Neutrophilic Inflammation in the Immune Responses of Chronic Obstructive Pulmonary Disease: Lessons from Animal Models
Table 1
Acute tobacco smoke exposure.
Treatment
Time
Response
Reference
Twice a day, 1 hour per section, 3 days
3 days
The numbers of neutrophils and the levels of proinflammatory mediators, keratinocyte chemoattractant (KC), macrophage inflammatory protein 2 (MIP-2), and interleukin 1 beta (IL-1β) are all increased in bronchoalveolar lavage fluid (BALF).
Acute exposure to cigarette smoke causes oxidative stress and increases the counts of leukocytes and macrophages and the levels of several proinflammatory cytokines, such as tumor necrosis factor alpha (TNF-α), IL-1β, interleukin 6 (IL-6), and KC.
Acute exposure to cigarette smoke increases the number of total cells, neutrophils, macrophages, and lymphocytes in BALF and increases the levels of KC and monocyte chemotactic protein 1 (MCP-1).
The numbers of mobilizing neutrophils and differentiating macrophages are significantly increased in BALF, and the levels of IL-1β, IL-6, interferon gamma (IFN-γ), TNF-α, and MCP-1 in BALF and lung are also increased.