Keseimbangan Sitokin Th1/Th2 Berperan Dalam Proliferasi Mastosit Jaringan Paru Pasca Pemberian Diet Tinggi Lemak pada Tikus
ABSTRACT: Asthma and obesity
are prevalent disorders, each with a significant public health impact, and a
large and growing body of literature suggests an association between the two.
The systemic inflammatory milieu in obesity leads to metabolic and
cardiovascular complications but this environment alters asthma risk or phenotype
is not yet known. Studies that evaluated the effects of leptin and obesity on
airway inflammation in response suggest that air way inflammation is enhanced
by leptin. Leptin is stimulate a Th1 cytokine profile and suppresses Th2
cytokine production. Whether resistance to the effects of the lung or on immune
function is unknown, but such resistance might be expected to polarize to a
Th2. The aim of this study is identify effect of leptin to lung mast cell
proliferation via shifting Th1/Th2 balance using diet-induced obese mice.
Because there are contradictive between leptin immune function in leptin
deficient and obese, to understand the effect of leptin in diet-induced obese
mice on immune function, lung mast cell proliferation and correlation with IL-4
as represent cytokine Th2 and IL-2 represent cytokine Th1 has been studied.To induced
obesity, wistar mice (Rattus novergicus) were fed high-fat diet for 12 weeks,
and control mice were fed standard diet for the same period. The result
suggested that the action of leptin in obese mice in vivo is differ from leptin
function on lymphocyte in vitro. These findings provide some evidence that
leptin can regulate the immune function in vivo, and suggest the role of leptin
on asthma pathophysiology.
Penulis: Rita Rosita, Muhamad
Rasjad Indra, Edi Widjajanto
Kode Jurnal: jpkedokterandd090140
