Biomedical Engineering Reference
In-Depth Information
Figure 2
Consequences of the innate inflammatory response and cigarette smoke
components on the lung (represented as an airway). Inflammation and smoke
products could break down tissues, and induce cell apoptosis and necrosis. These
products have potential antigenic determinants that will be taken up by the numer-
ous dendritic cells (DCs). If the innate inflammation is ''competent,'' it would create
the proper microenvironment for the DCs to mature and migrate to the draining
lymph nodes where they could present the antigens resulting from lung injury to
T-cells.
pathogen entry. Second, the innate immune system can induce an adaptive
immune response. Dendritic cells are the key cellular links between the
innate and adaptive immunity playing a pivotal role as sensors of infection
or injury for the initiation of adaptive immune responses (53).
It has been shown that recruitment of a wave of DCs into the respira-
tory tract mucosa is a universal feature of the acute cellular response to local
challenge with bacterial, viral, and soluble protein antigens (54). This sug-
gests that rapid amplification of specific antigen surveillance at peripheral
challenge sites is an integral feature of the innate immune response, and
serves as an ''early warning system'' to alert the adaptive immune system
to incoming pathogens or body injury. It seems, therefore, that DCs may
be evolution's answer to the problem posed by organisms that evade primi-
tive (innate) first line defense systems (54). There is evidence in the literature
that cigarette smoking is associated with an expansion in the DC population
in the lower respiratory tract (55) and with a marked increase in the number
of mature cells in the lung parenchyma (56). This is an indication that the
lung response to cigarette-smoke exposure follows the established immune
