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Volume 41, Number 3, June 2008

Host defense against Salmonella and rotaviral gastroenteritis: a serial study of transcriptional factors and cytokines

An-Yi Lin, Ching-Yuang Lin, Ching-Tung Chen, Woan-Ling Chen
Department of Pediatrics, Children’s Hospital, Changhua Christian Hospital, Changhua; and Children’s Medical Center and Graduate Institute of Clinical Medical Science, China Medical University and Hospital, Taichung, Taiwan

Received: March 5, 2005    Revised: April 1, 2006    Accepted: June 15, 2006   


Corresponding author:

Dr. Ching-Yuang Lin, M.D., Ph.D., Children’s Medical Center, China Medical University Hospital, No. 2, Yuh-Der Road, Taichung, Taiwan. E-mail: Dr. Ching-Yuang Lin This e-mail address is being protected from spam bots, you need JavaScript enabled to view it



Background and purpose: 

Common etiologies of acute enterocolitis in childhood include the intracellular pathogens Salmonella and rotavirus, along with extracellular pathogens. In order to elucidate differentiating immunologic parameters in patients with acute gastroenteritis of different etiologies, we investigated interferon (IFN)-gamma, interleukin (IL)-12, and T-bet of T-helper type 1 subsets, and IL-4 and GATA-3 of T-helper type 2 subsets.




From June 1, 2003 to December 31, 2003, 32 patients with acute gastroenteritis were enrolled. Sequential heparinized blood samples were obtained on the day of presentation (day 1) and on day 3 of hospitalization. Using reverse transcriptase-polymerase chain reaction, the mean ratios of IFN-gamma, T-bet and IL-12 mRNA levels relative to beta-actin were determined.



Salmonella infections induced stronger IFN-gamma and T-bet responses than either rotavirus infection or other enterocolitis (p<0.05). However, poor IL-12 response in Salmonella infections implied failed T-helper type 1 immunity, and probably accounted for the prolonged clinical course. In contrast, by day 3 of hospitalization, most patients with rotavirus enterocolitis were symptom-free.




IL-12 is the key factor in determining host response against and, hence, disease activity of Salmonella infections.



Key words:

Cytokines; Interferon type II; Rotavirus; Salmonella; T-lymphocytes, helper-inducer


J Microbiol Immunol Infect. 2008;41:265-271.