Journal: Frontiers in Immunology

Article Title: The free fatty acid 2 receptor regulates C5a induced neutrophil superoxide production and its sensitivity to inhibition by the antagonist avacopan

doi: 10.3389/fimmu.2026.1795719

Figure Lengend Snippet: TNF primes neutrophils and an allosteric FFA2R modulator turns C5a into a more potent activator of the NADPH oxidase. For priming, neutrophils were incubated with TNF (10 ng/mL) at 37 °C for 20 min and then stored on ice until used. The NADPH oxidase activity (O 2 - production) induced by C5a was measured continuously and expressed in mega couts per minute (Mcpm). (A) The response induced in naïve (non-primed; dashed line) and TNF primed neutrophils (solid line) by C5a (2 nM, added at the time point marked with an arrow) was measured. Inset: The priming effect of TNF on the NADPH oxidase activity expressed as peak values (Mcpm; mean ± SEM) of O 2 - production induced by C5a in naïve (n = 5) and TNF-primed neutrophils (n = 14). (B) Inhibition of the C5a-induced response by the specific C5aR1 antagonist avacopan. TNF-primed neutrophils were incubated without (solid line) or with avacopan (50 nM, dashed line) for 5 min before addition of C5a (2 nM; added at the time point marked with an arrow) and determination of the NADPH oxidase activity. Inset: The inhibitory effect of avacopan on the neutrophil NADPH oxidase activity expressed as peak values (Mcpm) of O 2 - production induced by C5a in absence and presence of the antagonist, respectively (mean ± SEM, n = 6). (C) Effects of the allosteric FFA2R modulator Cmp58 on the response induced by different concentrations of C5a in TNF-primed neutrophils. Neutrophils were incubated without (dashed lines) or with Cmp58 (1 µM, solid lines) for 5 min before addition of C5a (0.1 nM, grey lines, or 2 nM, black lines; added at the time point marked with an arrow) and determination of the NADPH oxidase activity. Inset: The effect of Cmp58 on the NADPH oxidase activity expressed as fold increase of O 2 - production induced by different C5a concentrations (0.1, 0.25 or 2 nM) in the absence and presence of Cmp58, respectively (mean ± SEM, n = 6). The horizontal dotted line in the bar graph represents a ratio of 1. (D) TNF-primed neutrophils were pre-incubated with and without Cmp58 (1 µM) for 5 min and activated with different concentrations of C5a as indicated. Superoxide production was recorded continuously and expressed as the peak value obtained in terms of percent of the activity induced by C5a alone (2 nM, mean ± SEM, n = 3).One representative experiment is shown in each subset (A–C) . Statistically significant differences in the insets were evaluated by an unpaired Student’s t -test (A) , a paired Student’s t -test (B) , or a repeated measures one-way ANOVA followed by Šίdák’s multiple comparison (C) and are denoted as *( p ≤ 0.05), ***( p ≤ 0.001), and ns = not significant.

Article Snippet: Recombinant human C5a (rhC5a) and AZ1729 was purchased from R&D Systems (Minneapolis, MN, USA) and avacopan was purchased from MedChemExpress (Princeton, NJ, USA).

Techniques: Incubation, Activity Assay, Inhibition, Comparison

Journal: Frontiers in Immunology

Article Title: The free fatty acid 2 receptor regulates C5a induced neutrophil superoxide production and its sensitivity to inhibition by the antagonist avacopan

doi: 10.3389/fimmu.2026.1795719

Figure Lengend Snippet: Antagonists selective for FFA2R and C5aR1, respectively, have inhibiting profiles beyond the expected receptor specificity. TNF-primed neutrophils were incubated with Cmp58 (1 µM; 5 min at 37 °C) and to determine the inhibitory effects of receptor specific antagonist, these cells were incubated without or with an antagonist (CATPB, 100 nM; avacopan, 50 nM) and the O 2 - production was measured continuously following an activation by different concentrations of C5a. (A-C) Inhibition by the antagonists (CATPB and avacopan) of the response in neutrophils incubated with Cmp58 and induced by C5a, at different concentrations, i.e., 2 nM (A; n = 3-8), 0.25 nM (B; n = 7), and 0.1 nM (C; n = 6), respectively. Inhibition is expressed as the remaining activity (peak value in percent) of neutrophils after activation with C5a in the presence of the respective antagonist. Bar graphs are presented as mean ± SEM. The statistical determinations are based on the difference between the C5a response without and with the antagonists. Statistically significant differences were evaluated by a repeated measures one-way ANOVA followed by Šίdák’s multiple comparison (C) or by a mixed effects analysis followed by Šίdák’s multiple comparison (A, B) and are denoted as *( p ≤ 0.05), **( p ≤ 0.01), ***( p ≤ 0.001), and ns = not significant.

Article Snippet: Recombinant human C5a (rhC5a) and AZ1729 was purchased from R&D Systems (Minneapolis, MN, USA) and avacopan was purchased from MedChemExpress (Princeton, NJ, USA).

Techniques: Incubation, Activation Assay, Inhibition, Activity Assay, Comparison

Journal: Frontiers in Immunology

Article Title: The free fatty acid 2 receptor regulates C5a induced neutrophil superoxide production and its sensitivity to inhibition by the antagonist avacopan

doi: 10.3389/fimmu.2026.1795719

Figure Lengend Snippet: Differential NADPH oxidase activity triggered by Cmp58 in neutrophils pretreated with C5a or propionate. (A) TNF-primed neutrophils pre-incubated with Cmp58 (1 µM, 5 min at 37 °C) were activated by C5a (0.1 nM, solid line) or propionate (25 µM, dashed line). The result obtained in one representative experiment is shown. Inset: The NADPH oxidase induced by the ligands C5a and propionate, in neutrophils pre-incubated (abbreviation Pre-inc.) with Cmp58, expressed as the peak values of O 2 - production (Mcpm; mean ± SEM, n = 5). (B) TNF-primed neutrophils incubated for 5 min at 37 °C with non-activating concentrations of C5a (solid line; 0.1 nM) or propionate (dashed line; 25 µM) were activated by Cmp58 (1 µM). The result obtained in one representative experiment is shown. Inset: The NADPH oxidase induced by Cmp58, in neutrophils pre-incubated (abbreviation Pre-inc.) with C5a and propionate, respectively, expressed as the peak values of O 2 - production (mean ± SEM, n = 5). Statistically significant differences in the insets were evaluated by a paired Student’s t -test and are denoted as *( p ≤ 0.05) and ns, not significant.

Article Snippet: Recombinant human C5a (rhC5a) and AZ1729 was purchased from R&D Systems (Minneapolis, MN, USA) and avacopan was purchased from MedChemExpress (Princeton, NJ, USA).

Techniques: Activity Assay, Incubation

Journal: Frontiers in Immunology

Article Title: The free fatty acid 2 receptor regulates C5a induced neutrophil superoxide production and its sensitivity to inhibition by the antagonist avacopan

doi: 10.3389/fimmu.2026.1795719

Figure Lengend Snippet: C5a triggers a transient increase in the cytosolic concentration of free calcium ions ([Ca 2+ ] i ) in neutrophils, which is not affected by the allosteric FFA2R modulator Cmp58. Fura-2 loaded neutrophils were activated by propionate (25 µM) or different concentrations of C5a (2, 0.25, 0.1, and 0.05 nM) in the absence (upper panel) or presence (lower panel) of the allosteric FFA2R modulator Cmp58 (1 µM, pre-incubated with the cells for 10 min at 37 °C prior addition of the agonist). Results obtained are shown as one representative experiment out of 3. The arrows show the time point for the addition of the agonists to the Fura-2 labelled neutrophils.

Article Snippet: Recombinant human C5a (rhC5a) and AZ1729 was purchased from R&D Systems (Minneapolis, MN, USA) and avacopan was purchased from MedChemExpress (Princeton, NJ, USA).

Techniques: Concentration Assay, Incubation

Journal: Frontiers in Immunology

Article Title: The free fatty acid 2 receptor regulates C5a induced neutrophil superoxide production and its sensitivity to inhibition by the antagonist avacopan

doi: 10.3389/fimmu.2026.1795719

Figure Lengend Snippet: Activation of FFA2R inhibits (heterologously desensitizes) the neutrophil response induced by C5a. TNF-primed neutrophils incubated with Cmp58 (1 µM), were either left in a resting state (dashed lines) or activated by an FFA2R activating/transactivating ligand (solid lines) and the O 2 - production was measured continuously and expressed in Mcpm. When the response induced by the FFA2R activating agonist was terminated, the two cell samples were activated by an addition of C5a (2 nM). The results obtained in one representative experiment is shown together with an inset showing the peak activities induced by C5a (mean ± SEM, n = 3). (A) Propionate (25 µM), (B) ATP (25µM), and (C) AZ1729 (1µM) were used as the FFA2R activating ligand (the time point for addition is marked by arrow 1). The time point for addition of C5a to the cells is marked by arrow 2. Statistically significant differences in the insets were evaluated by a paired Student’s t -test and are denoted as *( p ≤ 0.05).

Article Snippet: Recombinant human C5a (rhC5a) and AZ1729 was purchased from R&D Systems (Minneapolis, MN, USA) and avacopan was purchased from MedChemExpress (Princeton, NJ, USA).

Techniques: Activation Assay, Incubation

Journal: Frontiers in Immunology

Article Title: The free fatty acid 2 receptor regulates C5a induced neutrophil superoxide production and its sensitivity to inhibition by the antagonist avacopan

doi: 10.3389/fimmu.2026.1795719

Figure Lengend Snippet: C5a-induced desensitization in Cmp58-sensitized neutrophils. (A–C) TNF-primed neutrophils incubated with Cmp58 (1 µM, 5 min at 37 °C) were either left in a resting state (dashed lines) or activated by C5a (2 nM, solid line; the time point for addition is marked by arrow 1), and the O 2 - production was measured continuously and expressed as Mcpm. When the response, induced by the C5aR1 activating ligand was terminated, the two cell samples were activated by the addition of (A) propionate (25 µM, an FFA2R activating ligand), (B) ATP (50 µM, a P2Y 2 R activating ligand), or (C) AZ1729 (1 µM, an FFA2R activating ligand), and the time point for their addition is marked by arrow 2 (D–F) . The experimental setup differs from that described above, in that Cmp58 (1 µM), was added first when the response induced by C5a (time for addition marked by arrow 1), had settled. The neutrophils were then activated with either propionate [ (D) ; 25 µM)], ATP [ (E) ; 50 µM)], or AZ1729 [ (F) ; 1 µM)]. The time point for addition of the FFA2R activating/transactivating ligand is marked by arrow 2, and one representative experiment is depicted. The results obtained are shown together with an inset showing the peak activities induced by the FFA2R activating/transactivating ligands (mean ± SEM, n = 3). Statistically significant differences in the insets were evaluated by a paired Student’s t -test and are denoted as * ( p ≤ 0.05) and ns = not significant.

Article Snippet: Recombinant human C5a (rhC5a) and AZ1729 was purchased from R&D Systems (Minneapolis, MN, USA) and avacopan was purchased from MedChemExpress (Princeton, NJ, USA).

Techniques: Incubation

Journal: Frontiers in Immunology

Article Title: The free fatty acid 2 receptor regulates C5a induced neutrophil superoxide production and its sensitivity to inhibition by the antagonist avacopan

doi: 10.3389/fimmu.2026.1795719

Figure Lengend Snippet: A proposed model for how the neutrophil NADPH oxidase is turned to an active state by the C5aR1 agonist C5a in the absence and presence of the allosteric FFA2R modulator Cmp58. (A) Left: The neutrophil response induced by a 2 nM concentration of C5a. In the absence of Cmp58, the signals generated by the activated C5aR1 directly activate the O 2 -- generating NADPH oxidase and have also the capacity to transactivate FFA2R, but the naïve fatty acid receptor is not receptive to these signals. Right: In the presence of Cmp58, the signals generated by the activated C5aR1 directly activate the O 2 -- generating oxidase and transactivate the allosterically modulated FFA2R; the transactivated FFA2R does not directly potentiate the NADPH oxidase response but reduces the inhibitory effect on this response, of the C5aR1 specific antagonist avacopan. (B) Left: The neutrophil response induced by a 0.1 nM concentration of C5a. In the absence of Cmp58, the signals generated by the activated C5aR1 have no NADPH oxidase activating effect. The signals have, however, the capacity to transactivate FFA2R, but the naïve fatty acid receptor is not receptive to these signals. Right: In the presence of Cmp58, the signals generated by the activated C5aR1 activate the O 2 -- generating NADPH oxidase, and this activation is totally dependent of the signals generated by the allosterically modulated FFA2R, a receptor made receptive to the transactivating signals generated by C5aR1.

Article Snippet: Recombinant human C5a (rhC5a) and AZ1729 was purchased from R&D Systems (Minneapolis, MN, USA) and avacopan was purchased from MedChemExpress (Princeton, NJ, USA).

Techniques: Concentration Assay, Generated, Activation Assay

Journal: Biomolecules

Article Title: ACSL4 Drives C5a/C5aR1–Calcium-Induced Fibroblast-to-Myofibroblast Transition in a Bleomycin-Induced Mouse Model of Pulmonary Fibrosis

doi: 10.3390/biom15081106

Figure Lengend Snippet: Effects of blocking the C5a/C5aR1 signaling on the early stage of lung fibrosis: ( A ) Scheme for the BLM-induced lung fibrosis. The mice were treated with PMX53 (1 mg/kg) or vehicle 1 h before BLM exposure on day 0, and then once a day. Mice were euthanized on day 7 after BLM modeling. ( B ) Weight changes of the mice; n = 8 for each group. ( C ) Lung coefficients of the mice; n = 8 for each group. ( D ) H&E staining of the lung tissues. Representative images are shown. Original magnification: 200×. ( E ) The number of nuclei per high-power field of lung tissues; n = 8 for each group. ( F ) The inflammatory index of the alveoli; n = 8 for each group. ( G ) The Ashcroft score; n = 8 for each group. ( H , I ) The expression of Acta2 , Col1a1 , Col3 , and Fn1 in lung tissues was quantified by qPCR; n = 6 for each group. ( J ) The expression of αSMA protein in lung tissues. Representative immunohistochemical plots and statistical plots are shown. Original magnification: 200×; n = 8 for each group. ( K , L ) Immunohistochemical staining of collagen I in lung tissues. Representative images and relative IOD analyses are shown. Original magnification: 200×; n = 8 for each group. ( M ) Masson staining of the lung tissues. Representative images and collagen volume fraction analyses are shown. Original magnification: 200×; n = 8 for each group. ( N , O ) WB analysis of the ACSL4 and αSMA protein in lung tissues. Representative bands and statistical plots are shown; n = 6 for each group. ( P ) The expression of Acsl4 in lung tissues was quantified by qPCR; n = 6 for each group. ( Q ) Immunohistochemical staining of ACSL4 protein in the lung tissues. Representative images and relative IOD analyses are shown; n = 8 for each group. Data are the mean ± SEM; * p < 0.05, ** p < 0.01, *** p < 0.001 by two-way ANOVA followed by adjustments for multiple comparisons in panel ( B ), or Student’s t -test in panels ( C , E – J , L , M , O – Q ); ns = not significant.

Article Snippet: In some experiments, TGF-β1 (Sinobiological, Beijing, China, Cat#: 80116-RNAH-5), PRGL493, C5a (MCE, New Jersey, USA, Cat#: HY-P7695), or FK506 (Selleck, Texas, USA, Cat#: S5003) was added to the cell culture medium at the indicated concentrations and time points.

Techniques: Blocking Assay, Staining, Expressing, Immunohistochemical staining

Journal: Biomolecules

Article Title: ACSL4 Drives C5a/C5aR1–Calcium-Induced Fibroblast-to-Myofibroblast Transition in a Bleomycin-Induced Mouse Model of Pulmonary Fibrosis

doi: 10.3390/biom15081106

Figure Lengend Snippet: Inhibition of C5a/C5aR1 signaling reduced ACSL4 levels and attenuated lung inflammation and fibrosis in the chronic stage of pulmonary fibrosis: ( A ) Scheme of BLM-induced lung fibrosis. Mice were euthanized on day 21 after BLM modeling. ( B ) Weight changes of the mice; n = 6 for each group. ( C ) Lung coefficients of the mice; n = 6 for each group. ( D ) H&E staining of the lung tissues. Representative images are shown. Original magnification: 200×. ( E ) Number of nuclei per high-power field of the lung tissues; n = 6 for each group. ( F ) The inflammatory index of the alveoli; n = 6 for each group. ( G ) The Ashcroft score; n = 6 for each group. ( H , I ) The expression of Acta2 , Col1a1 , Col3 , and Fn1 in lung tissues was quantified by qPCR; n = 5 for each group. ( J ) Immunohistochemical staining of αSMA in lung tissues. Representative images and relative IOD analyses are shown. Original magnification: 200×; n = 6 for each group. ( K , L ) Immunohistochemical staining of collagen I in lung tissues. Representative images and relative IOD analyses are shown. Original magnification: 200×; n = 6 for each group. ( M ) Masson staining of lung tissues. Representative images and collagen volume fraction analyses are shown. Original magnification: 200×; n = 6 for each group. ( N , O ) WB analysis of the ACSL4 and αSMA proteins in lung tissues. Representative bands and statistical plots are shown; n = 6 for each group. ( P ) The expression of Acsl4 in lung tissues was quantified by qPCR; n = 6 for each group. ( Q ) Immunohistochemical staining of ACSL4 in lung tissues. Representative images and relative IOD analyses are shown; n = 6 for each group. Data are the mean ± SEM; * p < 0.05, ** p < 0.01, *** p < 0.001 by two-way ANOVA followed by adjustments for multiple comparisons in panel ( B ), or Student’s t -test in panels ( C , E – J , L , M , O – Q ); ns = not significant.

Article Snippet: In some experiments, TGF-β1 (Sinobiological, Beijing, China, Cat#: 80116-RNAH-5), PRGL493, C5a (MCE, New Jersey, USA, Cat#: HY-P7695), or FK506 (Selleck, Texas, USA, Cat#: S5003) was added to the cell culture medium at the indicated concentrations and time points.

Techniques: Inhibition, Staining, Expressing, Immunohistochemical staining

Journal: Biomolecules

Article Title: ACSL4 Drives C5a/C5aR1–Calcium-Induced Fibroblast-to-Myofibroblast Transition in a Bleomycin-Induced Mouse Model of Pulmonary Fibrosis

doi: 10.3390/biom15081106

Figure Lengend Snippet: Blocking ACSL4 reduced C5a/C5aR1 signaling-induced activation and migration of lung fibroblasts: ( A ) The expression of Acsl4 was quantified by qPCR; n = 6 for each group. ( B ) WB analysis of ACSL4 in lung fibroblasts. Representative bands and statistical plots are shown; n = 6 for each group. ( C , D ) The expression of Acta2 , Col1a1 , Col3 , and Fn1 was quantified by qPCR; n = 6 for each group. ( E ) WB analysis of αSMA in lung fibroblasts. Representative bands and statistical plots are shown; n = 6 for each group. ( F ) The expression of αSMA was tested by immunofluorescence. Representative plots are shown. Original magnification: 400×; αSMA (green) and DAPI (blue). ( G ) The cell scratch assay was used to assess lung fibroblasts’ migration. Representative images are shown. ( H ) The transwell assay. Representative plot and statistical plots of the transwell assay results are shown; n = 3 for each group. ( I ) The proliferation of fibroblasts was tested by CCK8. Data are the mean ± SEM; * p < 0.05, ** p < 0.01, *** p < 0.001 by Student’s t -test in panels ( A , B ), one-way ANOVA followed by adjustments for multiple comparisons in panels ( C – E , H ), or two-way ANOVA followed by adjustments for multiple comparisons in panel ( I ); ns = not significant.

Article Snippet: In some experiments, TGF-β1 (Sinobiological, Beijing, China, Cat#: 80116-RNAH-5), PRGL493, C5a (MCE, New Jersey, USA, Cat#: HY-P7695), or FK506 (Selleck, Texas, USA, Cat#: S5003) was added to the cell culture medium at the indicated concentrations and time points.

Techniques: Blocking Assay, Activation Assay, Migration, Expressing, Immunofluorescence, Wound Healing Assay, Transwell Assay

Journal: Biomolecules

Article Title: ACSL4 Drives C5a/C5aR1–Calcium-Induced Fibroblast-to-Myofibroblast Transition in a Bleomycin-Induced Mouse Model of Pulmonary Fibrosis

doi: 10.3390/biom15081106

Figure Lengend Snippet: Blockade of calcium signaling attenuated ACSL4 expression induced by the C5a/C5aR1 signaling: ( A ) The calcium concentration of lung fibroblasts was tested by calcium imaging. Representative plots and statistical plots are shown; n = 4 for each group. ( B , C ) The expression of Acta2 , Col1a1 , Col3 , and Fn1 was quantified by qPCR; n = 6 for each group. ( D ) WB analysis of ACSL4 and αSMA in lung fibroblasts. Representative bands and statistical plots are shown; n = 6 for each group. ( E ) The expression of αSMA was tested by immunofluorescence. Plots are shown. Original magnification: 400×; αSMA (green) and DAPI (blue). ( F , G ) The horizontal migration ability of lung fibroblasts was tested by the cell scratch assay. Representative plots and statistical plots are shown; n = 4 for each group. ( H ) The spatial migration ability of lung fibroblasts was tested by transwell assay. Representative plot and statistical plot are shown; n = 5 for each group. Data are the mean ± SEM; * p < 0.05, ** p < 0.01, *** p < 0.001, , **** p < 0.0001 by one-way ANOVA followed by adjustments for multiple comparisons in panels ( A – C , H ), Student’s t -test in panel ( D ), or two-way ANOVA followed by adjustments for multiple comparisons in panel ( G ); ns = not significant.

Article Snippet: In some experiments, TGF-β1 (Sinobiological, Beijing, China, Cat#: 80116-RNAH-5), PRGL493, C5a (MCE, New Jersey, USA, Cat#: HY-P7695), or FK506 (Selleck, Texas, USA, Cat#: S5003) was added to the cell culture medium at the indicated concentrations and time points.

Techniques: Expressing, Concentration Assay, Imaging, Immunofluorescence, Migration, Wound Healing Assay, Transwell Assay

Journal: Acta Pharmaceutica Sinica. B

Article Title: An anti-complement homogeneous polysaccharide from Houttuynia cordata ameliorates acute pneumonia with H1N1 and MRSA coinfection through rectifying Treg/Th17 imbalance in the gut–lung axis and NLRP3 inflammasome activation

doi: 10.1016/j.apsb.2025.04.008

Figure Lengend Snippet: HCPM and HCP inhibit the overactivation of intestinal complement in viral–bacterial coinfection mice. C57BL/6 mice were infected intranasally with 0.2 LD 50 H1N1 and then infected with 10 7 CFU MRSA three days later. Mice were treated with indicated drugs from Day 0 to Day 4 following H1N1 infection ( n = 6). The small intestines were obtained from different groups on Day 4 and Day 5. (A) Representative images of immunohistochemical staining for C3a in small intestines ( n = 4). (B, C) Quantitative analysis of the C3a-stained immunohistochemical images by ImageJ ( n = 4). (D) Representative images of immunohistochemical staining for C5a in small intestines ( n = 4). (E, F) Quantitative analysis of the C5a-stained immunohistochemical images by ImageJ ( n = 4). Scale bar = 50 μm. Data are represented as mean ± SD and analyzed by one-way ANOVA followed by Dunnett's multiple comparisons test. P values < 0.05 were considered statistically significant, ∗∗ P < 0.01 and ∗∗∗ P < 0.001 vs. coinfection; not significant (ns).

Article Snippet: Complement C5a (#PA5-78891) antibody was purchased from Thermo Fisher Scientific (Waltham, MA, USA).

Techniques: Infection, Immunohistochemical staining, Staining

Journal: Scientific Reports

Article Title: C5a in the peripheral plasma of female fibromyalgia patients is elevated but not related to pain sensitivity as in healthy controls

doi: 10.1038/s41598-025-01347-x

Figure Lengend Snippet: Mean peripheral C5a level in plasma. Means of C5a levels derived from 29 HCs and 30 FMs are compared ( p = 0.011.t-test), HC healthy control, FM Fibromyalgia, SD standard deviation.

Article Snippet: The plasma C5a level was measured by the use of MicroVue Complement C5a EIA (QuidelOrtho, USA), C3a with MicroVue Complement C3a Plus EIA (QuidelOrtho, USA), and Soluble C5b-9 with MicroVue complement SC5b-9 Plus EIA (QuidelOrtho, USA).

Techniques: Clinical Proteomics, Derivative Assay, Control, Standard Deviation

Journal: Scientific Reports

Article Title: C5a in the peripheral plasma of female fibromyalgia patients is elevated but not related to pain sensitivity as in healthy controls

doi: 10.1038/s41598-025-01347-x

Figure Lengend Snippet: Scatter plot of the C5a and CPT of the HC group ( a ) and FM group ( b ). CPTs of 1 HC and 1 FM were out of the measurable range and omitted. CPT Cold pain threshold. P values are obtained from Spearman’s rank correlation. HC Healthy control, FM Fibromyalgia, R Spearman’s rank correlation coefficient.

Article Snippet: The plasma C5a level was measured by the use of MicroVue Complement C5a EIA (QuidelOrtho, USA), C3a with MicroVue Complement C3a Plus EIA (QuidelOrtho, USA), and Soluble C5b-9 with MicroVue complement SC5b-9 Plus EIA (QuidelOrtho, USA).

Techniques: Control