Sepsis-induced lung inflammation is modulated by insulin.

Abstract:

BACKGROUND:We have previously shown that diabetic rats are more susceptible to sepsis, but that the Acute lung injury (ALI) secondary to sepsis is less intense than in non-diabetics. In the present study, we further investigated the ALI-secondary to sepsis in diabetic rats and the effect of insulin treatment. METHODS:Diabetes was induced in male Wistar rats by alloxan and sepsis by cecal ligation and puncture surgery (CLP). Some diabetic rats were given neutral protamine Hagedorn (NPH) insulin (4 IU, s.c.) 2 h before CLP. Six h later, the lungs were examined for edema, cell infiltration and prostaglandin-E2 (PGE2) levels in the bronchoalveolar lavage (BAL). RESULTS:The results confirmed that leukocyte infiltration and edema were milder in diabetic rats with sepsis. After insulin treatment, the lung inflammation in diabetics increased to levels comparable to the non-diabetics. The BAL concentration of PGE2 was also lower in diabetics with sepsis, and increased after insulin treatment. Sepsis was followed by early fibroblast activation in the lung parenchyma, evaluated by increased transforming growth factor (TGF)-β and smooth muscle actin (α-SMA) expression, as well as an elevated number of cells with myofibroblasts morphology. These events were significantly lower in diabetic rats and increased after insulin treatment. CONCLUSION:The results show that insulin modulates the early phase of inflammation and myofibroblast differentiation in diabetic rats.

journal_name

BMC Pulm Med

journal_title

BMC pulmonary medicine

authors

Filgueiras LR,Capelozzi VL,Martins JO,Jancar S

doi

10.1186/1471-2466-14-177

subject

Has Abstract

pub_date

2014-11-15 00:00:00

pages

177

issn

1471-2466

pii

1471-2466-14-177

journal_volume

14

pub_type

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