[1] The apical plasma membrane projects short microvilli to give an increased surface area for secretion.

Mucin within the granules stains pale in routine histology sections, primarily because these carbohydrate-rich proteins are washed out in the preparation of microscopy samples.

The main role of goblet cells is to secrete mucus in order to protect the mucous membranes where they are found.

[10] On the inner surface of the human intestine, it forms a 200 μm thick layer (less in other animals) that lubricates and protects the wall of the organ.

[13] Mucins are continuously made and secreted by goblet cells in order to repair and replace the existing mucus layer.

Anomalies in the number of goblet cells are associated with changes in the secretion of mucins, which can result in many of the abnormalities seen in asthma patients, such as clogged airways due to mucus hypersecretion, and eventual loss of lung function.

[13] Overexpression of MUC5AC alone does not result in the pathophysiology seen in asthma patients; it is the excessive production along with the speed of secretion that leads to the formation of thick mucus that cannot be removed by cilia or coughing action.

[17] These cells produce the thick mucins MUC5AC and MUC5B, which clog the airway, leading to the airflow obstruction characteristic of asthma.

[18] This results in docking of STAT6 monomers, which themselves are phosphorylated and then subsequently leave the receptor and congregate form STAT6 homodimers in the cytoplasm.

[18] These homodimers then enter the nucleus, where they bind to regulatory elements in the DNA, which affects the transcription of certain genes involved in mucus production.

[18] Induction of STAT6 signaling by IL-13 leads to increased of expression of 15-lipoxygenase (15-LO-1), which is an enzyme involved in the breakdown of unsaturated fatty acids.

[22] Studies of mice given monoclonal antibodies for IL-13 results in decreased expression of goblet cells in asthma patients.