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Cited by 84Fibromyalgia and Chronic Fatigue Syndrome ResearchPain Mechanisms and TreatmentsPsychosomatic Disorders and Their Treatments

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Fibromyalgia patients with elevated levels of anti–satellite glia cell immunoglobulin G antibodies present with more severe symptoms

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Krock, Emerson, Morado-Urbina, Carlos E., Menezes, Joana, Hunt, Matthew A., Sandström, Angelica, Kadetoff, Diana, Tour, Jeanette, Verma, Vivek, Kultima, Kim, Haglund, Lisbet, Meloto, Carolina B., Diatchenko, Luda, Kosek, Eva, Svensson, Camilla I.·2023·Pain
DOI 10.1097/j.pain.0000000000002881PMC PMC10348624
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Abstract

Transferring fibromyalgia patient immunoglobulin G (IgG) to mice induces pain-like behaviour, and fibromyalgia IgG binds mouse and human satellite glia cells (SGCs). These findings suggest that autoantibodies could be part of fibromyalgia pathology. However, it is unknown how frequently fibromyalgia patients have anti-SGC antibodies and how anti-SGC antibodies associate with disease severity. Here, we quantified serum or plasma anti-SGC IgG levels in 2 fibromyalgia cohorts from Sweden and Canada using an indirect immunofluorescence murine cell culture assay. Fibromyalgia serum IgG binding to human SGCs in human dorsal root ganglia tissue sections was also assessed by immunofluorescence. In the cell culture assay, anti-SGC IgG levels were increased in both fibromyalgia cohorts compared with control group. Elevated anti-SGC IgG was associated with higher levels of self-reported pain in both cohorts, and higher fibromyalgia impact questionnaire scores and increased pressure sensitivity in the Swedish cohort. Anti-SGC IgG levels were not associated with fibromyalgia duration. Swedish fibromyalgia (FM) patients were clustered into FM-severe and FM-mild groups, and the FM-severe group had elevated anti-SGC IgG compared with the FM-mild group and control group. Anti-SGC IgG levels detected in culture positively correlated with increased binding to human SGCs. Moreover, the FM-severe group had elevated IgG binding to human SGCs compared with the FM-mild and control groups. These results demonstrate that a subset of fibromyalgia patients have elevated levels of anti-SGC antibodies, and the antibodies are associated with more severe fibromyalgia symptoms. Screening fibromyalgia patients for anti-SGC antibodies could provide a path to personalized treatment options that target autoantibodies and autoantibody production.

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Figures

Figure 1. Fibromyalgia serum contains elevated levels of IgG that are reactive with satellite glia cells. Satellite glia cell–enriched cell cultures were incubated with serum from fibromyalgia (FM) or healthy control (HC) individuals and then stained for glutamine synthase (GS), a marker of SGCs. (A) Representative images of cultures incubated with FM or healthy control serum where human IgG is red and GS is green. (B) The percentage of SGCs that were bound by human IgG was determined for each serum sample tested. (C) The integrated density of IgG, as a measure of pixel intensity, was determined for each SGC that was imaged, and then, the mean integrated density was calculated for each serum sample. (D) Total IgG serum titres did not differ between the groups. Scale bar is 50 μm. N = 30 (FM) or 29 (HC); the difference between the percentage of IgG-positive cells was determined with a Mann–Whitney test, and the difference between integrated density was determined with a 2-tailed t test. Experimenters were blind to serum type during imaging and analysis. *Indicates P < 0.05, **indicates P < 0.01. SGC, satellite glia cell.
Figure 1. Fibromyalgia serum contains elevated levels of IgG that are reactive with satellite glia cells. Satellite glia cell–enriched cell cultures were incubated with serum from fibromyalgia (FM) or healthy control (HC) individuals and then stained for glutamine synthase (GS), a marker of SGCs. (A) Representative images of cultures incubated with FM or healthy control serum where human IgG is red and GS is green. (B) The percentage of SGCs that were bound by human IgG was determined for each serum sample tested. (C) The integrated density of IgG, as a measure of pixel intensity, was determined for each SGC that was imaged, and then, the mean integrated density was calculated for each serum sample. (D) Total IgG serum titres did not differ between the groups. Scale bar is 50 μm. N = 30 (FM) or 29 (HC); the difference between the percentage of IgG-positive cells was determined with a Mann–Whitney test, and the difference between integrated density was determined with a 2-tailed t test. Experimenters were blind to serum type during imaging and analysis. *Indicates P < 0.05, **indicates P < 0.01. SGC, satellite glia cell.CC BY · PubMed Central
Figure 2. Fibromyalgia plasma contains elevated levels of SGC-reactive IgG in a validation cohort, but osteoarthritis serum does not. SGC-enriched cultures were incubated with plasma collected from a regionally distinct FM cohort. (A) Representative images of cultures where human IgG is red and glutamine synthase (GS) is green. (B) The percentage of human IgG + SGCs and (C) the integrated density (intensity) of IgG binding to SGCs were determined. (D) Total IgG plasma titres did not differ between the groups. (E) SGC-enriched cultures were incubated with serum from osteoarthritis (OA) and HC individuals. (F) The percentage of IgG + SGCs and (G) binding intensity were determined. (H) Total IgG serum titres did not differ between the groups. (I) The percentage of IgG + SGCs and (J) the binding intensity were compared between the FM and OA cohorts. Scale bar is 50 μm. N = 36 (McGill FM), 34 (McGill HC), 10 (OA), or 30 (Karolinska FM). Percentages were assed using a Mann–Whitney test (B and F) or a Kruskal–Wallis test followed by Dunn post hoc test (H). Intensities were analyzed by 2-tailed t-tests (C and G) or a 1-way ANOVA followed by Tukey post hoc test. Experimenters were blind to serum or plasma type during imaging and analysis. *indicates P < 0.05, **indicates P < 0.01, ***indicates P < 0.001. ANOVA, analysis of variance; FM, fibromyalgia; HC, healthy control; SGC, satellite glia cell.
Figure 2. Fibromyalgia plasma contains elevated levels of SGC-reactive IgG in a validation cohort, but osteoarthritis serum does not. SGC-enriched cultures were incubated with plasma collected from a regionally distinct FM cohort. (A) Representative images of cultures where human IgG is red and glutamine synthase (GS) is green. (B) The percentage of human IgG + SGCs and (C) the integrated density (intensity) of IgG binding to SGCs were determined. (D) Total IgG plasma titres did not differ between the groups. (E) SGC-enriched cultures were incubated with serum from osteoarthritis (OA) and HC individuals. (F) The percentage of IgG + SGCs and (G) binding intensity were determined. (H) Total IgG serum titres did not differ between the groups. (I) The percentage of IgG + SGCs and (J) the binding intensity were compared between the FM and OA cohorts. Scale bar is 50 μm. N = 36 (McGill FM), 34 (McGill HC), 10 (OA), or 30 (Karolinska FM). Percentages were assed using a Mann–Whitney test (B and F) or a Kruskal–Wallis test followed by Dunn post hoc test (H). Intensities were analyzed by 2-tailed t-tests (C and G) or a 1-way ANOVA followed by Tukey post hoc test. Experimenters were blind to serum or plasma type during imaging and analysis. *indicates P < 0.05, **indicates P < 0.01, ***indicates P < 0.001. ANOVA, analysis of variance; FM, fibromyalgia; HC, healthy control; SGC, satellite glia cell.CC BY · PubMed Central
Figure 3. Fibromyalgia and osteoarthritis patients do not have elevated levels of sensory neuron binding IgG. Dorsal root ganglia neuron–enriched/satellite glia cell depleted cultures were incubated with serum from FM patients (A), plasma from FM patients (D), serum from osteoarthritis (OA) patients, or corresponding healthy control individuals (HC). (A, D, G) Neurons were identified by PGP 9.5 immunoreactivity (green); IgG binding was detected using an antihuman IgG antibody (red), and cultures were counterstained with Hoechst (blue). The percentage of neurons bound by IgG (B, E, H) and the intensity of the binding to neurons assessed by integrated density (C, F, I) were determined. Scale bar is 50 μm. In (A–C), n = 30 (FM) and 29 (HC); in (D–F), n = 36 (McGill FM) and 34 (McGill HC); in (G and H), n = 10 (OA and matched HC). Differences in percentages were determined using a Mann–Whitney test, and differences in intensity were determined using 2-tailed t-tests. Experimenters were blind to serum type during imaging and analysis. FM, fibromyalgia; PGP, protein gene product.
Figure 3. Fibromyalgia and osteoarthritis patients do not have elevated levels of sensory neuron binding IgG. Dorsal root ganglia neuron–enriched/satellite glia cell depleted cultures were incubated with serum from FM patients (A), plasma from FM patients (D), serum from osteoarthritis (OA) patients, or corresponding healthy control individuals (HC). (A, D, G) Neurons were identified by PGP 9.5 immunoreactivity (green); IgG binding was detected using an antihuman IgG antibody (red), and cultures were counterstained with Hoechst (blue). The percentage of neurons bound by IgG (B, E, H) and the intensity of the binding to neurons assessed by integrated density (C, F, I) were determined. Scale bar is 50 μm. In (A–C), n = 30 (FM) and 29 (HC); in (D–F), n = 36 (McGill FM) and 34 (McGill HC); in (G and H), n = 10 (OA and matched HC). Differences in percentages were determined using a Mann–Whitney test, and differences in intensity were determined using 2-tailed t-tests. Experimenters were blind to serum type during imaging and analysis. FM, fibromyalgia; PGP, protein gene product.CC BY · PubMed Central
Figure 4. Fibromyalgia IgG binding to satellite glia cells positively correlated with pain intensity. Comparisons of (A) age, (B) FM duration, (C) body mass index (BMI) measured as time from diagnosis, (D) maximum pain, and (E) average pain. Pain intensity was assessed with the visual analogue scale (VAS) of pain at Karolinska and with the numeric rating scale (NRS) of pain at McGill. Both scales have a range of 0 to 100. (F) A correlation matrix showing correlations between the percentage of IgG-positive cells and the binding intensity with total IgG levels, age, FM duration, pain duration, and average and maximum pain intensities were examined in FM serum (Karolinska) and plasma (McGill) samples only. The size of the dots and the colour (see colour legend) indicate the Spearman rank correlation coefficient. Only statistically significant correlations (P < 0.05) have coloured dots, whereas correlations that were not significant are blank. Differences in age, BMI, and pain intensity were assessed by 2-way ANOVA followed by Tukey post hoc test. Differences in FM duration were analyzed by a 2-tailed t test. *indicates P < 0.05, ***indicates P < 0.001. N = 30 (Karolinska FM), 36 (McGill FM), 29 (Karolinska HC), 34 (McGill HC), or 66 (FM correlations). ANOVA, analysis of variance; FM, fibromyalgia; HC, healthy control.
Figure 4. Fibromyalgia IgG binding to satellite glia cells positively correlated with pain intensity. Comparisons of (A) age, (B) FM duration, (C) body mass index (BMI) measured as time from diagnosis, (D) maximum pain, and (E) average pain. Pain intensity was assessed with the visual analogue scale (VAS) of pain at Karolinska and with the numeric rating scale (NRS) of pain at McGill. Both scales have a range of 0 to 100. (F) A correlation matrix showing correlations between the percentage of IgG-positive cells and the binding intensity with total IgG levels, age, FM duration, pain duration, and average and maximum pain intensities were examined in FM serum (Karolinska) and plasma (McGill) samples only. The size of the dots and the colour (see colour legend) indicate the Spearman rank correlation coefficient. Only statistically significant correlations (P < 0.05) have coloured dots, whereas correlations that were not significant are blank. Differences in age, BMI, and pain intensity were assessed by 2-way ANOVA followed by Tukey post hoc test. Differences in FM duration were analyzed by a 2-tailed t test. *indicates P < 0.05, ***indicates P < 0.001. N = 30 (Karolinska FM), 36 (McGill FM), 29 (Karolinska HC), 34 (McGill HC), or 66 (FM correlations). ANOVA, analysis of variance; FM, fibromyalgia; HC, healthy control.CC BY · PubMed Central
Figure 5. Level of satellite glia cell–reactive fibromyalgia IgG is associated with disease severity. The Karolinska cohort has expanded phenotypic data; therefore, additional correlations between IgG-positive cells and IgG binding intensity with various characteristics were examined in the FM samples. (A) Correlation matrix showing the relation between anti-SGC levels and additional phenotypic data. The size and colour (see colour legend) of the dots indicate the Spearman rank correlation coefficient, and only statistically significant correlations (P < 0.05) have coloured dots, whereas nonsignificant correlations are blank. The Karolinska FM cohort was divided into 2 groups based on FIQ, average pain intensity, and maximum pain intensity using a k-means cluster analysis. The cluster analysis resulted in a FM severe and a FM mild group (B-I). (J) The percentage of satellite glia cells bound by IgG and (K) the binding intensity were both greater in the FM severe group compared with the FM mild group and the healthy control group (HC). One-way ANOVAs with Tukey post hoc test (C–F, I–K) or 2-tailed t-tests (B, G, H) were used to examine differences between the groups. *indicates P < 0.05, **indicates P < 0.01, ***indicates P < 0.001. ANOVA, analysis of variance; BMI, body mass index; BDI, becks depression inventory; CPM, conditioned pain modulation; FIQ, fibromyalgia impact questionnaire; FM, fibromyalgia; PPT, pressure pain threshold; SGC, satellite glia cell.
Figure 5. Level of satellite glia cell–reactive fibromyalgia IgG is associated with disease severity. The Karolinska cohort has expanded phenotypic data; therefore, additional correlations between IgG-positive cells and IgG binding intensity with various characteristics were examined in the FM samples. (A) Correlation matrix showing the relation between anti-SGC levels and additional phenotypic data. The size and colour (see colour legend) of the dots indicate the Spearman rank correlation coefficient, and only statistically significant correlations (P < 0.05) have coloured dots, whereas nonsignificant correlations are blank. The Karolinska FM cohort was divided into 2 groups based on FIQ, average pain intensity, and maximum pain intensity using a k-means cluster analysis. The cluster analysis resulted in a FM severe and a FM mild group (B-I). (J) The percentage of satellite glia cells bound by IgG and (K) the binding intensity were both greater in the FM severe group compared with the FM mild group and the healthy control group (HC). One-way ANOVAs with Tukey post hoc test (C–F, I–K) or 2-tailed t-tests (B, G, H) were used to examine differences between the groups. *indicates P < 0.05, **indicates P < 0.01, ***indicates P < 0.001. ANOVA, analysis of variance; BMI, body mass index; BDI, becks depression inventory; CPM, conditioned pain modulation; FIQ, fibromyalgia impact questionnaire; FM, fibromyalgia; PPT, pressure pain threshold; SGC, satellite glia cell.CC BY · PubMed Central
Figure 6. Elevated FM IgG binding to human satellite glia cells. (A) Human DRG tissue sections were incubated with serum samples that had high levels or low levels of anti-SGC antibodies detected in mouse DRG–derived SGC cultures. Human SGCs (hSGCs) were identified with an antibody against glial fibrillary acidic protein (GFAP), and neurons were identified with an antibody against NF200. The normalized pixel intensity of serum IgG binding to (B) SGCs, (C) neuronal soma, (D) axons, and (E) GFAP-negative and NF200-negative objects was analyzed. (F) The pixel intensity of IgG binding to hSGCs correlated with the level of anti-SGC antibodies determined in cell culture by the percent of IgG positive mouse SGCs (mSGCs) and the binding intensity (integrated density). The size and colour of the dots indicate the Spearman rank correlation coefficient, and only statistically significant correlations (P < 0.05) have coloured dots, whereas nonsignificant correlations are blank. (G) Individuals in the FM severe group had elevated IgG binding to hSGCs compared with the FM mild group and HC group. One-way ANOVAs with Tukey post hoc test was used to determine differences, and experimenters were blind to serum type during imaging and analysis. *indicates P < 0.05, **indicates P < 0.01, n = 14/group. Scale bar is 50 μm. ANOVA, analysis of variance; DRG, dorsal root ganglia; FM, fibromyalgia; HC, health control; SGC, satellite glia cell.
Figure 6. Elevated FM IgG binding to human satellite glia cells. (A) Human DRG tissue sections were incubated with serum samples that had high levels or low levels of anti-SGC antibodies detected in mouse DRG–derived SGC cultures. Human SGCs (hSGCs) were identified with an antibody against glial fibrillary acidic protein (GFAP), and neurons were identified with an antibody against NF200. The normalized pixel intensity of serum IgG binding to (B) SGCs, (C) neuronal soma, (D) axons, and (E) GFAP-negative and NF200-negative objects was analyzed. (F) The pixel intensity of IgG binding to hSGCs correlated with the level of anti-SGC antibodies determined in cell culture by the percent of IgG positive mouse SGCs (mSGCs) and the binding intensity (integrated density). The size and colour of the dots indicate the Spearman rank correlation coefficient, and only statistically significant correlations (P < 0.05) have coloured dots, whereas nonsignificant correlations are blank. (G) Individuals in the FM severe group had elevated IgG binding to hSGCs compared with the FM mild group and HC group. One-way ANOVAs with Tukey post hoc test was used to determine differences, and experimenters were blind to serum type during imaging and analysis. *indicates P < 0.05, **indicates P < 0.01, n = 14/group. Scale bar is 50 μm. ANOVA, analysis of variance; DRG, dorsal root ganglia; FM, fibromyalgia; HC, health control; SGC, satellite glia cell.CC BY · PubMed Central
Figure 7. Human SGCs express epitopes for anti-SGC IgG across DRG donors. (A) DRG tissue from 6 human organ donors were incubated with an FM serum sample that had high levels of IgG against human SGCs and with an HC serum sample. Human SGCs were identified as glial fibrillary acidic protein (GFAP)–positive objects with a perineuronal location, and (B) the normalized pixel intensity of serum IgG binding to SGCs was quantified. Each symbol is the average normalized pixel intensity across 5 slides from a single DRG donor. Data were analyzed with a paired t test; experimenters were blind to serum type during imaging and analysis, *indicates P < 0.05, n = 6 DRGs/group. Scale bar is 50 μm and each symbol in (B) represents a single DRG donor. DRG, dorsal root ganglia; FM, fibromyalgia; HC, health control; SGC, satellite glia cell.
Figure 7. Human SGCs express epitopes for anti-SGC IgG across DRG donors. (A) DRG tissue from 6 human organ donors were incubated with an FM serum sample that had high levels of IgG against human SGCs and with an HC serum sample. Human SGCs were identified as glial fibrillary acidic protein (GFAP)–positive objects with a perineuronal location, and (B) the normalized pixel intensity of serum IgG binding to SGCs was quantified. Each symbol is the average normalized pixel intensity across 5 slides from a single DRG donor. Data were analyzed with a paired t test; experimenters were blind to serum type during imaging and analysis, *indicates P < 0.05, n = 6 DRGs/group. Scale bar is 50 μm and each symbol in (B) represents a single DRG donor. DRG, dorsal root ganglia; FM, fibromyalgia; HC, health control; SGC, satellite glia cell.CC BY · PubMed Central

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Metadata

Authors
Krock, E., Morado-Urbina, C. E., Menezes, J., Hunt, M. A., Sandström, A., Kadetoff, D., Tour, J., Verma, V., Kultima, K., Haglund, L., Meloto, C. B., Diatchenko, L., Kosek, E., & Svensson, C. I.
Affiliations
  • Karolinska Institutet (SE)
  • Harvard University (US)
  • McGill University (CA)
  • Uppsala University (SE)
Corresponding author
Svensson, Camilla I.
ORCID
Venue
Pain
Publisher
Ovid Technologies (Wolters Kluwer Health)
Published
2023-03-22
Volume
164
Issue
8
Pages
1828-1840
ISSN
  • 0304-3959 (ISSN-L)
  • 1872-6623
DOI
10.1097/j.pain.0000000000002881
PMC
PMC10348624
OpenAlex
W4328048178
Cited by
84
References
6
Citations by year
2026: 21 · 2025: 40 · 2024: 17 · 2023: 5
FWCI
16.90
Type
journal article
Language
en
Open access
Licence
Locations
  • Pain (publishedVersion, cc-by)
  • PubMed Central (publishedVersion, cc-by)
  • PubMed (publishedVersion)
Funders
  • Pfizer
  • European Commission (2007–2013, FP7 2007-2013, HORIZON2020, FP7/2007, 764860, 602919)
  • Canada Excellence Research Chairs, Government of Canada (CERC09)
  • Karolinska Institutet
  • Knut och Alice Wallenbergs Stiftelse (018.0161)
  • Stockholms Läns Landsting
  • Vetenskapsrådet (542-2013-8373, FP7/2007-2013, 2016-01556, 2013-08373)
  • Reumatikerförbundet
  • Foundation for Research in Rheumatology
  • Pfizer Canada
  • Canadian Institutes of Health Research (145102_1, CERC09)
  • H2020 European Research Council (866075)
Topics
  • Health Sciences › Medicine › Psychiatry and Mental health › Fibromyalgia and Chronic Fatigue Syndrome Research
  • Health Sciences › Medicine › Physiology (medical) › Pain Mechanisms and Treatments
  • Health Sciences › Medicine › Psychiatry and Mental health › Psychosomatic Disorders and Their Treatments
Keywords
fibromyalgia, autoantibodies, disease severity, pressure sensitivity, dorsal root ganglia, IgG, Fibromyalgia Impact Questionnaire, autoantibody detection, personalized treatment
MeSH terms
Animals, Autoantibodies, Fibromyalgia, Humans, Immunoglobulin G, Pain, Surveys and Questionnaires, Mice

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

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