Abstract
Although mucins are essential for the protection of internal epithelial surfaces, molecular responses involving mucin production and secretion in response to various infectious agents in the airway have not been fully elucidated. The present study analysed airway goblet cell mucins in rats infected with the nematode Nippostrongylus brasiliensis, which migrates to the lungs shortly after infection. Goblet cell hyperplasia occurred in the bronchial epithelium 3–10 days after infection. The high iron diamine-alcian blue staining combined with neuraminidase treatment showed that sialomucin is the major mucin in hyperplastic goblet cells. Immunohistochemical studies demonstrated that goblet cell mucins were immunoreactive with both the major airway mucin core peptide, Muc5AC, and the major intestinal mucin core peptide Muc2. Reverse transcription real-time PCR studies demonstrated upregulation of gene transcription levels of Muc5AC, Muc2, the sialyltransferase St3gal4, and the resistin-like molecule beta (Retnlb) in the lungs. These results showed that nematode infection induces airway epithelial responses characterised by the production of sialomucin with Muc5AC and Muc2 core peptides. These mucins, as well as Retnlb, might have important roles in the protection of mucosa from migrating nematodes in the airway.
Highlights
Parasitic gastrointestinal nematodes are one of the most commonly acquired infections in the world, affecting approximately one-quarter of the human population [1]
We have previously shown that nematode infection induced intestinal epithelial responses that were characterised by goblet cell hyperplasia and led to an increase in production of sialomucin, sulfomucin, Muc2, the resistin-like molecule beta (Retnlb), and St3gal4 [16,17,18]
We previously reported that sialomucin and sulfomucin-positive goblet cells in intestinal epithelium were upregulated after nematode infection [18]
Summary
Parasitic gastrointestinal nematodes are one of the most commonly acquired infections in the world, affecting approximately one-quarter of the human population [1]. Parasitic helminths place a considerable constraint upon the livestock industry, representing a major economic burden; one recent estimate suggested that £1.7 billion is spent annually on their control [2] They cause relatively little mortality, infections result in high levels of morbidity that can result in developmental consequences in infected children [3] and cause significant economic loss in infected animals [2]. The morbidity induced by these infections is thought to be mediated through a combination of effects on both the nutrition and immunological responses of the host [3] Certain intestinal nematodes, such as Ascaris, hookworms, and Strongyloides, migrate to the lungs before homing to their final habitat, the small intestine. Little is known about the molecular aspects of the responses such as the species of mucins and nonmucin secretory peptides produced in the bronchial
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