Comparison of Inflammatory Cell Counts
Increased inflammatory cells and platelets count in the peripheral blood is an indication of inflammatory reaction in the host. In the present study, the total white blood cells, neutrophils and platelets counts were higher in the woodworkers. This is consistent with the result of Gripenbäck et al., (2005) who found a significantly increased number of neutrophils in the peripheral blood of healthy volunteers who were exposed to pinewood dust. The lymphocyte count was not significantly high in the woodworkers. This result is consistent with the findings of Gripenbäck, et al., (2005) who found significant decreased lymphocytes numbers in the peripheral blood of healthy volunteers exposed to wood dust and also found increased lymphocytes in the bronchoalveolar lavage (BAL) fluid. The increased inflammatory cells in the peripheral blood in this study suggest that the wood dust may have induced inflammatory reactions in the woodworkers.
Comparison of Cytokine levels among woodworkers and non-exposed workers
Cytokines are inflammatory and immunomodulating mediators that exhibit both negative and positive regulatory effects on various target cells (Sultani et al 2012), hence the serum levels of various cytokines may give information on the presence of inflammatory processes (Cavaillon, 2001). This study investigated the cytokine profile of the different classes of cytokines in the woodworkers:
Proinflammatory cytokines promote inflammation by activating a variety of pro-inflammatory genes, including phospholipase A2, cyclooxygenase 2 (COX-2), inducible nitric oxide synthase (iNOS), and other cytokines and chemokines to initiate inflammation (Dinarello, 2000; Apte and Voronov, 2002 Mizgerd, 2002). IL-1β and IL-6 also promote the development of T helper (Th17) cells and Th1 cell lineage (Aldrich and Vigil-Cruz 2003; Borish and Steinke, 2003). The proinflammatory cytokines (IL-1β and IL-6) were increased in the woodworkers in this study, which suggests that the wood dust induces proinflammatory cytokines and therefore may promote inflammatory reaction in the woodworkers. This observation is similar to the result of Long et al., (2004); Bornholdt et al., (2007) and Määttä, et al., (2008) in which wood dust of all the tested wood species induced proinflammatory cytokine expression in the human lung tissue and animal model studies. The present study, therefore, supports the previous observation that the wood dust induces an inflammatory response in the woodworkers
The CD4+ effector subset Th1, Th2, Th17 and Treg cytokines were higher in the woodworkers, which suggests that the wood dust may have induced Th1, Th2, Th17 and Treg immune response in the woodworkers. However, no significant changes have been reported in previous studies on the expression of Th1, Th2, Th17 and Treg cytokines in woodworkers, human tissue or animals exposed to wood dust (Määttä et al., 2005; Bornholdt 2007). Again, there were no studies reported on CD4+ effector subset cytokines induction in woodworkers exposed to tropical hardwood.
The Th1 cytokines (IFN-γ and IL-12) are known to mediate the killing of intracellular pathogens by activating monocytes and macrophages to increase their cytokines secretion and antigen presentation. However, they also resist the Th2 cell cytokine function and Th2 response (allergic response) (Moldoveanu et al., 2009; Murdock and Lloyd, 2010). Th1 cytokines also downregulate eosinophils differentiation by suppressing the development of Th2 cells in allergic inflammation (Teran, et al., 1999). This study, therefore, suggests that the increased Th1 cytokine levels observed in the woodworkers may contribute to resisting allergic inflammatory reactions that may be induced due to the increase Th2 level in the woodworkers.
This is consistent with the findings that, altering the cytokine-producing profile of Th2 cells by inducing Th1 responses is protective against Th2-related disorders such as asthma and allergy (Teixeira et al 2005). This study suggests that the Th1 response induced by the wood dust may contribute to resisting allergic response in woodworkers. This may have contributed to the normal lung function indices observed in the woodworkers in our study (not published).
The Th2 cytokines (IL-4 and IL-13) were higher in the woodworkers compared to the non-exposed workers, suggesting that the wood dust may have contributed to induce of Th2 response in the woodworkers. Th2 cytokines are important in hypersensitivity reactions and allergic immunopathology. They are known to enhance mucus release, class switching of B cells to produce IgE, and fibrosis (Gripenbäck et al., 2005). The action of the Th2 immune response can result in IgE production, inflammation of the airways and tissue remodelling (Teran et al., 1999). Although IgE was not measured in the present study, the increased Th2 cytokines may support the high level of IgE found in a previous study of exposed tropical hardwood workers in Accra (Ennin, 2009). The increased Th2 cytokines in the woodworkers in the present study may have contributed to allergic respiratory symptoms such as sneezing and catarrh and mucous release woodworkers. This is consistent with the findings of Gripenbäck et al., (2005) and Shum et al., (2008), that elevated production of the Th2 cytokines contribute to allergic airway inflammation. The high levels of the Th1 cytokines (IFN-γ and IL-12) observed in the present study may be attributed to the high level of Th2 cytokines (IL-4) to antagonize the development of Th2 response and downregulate the Th2 inflammatory reactions in the woodworkers (Shum et al., 2008; Murdoch and Lloyd 2010).
The Th17 cytokine IL-17A was higher in the woodworkers suggesting that the wood dust may have induced a Th17 response in the woodworkers. IL-17A is known to stimulate the production of other proinflammatory cytokines and play protective roles in host resistance against pathogens at epithelial and mucosal barriers (Onishi and Gaffen, 2010; Jin and Dong, 2013). Elevated levels of IL-17A have been observed in the airways of asthmatics and are associated with neutrophil influx (Shum et al., 2008). In the present study, the IL-17A level was higher in the woodworkers this indicating that IL-17A may contribute to the induction of inflammation reaction in the woodworkers.
The woodworkers had a higher Treg cytokine (IL-10) level than the non-exposed workers suggesting an increased Treg response in the woodworkers. Activated Treg produces IL-10 which inhibits the synthesis of pro-inflammatory cytokines or suppresses their activities hence negatively modulating inflammatory response (Opal and DePalo, 2000). It also reduces airway hyper-reactivity (AHR), lung eosinophil infiltration and Th2 cytokine production which are characteristics of allergic airway inflammation. IL-10 together with IL-4 and IL-13 downregulate immunological response in the lungs (Baldacci et al., 2001; Moldoveanu et al., 2009; Murdoch and Lloyd 2010 and Erjefält 2014). The higher level of Treg cytokine in the present study suggests that the increased Treg cytokine in the woodworkers may contribute to the suppression of allergic and inflammatory reactions induced by wood dust to limit the immuno-pathological occurrence in the woodworkers.