Department of Pharmacology and Toxicology, Faculty of Veterinary Medicine, University of Warmia and Mazury, Oczapowski Street 13, 10-718 Olsztyn, Poland.
Res Vet Sci. 2013 Jun;94(3):662-74. doi: 10.1016/j.rvsc.2012.12.005. Epub 2012 Dec 31.
The aim of undertaken research was an in vitro evaluation of the effects of dexamethasone and meloxicam on selected bovine CD8(+) T lymphocyte subpopulations. Dexamethasone induced a fast-occurring and lasting depletion of CD25(-)CD8(+) cells. This was primarily the result of the proapoptotic effect of dexamethasone, but the antiproliferative effect of the drug was clearly responsible for the deepening of this disturbance. Dexamethasone transiently increased the relative and absolute CD25(high)CD8(+) and CD25(low)CD8(+) cell numbers. This effect was not a consequence of increased proliferation, but at least partly resulted from the antiapoptotic effect of the drug on these cells. The obtained results indicate that induction of CD8(+) lymphocyte depletion and impairment of IFN-γ production by these cells participate in the production of the anti-inflammatory and immunosuppressive effect of dexamethasone in cattle. An increase in Foxp3, IL-10 and TGF-β production by CD8(+) lymphocytes is not involved in the production of these effects because the drug did not affect the percentage of TGF-β(+)CD8(+) cells, while paradoxically reducing the percentage of cells with the suppressive phenotype, i.e. IL-10(+)CD25(low)CD8(+) and Foxp3(+)CD25(low)CD8(+) cells. Meloxicam did not substantially affect CD8(+) lymphocytes as to their percentage, absolute number, apoptosis, proliferation, Foxp3 expression and IFN-γ, IL-10 and TGF-β production. Thus, in the context of the parameters being estimated, meloxicam seems a relatively safe anti-inflammatory drug to be used in infectious diseases in cattle.
本研究的目的是体外评估地塞米松和美洛昔康对牛 CD8(+)T 淋巴细胞亚群的影响。地塞米松诱导 CD25(-)CD8(+)细胞快速耗竭并持续存在。这主要是地塞米松诱导细胞凋亡的结果，但药物的抗增殖作用显然是导致这种紊乱加深的原因。地塞米松短暂增加 CD25(high)CD8(+)和 CD25(low)CD8(+)细胞的相对和绝对数量。这种作用不是由于细胞增殖增加引起的，而是至少部分是由于药物对这些细胞的抗凋亡作用。所得结果表明，牛体内地塞米松诱导 CD8(+)淋巴细胞耗竭和损害这些细胞产生 IFN-γ的能力参与了地塞米松的抗炎和免疫抑制作用的产生。CD8(+)淋巴细胞中 Foxp3、IL-10 和 TGF-β的产生增加不参与这些作用的产生，因为该药物不影响 TGF-β(+)CD8(+)细胞的百分比，而矛盾的是降低了具有抑制表型的细胞的百分比，即 IL-10(+)CD25(low)CD8(+)和 Foxp3(+)CD25(low)CD8(+)细胞。美洛昔康对 CD8(+)淋巴细胞的百分比、绝对数量、凋亡、增殖、Foxp3 表达以及 IFN-γ、IL-10 和 TGF-β的产生没有明显影响。因此，在所评估的参数范围内，美洛昔康似乎是一种相对安全的抗炎药物，可用于牛的感染性疾病。
