Published online Oct 7, 2021. doi: 10.3748/wjg.v27.i37.6248
Peer-review started: March 2, 2021
First decision: April 17, 2021
Revised: April 29, 2021
Accepted: August 9, 2021
Article in press: August 9, 2021
Published online: October 7, 2021
Processing time: 211 Days and 1 Hours
Shigella infection is a major public health concern around the world. Shigella flexneri (S. flexneri) is a major pathogen causing acute intestinal infection and is more frequently fatal than other Shigella species. The white blood cell (WBC) count and levels of C-reactive protein (CRP) and cytokines have always been used to evaluate the severity of Shigella-induced infection. Because RNA oxidation plays a substantial role in the progression of multiple diseases, the RNA oxidative product 8-oxo-7,8-dihydroguanosine (8-oxo-Gsn) may be useful as a biomarker for predicting infectious disease progression and severity.
There is no information regarding the diagnostic value of urinary 8-oxo-Gsn and 8-oxo-7,8-dihydro-2-deoxyguanosine (8-oxo-dGsn) in intestinal infection induced by S. flexneri. In addition, the correlation of blood inflammatory-related cytokines with RNA oxidative metabolites is unclear. Furthermore, the systematic tissue oxidative damage during Shigella-induced intestinal infection has not been investigated.
To determine the systemic RNA oxidative damage incurred in S. flexneri-induced intestinal infection and to evaluate the diagnostic value of the RNA oxidative metabolites 8-oxo-Gsn in urine.
Sprague-Dawley rats were used to establish an acute intestinal infection model by oral gavage of S. flexneri strains. The CRP level was measured by ELISA, and cytokines were detected using the MILLIPLEX MAP Kit according to the manufacturer's protocol. Hematoxylin and eosin staining was performed to detect tissue inflammation. Liquid chromatography with tandem mass spectrometry was used to determine the 8-oxo-dGsn and 8-oxo-Gsn levels in urine. Immunohistochemical staining was performed to detect the expression of 8-oxo-Gsn and 8-oxo-dGsn in the ileum, colon, liver, spleen, and brain.
Intestinal infection induced by S. flexneri caused an increase in inflammation-related markers in the blood [WBCs, CRP, tumor necrosis factor α (TNF-α), interleukin (IL)-6, IL-10, IL-1β, IL-4, and IL-17a] and RNA oxidative damage-related markers in the urine (8-oxo-Gsn). The urinary 8-oxo-Gsn level increased after infection and returned to the baseline level after recovery from infection. A correlation analysis showed that urinary 8-oxo-Gsn was positively correlated with the WBC count and the cytokines IL-6, TNF-α, IL-10, IL-1β, and IL-17α. The evaluation of oxidation in different tissues showed that intestinal infection caused by S. flexneri induced an increase in RNA oxidative damage in various tissues, including the intestine, liver, spleen, and brain.
This study demonstrated that acute intestinal infection induced by S. flexneri not only causes RNA oxidative damage in the intestine but also other tissues as well (liver, spleen, and brain). Furthermore, the urinary metabolite of RNA oxidation 8-oxo-Gsn was shown to be useful as a diagnostic index to evaluate the infection status.
Urinary 8-oxo-Gsn can be used as a noninvasive diagnostic biomarker to evaluate the severity and prognosis of infection in clinical practice.