Chemokines in COPD

Barnes, Peter J.; Stockley, Robert A.; Rennard, Stephen I.; Rabe, Klaus F.; Celli, Bartolomé R.

doi:10.1002/9780470755976.ch70

Cited by 1 publication

(1 citation statement)

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“…An accumulation of inflammatory cells such as neutrophils, macrophages, dendritic cells and CD8+ T lymphocytes is seen, although the cellular and molecular pathways behind this increased cellular influx are still incompletely unraveled. However, CC-chemokines (MIP-1alpha, MIP-3alpha, RANTES and MCP-1) [ 6 ] and CXC-chemokines (IL-8, GCP-2) [ 7 ], binding to their respective receptors play an important role. Moreover, the role of lymphocytes in the development of COPD is demonstrated by the fact that chronic cigarette smoke (CS) exposure leads to an increase in peribronchial lymphoid follicles in both mice and humans [ 8 , 9 ], although the importance of these lymphoid follicles remains unclear [ 10 ].…”

Section: Introductionmentioning

confidence: 99%

Different regulation of cigarette smoke induced inflammation in upper versus lower airways

et al. 2010

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BackgroundCigarette smoke (CS) is known to initiate a cascade of mediator release and accumulation of immune and inflammatory cells in the lower airways. We investigated and compared the effects of CS on upper and lower airways, in a mouse model of subacute and chronic CS exposure.MethodsC57BL/6 mice were whole-body exposed to mainstream CS or air, for 2, 4 and 24 weeks. Bronchoalveolar lavage fluid (BAL) was obtained and tissue cryosections from nasal turbinates were stained for neutrophils and T cells. Furthermore, we evaluated GCP-2, KC, MCP-1, MIP-3α, RORc, IL-17, FoxP3, and TGF-β1 in nasal turbinates and lungs by RT-PCR.ResultsIn both upper and lower airways, subacute CS-exposure induced the expression of GCP-2, MCP-1, MIP-3α and resulted in a neutrophilic influx. However, after chronic CS-exposure, there was a significant downregulation of inflammation in the upper airways, while on the contrary, lower airway inflammation remained present. Whereas nasal FoxP3 mRNA levels already increased after 2 weeks, lung FoxP3 mRNA increased only after 4 weeks, suggesting that mechanisms to suppress inflammation occur earlier and are more efficient in nose than in lungs.ConclusionsAltogether, these data demonstrate that CS induced inflammation may be differently regulated in the upper versus lower airways in mice. Furthermore, these data may help to identify new therapeutic targets in this disease model.

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