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Goblet cell hyperplasia

The morbidity and mortality that are often associated with human GI helminth infections reflect in part the nutritional consequences of diarrhoea and malabsorption, and the resulting malnutrition that can accentuate the effects of infection by suppressing the protective immune response as well as compromising intestinal repair (Ferguson et al., 1980 Keymer and Tarlton, 1991 Cooper et al, 1992). In experimental rodents the pathology associated with infection is characterized by villus atrophy, crypt hyperplasia, goblet cell hyperplasia and infiltration of the mucosa by a variety of... [Pg.382]

Muc2 and Muc3, and mucin mRNA are coordinately upregulated in response to T. spiralis infection and may form the basis of an innate mucosal response independent of specific IFN-y, TNF and IL-4 cytokines. Importandy, this study also demonstrated that goblet cell hyperplasia and upregulated mucin secretion are not essential components of the protective immune response to GI helminths. [Pg.393]

Information regarding respiratory effects in orally-exposed animals is limited to a report of a significantly increased incidence of nasal lesions (goblet cell hyperplasia and inflammation of nasal turbinates) following 90 days of exposure to chlorine dioxide in the drinking water at concentrations that resulted in estimated doses as low as 2 mg/kg/day in males and 8 mg/kg/day in females (Daniel et al. 1990). These nasal effects were likely caused by inhalation of chlorine dioxide vapors released from the water rather than a systemic respiratory effect following oral exposirre. [Pg.45]

Immediate effects included dyspnea, coughing, irritation of the eyes and throat, headache, giddiness, chest pain, abdominal discomfort. Subjects also exhibited hilar congestion, bronchial vasculature markings, respiratory incapacitation, tracheobronchial congestion, chronic bronchitis, scattered hemorrhages, bronchial erosion. Bronchial smears taken from 28 subjects 5 d after exposure showed basal-cell and goblet-cell hyperplasia, acute inflammation, and chromatolysis... [Pg.127]

Haswell LE, Hewitt K, Thorne D et al (2010) Cigarette smoke total particulate matter increases mucous secreting cell numbers in vitro a potential model of goblet cell hyperplasia. Toxicol In Vitro 24(3) 981-987... [Pg.120]

If IL-4 is targeted to the airway epithelium, an enhancement of goblet cell hyperplasia is observed (416). These experiments showed the multiple functions IL-4 can exert over different cell types. [Pg.176]

A chronic inhalation MRL of 0.008 ppm was derived based on a minimal LOAEL of 0.24 ppm for histological evidence of mild damage to the nasal epithelial tissue (squamous metaplasia, loss of ciliated cells, goblet cell hyperplasia, and mild dysplasia in biopsied tissue) in formaldehyde exposed chemical workers (Holmstrom et al. 1989c). To derive the MRL, the minimal LOAEL was divided by an uncertainty factor of 30 (3 for the use of a minimal LOAEL and 10 for human variability). [Pg.355]

Read, Goblet cell hyperplasia is a feature of the adaptive response to jejunoileal bypass in rats. Gut, 25 62-68 (1984). [Pg.180]


See other pages where Goblet cell hyperplasia is mentioned: [Pg.363]    [Pg.30]    [Pg.236]    [Pg.245]    [Pg.363]    [Pg.384]    [Pg.191]    [Pg.201]    [Pg.202]    [Pg.40]    [Pg.495]    [Pg.197]    [Pg.203]    [Pg.666]    [Pg.163]    [Pg.363]    [Pg.2329]    [Pg.2330]    [Pg.112]    [Pg.2254]    [Pg.111]    [Pg.182]    [Pg.69]    [Pg.70]    [Pg.223]    [Pg.452]    [Pg.9]    [Pg.10]    [Pg.121]    [Pg.259]    [Pg.261]    [Pg.13]    [Pg.89]    [Pg.89]    [Pg.90]    [Pg.98]    [Pg.167]    [Pg.282]    [Pg.282]    [Pg.193]    [Pg.196]    [Pg.200]    [Pg.252]   
See also in sourсe #XX -- [ Pg.374 ]




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