Acta Med. 2013, 56: 57-66

https://doi.org/10.14712/18059694.2014.25

TLR2 AND TLR4 EXPRESSION ON BLOOD MONOCYTES AND GRANULOCYTES OF CARDIAC SURGICAL PATIENTS IS NOT AFFECTED BY THE USE OF CARDIOPULMONARY BYPASS

Jan Krejseka, Martina Koláčkováa, Jiří Manďákb, Pavel Kunešb, Zdeňka Holubcováb, Drahomíra Holmannováa, Mouhammed AbuAttieha, Ctirad Andrýsa

aCharles University in Prague, Faculty of Medicine and University Hospital in Hradec Králové, Czech Republic: Department of Clinical Immunology
bCharles University in Prague, Faculty of Medicine and University Hospital in Hradec Králové, Czech Republic: Department of Cardiac Surgery

Cardiac surgery is inseparably linked to the activation of innate immunity cells recognizing danger signals of both endogenous and exogenous origin via pattern recognition receptors such as TLR receptors. Therefore, we followed by flow cytometry TLR2 and TLR4 expression on blood monocytes and granulocytes of patients who underwent coronary artery bypass grafting using beating heart surgery (off-pump, n = 34), with use of standard cardiopulmonary bypass (CPB), (on-pump, n = 30), and miniinvasive CPB (mini on-pump, n = 25), respectively, before, during surgery, and up to 7th postoperative day. TLR2 and TLR4 expression both on monocytes and granulocytes was significantly diminished already at the end of CPB being highly significantly decreased at the end of surgery in all patients’ groups. TLR2 and TLR4 expression reached preoperative value at the 1st postoperative day being significantly higher at the 3rd postoperative day. Using intracellular staining we found the peak of TLR2 and TLR4 expression inside of monocytes and granulocytes at the first postoperative day in a subgroup of on-pump patients. In conclusion, TLR2 and TLR4 expression is significantly modulated in patients undergoing coronary artery bypass grafting as a part of adaptive homeostatic mechanisms induced by major surgery. The very surgical trauma is responsible for TLR2 and TLR4 modulation. Surprisingly, cardiopulmonary bypass itself was little contributing to the modulation of TLR2 and TLR4 expression.

References

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