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Review
. 2006 Aug;118(2):295-302; quiz 303-4.
doi: 10.1016/j.jaci.2006.05.025.

Respiratory viral infections drive chemokine expression and exacerbate the asthmatic response

Matthew Schaller  1 , Cory M Hogaboam, Nicholas Lukacs, Steven L Kunkel
Affiliations
Review

Respiratory viral infections drive chemokine expression and exacerbate the asthmatic response

Matthew Schaller et al. J Allergy Clin Immunol. 2006 Aug.

Abstract

A number of investigations have linked respiratory viral infections and the intensity and subsequent exacerbation of asthma through host response mechanisms. For example, it is likely that the immune-inflammatory response to respiratory syncytial virus can cause a predisposition toward an intense inflammatory reaction associated with asthma, and adenovirus might cause exacerbation of the immune response associated with chronic obstructive pulmonary disease. In each of these situations, the host's immune response plays a critical mechanistic role through the production of certain cytokines and chemokines. Specific aspects of these augmented immune responses are determined by the biology of the virus, the genetic variability of the host, and the cytokine-chemokine phenotype of the involved tissue. For instance, the type 1/type 2 cytokine ratio in the airways during infection with rhinovirus determines how long the viral infection endures. By this same theory, it has been demonstrated that chemokine levels produced during respiratory syncytial virus infection determine host responses to later immune stimuli in the lung, with the potential to augment the asthmatic response. Further research in this area will clarify cytokines, chemokines, or cell targets, which will provide the basis for next-generation therapies.

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Figures

Fig 1
Fig 1
Chemokine profiles of epithelial cells and PBMCs infected with various respiratory viruses. The production of CCL3, CCL5, CCL11, and CXCL8 is depicted with respect to infection with 4 different respiratory viruses. References to relevant research are included in the tables.
Fig 2
Fig 2
The various biologic activities of chemokines can contribute to the pathology associated with respiratory virus–exacerbated asthma, including (1) effect on epithelial cells, (2) induction of cell proliferation, (3) matrix deposition, and (4) recruitment of specific leukocyte populations to the lungs.
Fig 3
Fig 3
Chemokines play an important role in respiratory virus–induced asthma because they provide one of the mechanisms for the successful delivery of specific blood borne leukocytes to the airways of the lung. In particular, CCL11 (eotaxin), CCL5 (RANTES), and CCL3 (macrophage inflammatory protein 1α) and their respective receptors CCR3, CCR1, and CCR5 have been identified as important to the exacerbation of experimentally induced asthma.
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