Modulation of peripheral blood mononuclear cell activation status during Salmonella-triggered reactive arthritis.
OBJECTIVE
To determine the activation status of mononuclear cells in the peripheral circulation during the acute phase and the recovery phase of Salmonella-triggered reactive arthritis (ReA).


METHODS
Peripheral blood mononuclear cells (PBMC) were obtained from 8 patients with Salmonella infection (4 with ReA and 4 without) and were studied by reverse transcription-polymerase chain reaction for messenger RNA (mRNA) of proinflammatory and antiinflammatory cytokines, by flow cytometry (FC) for cell surface activation and adhesion molecules, by immunofluorescence (IF) microscopy for bacterial antigens, and by FC, IF, and DNA fragmentation on gel for signs of apoptosis.


RESULTS
During the acute phase of the infection, PBMC were activated in all patients, as characterized by high levels of expression of CD14, CD11b, and CD11c on monocytes. In the patients with ReA, PBMC also had the capacity to produce interleukin-1beta (IL-1beta), IL-6, IL-8, IL-10, and tumor necrosis factor alpha. During the amelioration of disease, monocyte activation was decreased in all patients. A complete down-regulation of CD14 was detected only in the patients with ReA, whereas the expression of CD14 in the patients without ReA was positive and was similar to that in healthy controls. In addition, cytokine mRNA levels decreased regardless of the presence of Salmonella antigens in blood cells in all 4 patients with ReA.


CONCLUSIONS
High levels of expression of some activation and adhesion molecules and elevated levels of mRNA for certain cytokines that are predominantly produced by monocytes were found in PBMC from patients with acute Salmonella-triggered ReA, which suggests that these cells are activated. On the other hand, complete down-regulation of CD14 and a marked decrease in the cytokine production capacity during amelioration of the disease suggest that suppression of PBMC activity might be involved in recovery from ReA.
Kirveskari
J
J
National Public Health Institute, Turku, Finland.
He
Q
Q
Holmström
T
T
Leirisalo-Repo
M
M
Wuorela
M
M
Mertsola
J
J
Granfors
K
K
D000210:Acute-Phase Reaction / Q000209:etiology / Q000276:immunology; D000328:Adult; D015703:Antigens, CD / Q000096:biosynthesis* / Q000276:immunology; D016918:Arthritis, Reactive / Q000097:blood / Q000209:etiology* / Q000276:immunology*; D016207:Cytokines / Q000096:biosynthesis* / Q000276:immunology; D005434:Flow Cytometry; D006801:Humans; D007963:Leukocytes, Mononuclear / Q000276:immunology*; D008297:Male; D008875:Middle Aged; D016133:Polymerase Chain Reaction; D000091402:Prohibitins; D012333:RNA, Messenger / Q000032:analysis; D012480:Salmonella Infections / Q000150:complications* / Q000276:immunology
D015703:Antigens, CD; D016207:Cytokines; C000717331:PHB2 protein, human; D000091402:Prohibitins; D012333:RNA, Messenger