Altered release of chemokines by phagocytes from fibromyalgia patients: a pilot study

Abstract

Fibromyalgia (FM) is a syndrome characterized by widespread chronic pain and is associated with elevated systemic inflammatory biomarkers, and an elevated innate cellular response. The aim of this study was to determine if fibromyalgia patients have altered ability to release pro-inflammatory chemokines by isolated neutrophils and monocytes. The study participants were women diagnosed with FM (n ¼ 6) and a control group of healthy women (HW) (n ¼ 6). Supernatant concentrations of eotaxin (CCL11), human macrophage-derived chemokine (MDC) (CCL22) and growth regulatedoncogene (GRO-a) (CXCL1) released by both monocytes and neutrophils either resting or stimulated by LPS were determined by ELISA and compared between the FM and HW groups. Both resting and activated monocytes from FM patients released more eotaxin, MDC and GRO-a than those from HW. However, there were no significant differences in the release of chemokines from neutrophils of FM patients and the ones from healthy women. In conclusion, monocytes from women with FM are deregulated, releasing higher amounts of eotaxin, MDC and GRO-a than healthy individuals. This fact does not occur in neutrophils from women with FM.

Value of Circulating Cytokine Profiling During Submaximal Exercise Testing in Myalgic Encephalomyelitis/Chronic Fatigue Syndrome

“…CXCL1 also demonstrated high relative centrality within the network participants with ME/CFS. Interestingly, increased CXCL1 production by neutrophils has been seen in patients with fibromyalgia, however, considering the small numbers within the studies, these findings should be considered exploratory and further investigation is required to define their clinical implications 20 .…”

Natural product HTP screening for attenuation of cytokine-induced neutrophil chemo attractants (CINCs) and NO2− in LPS/IFNγ activated glioma cells

“…Inflammatory processes occurring within CNS (by glial cells) contribute vulnerability by initiating vascular damage (Doyle et al, 2015, Weaver et al, 2010) neurological insult (Bodnar et al, 2015, Garcia et al, 2016) and destruction to the blood brain barrier (BBB). (Adelson et al, 1998) While CNS glial cells exert an influential role in neurodevelopment, neuronal homeostasis and CNS detoxification, on the flip side, detrimental inflammatory processes can arise from head trauma (Lopez-Rodriguez et al, 2015), ischemia (Li et al, 2015c) infection (Ben Haim et al, 2015a) lysosomal storage diseases (Rama Rao and Kielian, 2015) and protein aggregates of amyloid β (Aβ) (Ben Haim, Carrillo-de Sauvage, 2015a) and α-synuclein A53T (Ben Haim, Carrillo-de Sauvage, 2015a, Yang et al, 2015) common to AD and PD, respectively.…”

Pain and the biochemistry of fibromyalgia: patterns of peripheral cytokines and chemokines contribute to the differentiation between fibromyalgia and controls and are associated with pain, fat infiltration and content

“…The two most important chemokines were MDC/CCL22 and MIP-1α/CCL3 ( Supplementary Table 8 , right part). The pro-inflammatory chemokine MDC/CCL22 is increased in serum and in monocytes from FM patients, ( 83 , 147 ); increased levels were also found in ischemic heart disease ( 148 ). MIP - 1 α /CCL3 was also important for group differentiation, IL - 1 - Ra was a significant regressor of pain intensity in FM, and M - CSF/CSF - 1 was important for PPT (see above).…”