Specifically with regards to the recruitment and potential stimulation of B cells. In our murine respiratory inhalation model, mice are challenged with the clinically relevant P. aeruginosa Liverpool epidemic strainisolate LESB65, which Eleutheroside-E establishes a stable 7 day infection that is restricted to the airway. In contrast to models using non-colonising P. aeruginosa strains that are rapidly cleared by components of the innate Cryptochlorogenic-acid immune system or more aggressive strains that cause sepsis and host death, this model allows the lung response to in situ infection to develop over a longer time period, such as occurs in CF. Our results demonstrate for the first time the kinetics of B cell chemoattractant and differentiation factor responses both following P. aeruginosa infection and in relation to lung B cell recruitment in a murine model. An elevated level of BAFF was found to be associated with the paediatric CF airway, irrespective of the presence or absence of pseudomonal infection, implying that the expression is not specific to pseudomonas infection and may be a feature of the CF airway. The importance of the B cell response in the CF lung remains unclear and its effectiveness is complicated by other factors predisposing to poor bacteria eradication such as impaired mucocilary clearance. Although many studies have focused on the mechanism and importance of inflammatory cell recruitment into the lung following P. aeruginosa infection, few studies have examined the B cell response within the airway. Here we demonstrate, to our knowledge for the first time, that BAFF expression is increased in BAL from the lungs of patients with CF. Furthermore, using a respiratory inhalation model of stable long-term lung infection with P. aeruginosa LESB65 in mice, we show, to our knowledge for the first time, recruitment of both B and T lymphocytes, expression of the B cell chemo-attractant cytokines CXCL13, CCL19 and CCL21 and up-regulation of the B cell differentiation factor BAFF. We have previously shown that the B cell differentiation factor BAFF, a major B cell growth factor that promotes B cell maturation and antibody production is expressed in the human airway during a range of viral infections including respiratory syncytial virus. To determine if BAFF expression is a component of the human airway response to P. aeruginosa infection, we measured BAFF expression in BAL from children with CF both with and without P. aeruginosa infection. Both groups showed significant elevation in BAFF expression in comparison to the control group. The P. aeruginosa negative CF patient group, some of whom were culture positive for other bacterial infections, also showed elevated BAFF expression, indicating that this response is not P. aeruginosa-specific. The recent observation that BAFF is expressed during Mycobacterial infection is consistent with this suggestion. Furthermore, our previous finding that BAFF expression occurs in response to a range of viral infections, supports this being a general mechanism in airway defence. The findings presented here cannot discount the possibility that elevated BAFF expression may be an innate characteristic of the CF airway associated with the underlying CFTR defect or of immune or inflammatory processes within the CF airway. To further determine if expression of this B cell differentiation factor correlated with increased expression of B cell recruitment factors and increased B cell numbers in the lung.