Background Surfactant protein-D (SP-D) belongs to the collectin family of the innate immune system. It has pro- and anti-inflammatory activities according to its oligomerization. Microbial opsonization and scavenging of nuclear debris are among its important properties. Serum SP-D exhibits a biphasic course with acute bacterial infections and increases during flares of COPD. Conversely, in rheumatoid arthritis (RA) we recently reported that individuals with newly diagnosed disease had subnormal circulating levels of SP-D at baseline and 4 years on despite a treatment to target strategy. In addition we found that SP-D and CRP were inversely correlated at baseline suggesting that SP-D is implicated in the RA pathogenesis. Spondyloarthritis (SpA) and psoriatic arthritis (PsA) are chronic and usually seronegative arthritides belonging to the SpA complex. The etiopathogenesis is incompletely understood although there is evidence for an effect of genes and environmental triggers, HLA-B27 and bacterial antigens in particular. The present investigation was conducted to extend our previous studies on SP-D in RA by assessing the pattern of SP-D expression in serum among patients with SpA and PsA.
Objectives To compare the serum level of SP-D in SpA and PsA with that in healthy controls.
Methods Patients with SpA according to the ASAS criteria, age 18-63 years (n=108) and PsA patients fulfilling the CASPAR criteria, age 21-53 years (n=98) were included. Demographic and clinical disease measures were recorded including HAQ, BAS and hs-CRP. Healthy twin individuals, age 18-67 years (n=1476) served as controls. SP-D in serum was quantified by ELISA. SP-D was compared across patient groups and with controls using non parametric statistics. Stepwise multiple linear regression with a significance level of 0.05 was performed to study associations between SP-D, patient characteristics and disease activity measures. The model fit was assessed using appropriate residual and goodness of fit statistics.
Results SP-D did not differ between patients with SpA, 1054 ng/ml (677;1462 p=0.23) and PsA patients, 962 ng/ml (730;1506 p=0.57) or healthy controls, 913 ng/ml (680;1387). Linear regression analysis showed that SP-D was positively associated with sex, patient global (VAS) and negatively associated with BMI and hs-CRP in SpA. By contrast, SP-D was only associated with smoking in PsA patients (Table).
Conclusions Serum SP-D did not differ between patients with SpA, PsA and healthy controls. However, while SP-D did not associate with disease activity measures in PsA, SP-D correlated positively with clinical disease activity, and negatively with hs-CRP in axial SpA. These distinctive association profiles may relate to underlying pathogenetic disparities. The negative association between SP-D and hs-CRP in SpA may reflect that SP-D and hs-CRP are regulated in a coordinated manner, increased consumption or complex formation with inflammatory debris in active disease.
Disclosure of Interest : None declared
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