 HCl RSV-infected mouse studies, the induction of Th2 cytokines (including IL-4 and IL-5) is not observed in bronchial alveolar lavage (BAL) fluid or the lung cells of RSV-infected mice (Peebles et al., 2001; Chavez-Bueno et al., 2005; Lee et al., 2008). A comparison of mouse strains showed that BALB/c and DBA/2 mice experienced a significantly higher airway hyper-reactivity over almost the entire time program up to 20 days after RSV exposure, compared with C57BL/6 mice (Tekkanat et al., 2001). However, actually the BALB/c mice required NSC-23766 HCl a very high intranasal or intratracheal inoculum (105 or 106 PFUs) to elicit airway hyper-responsiveness (AHR; Tekkanat et al., 2001; Wang et al., 2004). Consequently, both the mouse strains and the.