A +1444 C>T polymorphism in the CRP gene has been associated with differences in CRP concentration. These results suggest that CRP, although not an initiating insult in ARDS, may contribute to the subsequent abnormalities of surfactant function and thus the pathogenesis of the pulmonary dysfunction seen in ARDS.« lessĬ-reactive protein (+1444 C>T) polymorphism influences CRP response following a moderate inflammatory stimulus.ĭ'Aiuto, Francesco Casas, Juan P Shah, Tina Humphries, Steve E Hingorani, Aroon D Tonetti, Maurizio SĮlevations in C-reactive protein ( CRP) concentration are associated with an increased risk of future coronary events in prospective studies and it has been suggested that CRP could be used to aid risk prediction. In contrast, human serum albumin (HSA) at 500 and 900 micrograms/ml had no inhibitory effect on Surfactant TA surface activity. Furthermore, the surface activity of a clinically used surfactant replacement, Surfactant TA (2 mg/ml), was also severely impaired by CRP in a dose-dependent manner (doses used ranging from 24.5 to 1,175 micrograms/ml). As a result of this interaction, CRP inhibits the surface activity of a PG-DPPC mixture when tested with a Wilhelmy surfactometer or with the Enhorning pulsating bubble apparatus. Our results show that CRP binds to liposomes containing DPPC and phosphatidylglycerol (PG). 4.04more » +/- 2.2 micrograms/mg total protein in normals). ![]() Our results showed that CRP levels in the bronchoalveolar fluid (BALF) was increased in patients with ARDS (97.8 +/- 84.2 micrograms/mg total protein vs. The structural homology between PC and the major phospholipid component of surfactant, dipalmitoyl phosphatidylcholine (DPPC), led to the present study in which we examined if CRP levels might be increased in patients with adult respiratory distress syndrome (ARDS), and subsequently interfere with surfactant function. CRP binds to phosphorylcholine (PC) in a calcium-ion dependent manner. Plasma levels of the acute-phase reactant, C-reactive protein ( CRP), increase up to one thousand-fold as a result of trauma or inflammation. Impact of C-reactive protein ( CRP) on surfactant function This might constitute another level of complement regulation, which has implications for systemic lupus erythematosus where CRP is often low despite flare-ups.« less We propose that the underlying mechanism depends on fluid-phase interaction between C1q and CRP. Using radial immunodiffusion, CRP-C1q interaction was observed in serum samples with high CRP concentrations. Unexpectedly, the activation was efficientlymore » down-regulated at CRP levels >150 mg/L. The binding of serum CRP to PC-KLH dose-dependently triggered activation of the classical pathway. The total serum protein deposition was quantified and deposition of IgG, C1q, C3 c, C4, factor H, and CRP detected with polyclonal antibodies. A low- CRP serum with different amounts of added CRP was exposed to the PC-surfaces. PC conjugated with keyhole limpet hemocyanin (PC-KLH) was immobilized to cross-linked fibrinogen. The aim was to characterize CRP-induced complement activation by ellipsometry. Sjoewall, Christopher Wetteroe, Jonas Bengtsson, TorbjoernĬ-reactive protein ( CRP) interacts with phosphorylcholine (PC), Fc receptors, complement factor C1q and cell nuclear constituents, yet its biological roles are insufficiently understood. Solid-phase classical complement activation by C-reactive protein ( CRP) is inhibited by fluid-phase CRP-C1q interactionĭOE Office of Scientific and Technical Information (OSTI.GOV)
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