{'fraction_non_alphanumeric': 0.0332409972299169, 'fraction_numerical': 0.024238227146814405, 'mean_word_length': 5.598173515981735, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Pulmonary cryptosporidiosis: role of COX2 and NF‐kB

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.