Temporal changes in cytokine/chemokine profiles and pulmonary involvement in severe acute respiratory syndrome.
OBJECTIVE
Pathological changes in severe acute respiratory syndrome (SARS) suggest that SARS sequelae are associated with dysregulation of cytokine and chemokine production. To improve understanding of the immuno-pathological processes involved in lung injury associated with SARS, the temporal changes in cytokine/chemokine profiles in the sera of SARS patients were compared with those of patients with community-acquired pneumonia (CAP), according to the degree of lung involvement.


METHODS
Serum levels of 11 cytokines and chemokines, in 14 patients with SARS and 24 patients with CAP, were serially checked using a bead-based multiassay system. Sera from 12 healthy subjects were used as normal controls.


RESULTS
The serum levels of interferon-gamma-inducible protein-10 (IP-10), IL-2 and IL-6 were significantly elevated during SARS infection. In patients with CAP, but not in those with SARS, the levels of interferon-gamma, IL-10, IL-8 and monokine induced by interferon-gamma (MIG) were significantly elevated compared with the levels in healthy controls. Among the chemokines/cytokines, IL-6 levels correlated most strongly with radiographic scores (r=0.62). The elevation of IP-10 and IL-2 antedated the development of chest involvement and reached peak levels earlier than the radiographic scores. In contrast, the dynamic changes in IL-6, C-reactive protein and neutrophils occurred synchronously with the changes in radiographic scores. The mean ratio of IL-6 to IL-10 in SARS patients (4.84; range 0.41-21) was significantly higher than that in CAP patients (2.95; range 0.02-10.57) (P=0.04).


CONCLUSIONS
The early induction of IP-10 and IL-2, as well as the subsequent over-production of IL-6 and lack of IL-10 production, probably contribute to the main immuno-pathological processes involved in lung injury in SARS. These changes in cytokine/chemokine profile are remarkably different from those observed in CAP patients.
Chien
Jung-Yien
JY
Department of Internal Medicine, National Taiwan University Hospital (Yun-Lin Branch), Douliu, Taiwan.
Hsueh
Po-Ren
PR
Cheng
Wern-Cherng
WC
Yu
Chong-Jen
CJ
Yang
Pan-Chyr
PC
D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D016022:Case-Control Studies; D054357:Chemokine CXCL10; D018925:Chemokines / Q000097:blood* / Q000235:genetics; D019743:Chemokines, CXC / Q000235:genetics / Q000378:metabolism; D017714:Community-Acquired Infections / Q000097:blood / Q000000981:diagnostic imaging / Q000276:immunology / Q000503:physiopathology; D016207:Cytokines / Q000097:blood* / Q000235:genetics; D005260:Female; D005786:Gene Expression Regulation; D006801:Humans; D016753:Interleukin-10 / Q000235:genetics / Q000378:metabolism; D007376:Interleukin-2 / Q000235:genetics / Q000378:metabolism; D015850:Interleukin-6 / Q000235:genetics / Q000378:metabolism; D008168:Lung / Q000000981:diagnostic imaging / Q000473:pathology*; D008297:Male; D008875:Middle Aged; D011014:Pneumonia / Q000097:blood / Q000000981:diagnostic imaging / Q000276:immunology / Q000503:physiopathology; D011446:Prospective Studies; D011859:Radiography; D045169:Severe Acute Respiratory Syndrome / Q000097:blood / Q000000981:diagnostic imaging / Q000276:immunology* / Q000503:physiopathology*
D054357:Chemokine CXCL10; D018925:Chemokines; D019743:Chemokines, CXC; D016207:Cytokines; D007376:Interleukin-2; D015850:Interleukin-6; D016753:Interleukin-10