CD11b expression on polymorphonuclear leukocytes from patients with ankylosing spondylitis in a lipopolysaccharide-stimulated whole blood ex vivo model.

Aim: Ankylosing spondylitis (AS) is a chronic inflammatory disease that compromises the axial skeleton, causing pain and disability. The involved mechanisms are not completely understood, but evidence suggests a role of the gut microbiota in eliciting innate immune responses. We conducted an experimental study to determine if AS patients exhibit an enhanced inflammatory response to microbial compounds.

Method: We incubated whole peripheral blood of AS patients and healthy controls with phosphate-buffered saline (PBS) or lipopolysaccharide (LPS) for 48 h with saturating levels of labeled antibodies (CD66b, CD11b and human leukocyte antigen type DR [HLA-DR]) for flow cytometry. CD11b and HLA-DR expression levels were assessed in polymorphonuclear leukocytes (PMN) (CD66b high - HLA-DR low). We also measured basal CD11b and HLA-DR levels on circulating PMN (without incubation).

Results: We found that CD11b and HLA-DR levels were similarly elevated in response to LPS on PMNs from healthy controls (HC) and AS patients. Basal levels of CD11b and HLA-DR on circulating PMN from AS patients and HC were similar. However, significantly lower levels of CD11b and HLA-DR were observed in PMNs from AS patients than HC in response to incubation with PBS for 48 h.

Conclusion: We concluded that the response of AS innate immune cells to LPS is similar to that observed in immune cells from HCs, and suggested that the lower PMN activation of AS patients after 48 h saline incubation is mainly due to anti-inflammatory medication.