DOWNREGULATION OF TOLL-LIKE RECEPTOR 4 AND ACUTE PHASE CYTOKINES MEDIATED DEXAMETHASONE IMMUNOSUPPRESSANT MECHANISM DURING CRYPTOSPORIDIUM-PARVUM INFECTION | ||||
| Journal of the Egyptian Society of Parasitology | ||||
| Article 27, Volume 50, Issue 1, April 2020, Page 197-202 PDF (1.04 MB) | ||||
| Document Type: Original Article | ||||
| DOI: 10.21608/jesp.2020.88837 | ||||
 View on SCiNiTO | ||||
| Authors | ||||
| TAREK K. ZAALOUK1; GAMAL A. ABO SHEISHAA1; IBRAHIM R. SHALASH2 | ||||
| 1Department of Medical Parasitology, Faculty of Medicine, Al-Azhar University, Nasr City, Cairo, Egypt. | ||||
| 2Theodor Bilharz Research Institute2, Imbaba P.O.B. 30, Giza, Egypt. | ||||
| Abstract | ||||
| TLRs in enterocytes play an important role in protecting the mucosal surface by promoting the innate inflammatory immune response following infection. Cryptosporidium parvum generally causes a short-term diarrheal illness that resolves spontaneously in immunocompetent hosts. But, in immunocompromised hosts, (e.g. on steroid therapy), it may cause a life-threatening, chronic, cholera-like illness. The mechanisms by which steroids reduced the host resistance to C. parvum infection are poorly understood. It was hypothesized that steroid may interfere with TLR activation and reduced proinflammatory cytokines production required for early infection containment. To test this hypothesis, sixty C57BL/6 mice were equally divided into three subgroups; G1 was daily given intraperitoneally dexamethasone (DEX) for 14 days before oocyst inoculation and throughout the study. G2 was non-immunosuppressed mice. G1 & G2 were inoculated intragastrically with C. parvum (106 oocysts). G3 was retained as naïve non-infected control. Length and severity of infections were determined by monitoring oocyst shedding in fecal pellets using acid-fast (Ziehl-Neelsen) stained smear prepared from fresh pellets, by counting the number of oocysts in 10 microscopic fields under x100 for each mice group. Expression of TLR4 was assessed by immunohistochemistry, serum of proinflammatory cytokines level was determined by ELISA. The results showed that DEX immunosuppressed mice developed chronic cryptosporidiosis that lasted until the study end. Non-immunosuppressed mice developed a patent infection and the majority of them overcame the infection by the 21st day. The mean oocyst count was significantly higher in the immunosuppressed mice than in non-immunosuppressed ones, with a longer patent period in immunosuppressed mice. Expression of TLR4 was significantly increased in mice gut post-infection. Expression of TLR was significantly decreased in DEX immunosuppressed infected mice, with a significant decr ease was in proinflammatory cytokines serum levels compared to non-immunosuppressed ones. | ||||
| Keywords | ||||
| Mice; Cryptosporidium parvum; Toll-Like Receptor; Acute phase cytokines | ||||
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