The ACE inhibitors enalapril and captopril modulate cytokine responses in Balb/c and C57Bl/6 normal mice and increase CD4+CD103+CD25negative splenic T cell numbers
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Abstract
Increasing evidence implies beneficial effects of angiotensin-converting enzyme (ACE)
inhibitors beyond those of their original indications to control hypertension. One
of the most attractive non-hemodynamic properties of ACE inhibitors is their ability
to regulate cytokine production. The mechanism(s) underlying the role of ACE inhibitors
on cytokine synthesis are not well understood but they have traditionally been attributed
to the inhibition of angiotensin (Ang) II formation. In fact, it has been extensively
demonstrated that ACE inhibitors decrease Ang II-induced production of proinflammatory
cytokines and chemokines. However, it is not well described if inhibition of endogenous
Ang II generation by ACE inhibitors modulates systemic cytokine production in mice.
To verify that, in this work, we investigated the effects of treatment with the ACE
inhibitors enalapril and captopril on cytokine synthesis in C57Bl/6 and Balb/c mice.
Our results show that enalapril up regulates IL-10 produced by splenocytes from Balb/c
and C57Bl/6 mice and captopril increased it only in Balb/c mice. Furthermore, CD4(+)CD103(+)
presented increased IL-10 production after enalapril treatment. Enalapril as well
as captopril short-term treatment enhanced IL-2 synthesis in Balb/c mice. Besides,
enhanced IL-2 and IL-10 levels correlates with increased CD4(+)CD103(+)CD25(negative)
T cells numbers in spleens from enalapril-treated mice.