The effect of Helicobacter pylori infection on expression of macrophage migration inhibitory factor by T cells and macrophages in gastric mucosa.
BACKGROUND
Macrophage migration inhibitory factor (MIF) plays a pivotal role in inflammatory and immune-mediated diseases. However, its molecular function and role in gastrointestinal diseases has rarely been studied and thus warrants an in-depth investigation. This study was designed and conducted to determine MIF expression in Helicobacter pylori (H. pylori)-induced gastritis and the effect of H. pylori on MIF expression in monocytes in vitro.


METHODS
Gastric specimens of 62 patients with chronic gastritis were obtained through endoscopic biopsies. Both gastric antrum and body were examined for histopathologic changes. Positive H. pylori was determined through rapid urease test and histopathological examination. A patient was classified as H. pylori positive if both tests showed positive results. The updated Sydney System was employed to assess the severity and activity of gastric inflammation. Double immunoassaying for MIF/T-cells (CD45RO) and MIF/macrophage (KP1), as well as in situ hybridization for the expression of MIF mRNA were used for the current analysis. THP-1, a monocyte cell line, was co-incubated with H. pylori strains (ATCC26695) and subsequently examined for the expression of MIF protein and mRNA by enzyme linked immunosorbent assay and retrospective transcription-polymerase chain reaction, respectively.


RESULTS
Among 62 patients with chronic gastritis, significant increase in total T-cells, MIF+ T-cells, total macrophages, MIF+ macrophages and MIF mRNA+ cells was observed in 42 H. pylori positive patients compared to H. pylori negative patients. Moreover, the increase of the MIF mRNA+ cells was highly correlated with the severity of the disease (number of MIF mRNA+ cells/mm(2), mild: 2834 +/- 382, moderate: 3569 +/- 123, severe: 3881 +/- 118, P < 0.01). In vitro results showed that the expression of MIF protein and mRNA in monocytes was significantly increased after incubation with H. pylori strains.


CONCLUSIONS
Overexpression of MIF is common in H. pylori-induced gastric inflammation, which suggests MIF may play an important role in the initiation and development of this disease.
He
Xing-xiang
XX
Department of Gastroenterology, the Second Affiliated Hospital of Guangzhou Medical College, Guangzhou 510260, China. xingxianghe@medmail.com.cn
Yang
Jun
J
Zheng
Xue-ling
XL
Ding
Yuan-wei
YW
Shen
Qing-yan
QY
Liu
Wei
W
Zhao
Ying-heng
YH
D005260:Female; D005753:Gastric Mucosa / Q000737:chemistry / Q000378:metabolism*; D005756:Gastritis / Q000209:etiology / Q000378:metabolism / Q000382:microbiology; D016481:Helicobacter Infections / Q000378:metabolism*; D016480:Helicobacter pylori; D006801:Humans; D008263:Macrophage Migration-Inhibitory Factors / Q000032:analysis* / Q000235:genetics; D008264:Macrophages / Q000737:chemistry / Q000378:metabolism*; D008297:Male; D008875:Middle Aged; D009000:Monocytes / Q000378:metabolism; D012333:RNA, Messenger / Q000032:analysis; D013601:T-Lymphocytes / Q000737:chemistry / Q000378:metabolism*
D008263:Macrophage Migration-Inhibitory Factors; D012333:RNA, Messenger