Pulmonary cryptosporidiosis:: role of COX2 and NF-κB

In the present study we investigated whether the pathological changes induced by Cryptosporidium in the lungs are mediated through the activation of COX-2, and whether the pathway employed for this activation involves NF-kB. 70 albino rats were submitted for this work. They were categorized into 3 groups: 30 immunocompetent (IC) rats infected with Cryptosporidium oocysts, 30 immunosuppressed (IS) rats infected with Cryptosporidium oocysts, and 10 IC, non-infected rats. Immunohistochemical expression of COX2 and NF-kB in lung tissues of the rats was examined. 43.3% of IC rats showed chronic pneumonia and fibrosis, 40% COX2 positivity, and 36.67% NF-kB positivity. 96.7% of IS rats showed chronic pneumonia and fibrosis, 56.7% non-caseating granuloma with Cryptosporidium oocysts, and 66.7% positivity for both COX2 and NF-kB. Density of inflammatory infiltration was statistically correlated with quickscore of both COX2 and NF-kB in both IC and IS groups. An association between quickscores of COX2 and NF-kB was found in our studied material. These data could demonstrate that Cryptosporidium infection induces upregulation of COX2 possibly through the NF-kB pathway, which suggests the events that contribute to the pathogenesis of Cryptosporidium. These findings could indicate potential therapeutic pharmacological target-mediating treatment of lesions caused by Cryptosporidium.