There is increasing evidence that obesity is a proinflammatory state (33). Initial studies have focused mainly on the association of obesity and tumor necrosis factor (TNF), IL-6, IL-1P, and C-reactive protein. IL-6 and TNF are constitutively expressed by adipocytes and correlate with total fat mass. TNF is increased in asthma, and it increases further with allergen exposure. Thus, the TNF inflammatory pathway is common to both obesity and asthma, and it is plausible that it is upregulated by the presence of both conditions (28,29).
Recent research shows that in obese humans, even in the absence of any overt inflammatory insult, there is chronic, low-grade systemic inflammation characterized by increased circulating leukocytes and increased serum concentration of cytokines, cytokine receptors, chemokines, and acute-phase proteins (34). Similar results are obtained in obese mice. The origin of this inflammation appears to be, at least in part, the adipose tissue itself, because expression of a variety of inflammatory genes is upregulated in adipose tissue from obese humans or mice. The cellular source of some of these factors appear to be macrophages that infiltrate adipose tissue (35,36). Systemic inflammatory markers in humans correlate with the presence of diseases common to obesity, including type 2 diabetes and atherosclerosis, suggesting that the inflammation is functionally important. Obese Cpefat mice display innate airway hyper-responsiveness, as well as increased airway responsiveness and inflammation following ozone (O3) exposure. These increased effects of O3 appear to be independent of changes in lung volume or lung mass, suggesting that obesity augments the airway response to O3 in mice (34).
Adiponectin is one of the most abundant gene products in adipose tissue. In contrast with many of the other adipokines, the levels of which rise in obesity, plasma adiponectin levels are decreased in obesity, and levels increase following weight loss. The predominant metabolic effects of adiponectin are in the liver and in skeletal muscle and include increased glucose uptake, inhibition of gluconeogenesis, and increased fatty acid oxidation (37). Adiponectin also has anti-inflammatory properties. Pertaining to asthma, adiponectin inhibits proliferation and migration of cultured vascular smooth muscle cells induced by mitogens (38). It will be important to determine whether adiponectin has similar effects on airway smooth muscles (ASM), especially because both the AdipoR1 and AdipoR2 receptors are expressed in cultured human ASM cells. In this context, it should be noted that increased ASM mass is a feature of human asthma, and modeling studies have shown that increased muscle mass alone can account for a large part of the AHR of asthma. Taken together, the anti-inflammatory effects of adiponectin and the possibility that adiponectin may have antimitogenic effects on ASM suggest that the decreased serum concentration of adiponectin observed in the obese may contribute to the propensity toward AHR in this population (29).
There are also limited data showing greater systemic inflammation in obese vs lean asthmatics, as measured by serum amyloid A, fibrinogen, and C-reactive protein (39). Such changes are to be expected because levels of these acute-phase proteins are also elevated in nonasthmatic obese versus lean subjects. However, in some cases, obese asthmatics had higher serum acute-phase proteins than lean asthmatics even after correction for BMI, suggesting that systemic as well as airway inflammation exists in asthma (29).
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