Increase of interferon-gamma inducible alpha chemokine CXCL10 but not beta chemokine CCL2 serum levels in chronic autoimmune thyroiditis.
OBJECTIVE
To measure serum levels of CXCL10 and CCL2 prototype chemokines of the two major subclass (CXC and CC) in patients with newly diagnosed chronic autoimmune thyroiditis (AT), and relate the findings to the clinical phenotype.


METHODS
Serum CXCL10 and CCL2 were assayed in 70 consecutive patients with newly diagnosed chronic AT, in sex- and age-matched healthy volunteers (n = 37) and in 20 patients with non-toxic multinodular goiter, extracted from a random sample of the general population from the same geographic area.


RESULTS
CXCL10 serum levels were significantly higher in patients with thyroiditis than in controls or multinodular goiter patients, while comparable CCL2 levels were found between groups. CXCL10 levels were significantly increased in hypothyroid patients and in those with an hypoechoic pattern (P = 0.0004 and P = 0.0001, respectively) while serum CCL2 levels were significantly increased in patients older than 50 years and in those with hypothyroidism (P = 0.0001 and P = 0.03, respectively). No correlation between CXCL10 and CCL2 serum levels could be demonstrated. CXCL10 and CCL2 were studied separately in relation to clinical features of AT patients. Two separate multiple linear regression models for CXCL10 and CCL2 were performed, including age, thyroid volume, thyroid stimulating hormone (TSH), FT4, anti-thyroid peroxidase (AbTPO), hypoechoic pattern, and the presence of hypervascularity, demonstrating that ln of serum CXCL10 levels was associated with TSH independently of other possible confounders levels [regression coefficient (R.C.) 0.143 confidence interval (C.I.) (0.042-0.245); P = 0.0059], while serum CCL2 were significantly associated only with age [R.C. 5.412 C.I. (3.838-6.986); P < 0.0001].


CONCLUSIONS
Our results, obtained in a large cohort of newly diagnosed AT patients demonstrate increased CXCL10 especially in hypothyroid patients with a more aggressive disorder, and normal CCL2 serum levels in AT.
Antonelli
Alessandro
A
Metabolism Unit, Department of Medicine and CNR Institute of Clinical Physiology, University of Pisa School of Medicine, Pisa, Italy. a.antonelli@med.unipi.it
Rotondi
Mario
M
Fallahi
Poupak
P
Romagnani
Paola
P
Ferrari
Silvia Martina
SM
Paolicchi
Aldo
A
Ferrannini
Ele
E
Serio
Mario
M
D000328:Adult; D001323:Autoantibodies / Q000097:blood; D018932:Chemokine CCL2 / Q000097:blood*; D054357:Chemokine CXCL10; D019743:Chemokines, CXC / Q000097:blood*; D002908:Chronic Disease; D015331:Cohort Studies; D005260:Female; D006801:Humans; D007037:Hypothyroidism / Q000097:blood / Q000276:immunology; D007371:Interferon-gamma / Q000378:metabolism*; D008297:Male; D008875:Middle Aged; D010641:Phenotype; D013961:Thyroid Gland / Q000276:immunology; D013967:Thyroiditis, Autoimmune / Q000097:blood* / Q000276:immunology*; D013972:Thyrotropin / Q000097:blood
D001323:Autoantibodies; C111835:CCL2 protein, human; C114753:CXCL10 protein, human; D018932:Chemokine CCL2; D054357:Chemokine CXCL10; D019743:Chemokines, CXC; D007371:Interferon-gamma; D013972:Thyrotropin