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Gob-5 contributes to goblet cell hyperplasia and modulates pulmonary tissue inflammation.

Gob-5 is a member of the calcium-activated chloride channel family and has been associated with allergic response in mouse models of pulmonary inflammation. Gene expression of Gob-5 has been shown to be induced in allergic airways and has been strongly associated with mucin gene regulation and goblet cell hyperplasia. We investigated the physiologic role of Gob-5 in murine models of pulmonary inflammation using mice deficient in Gob-5. After sensitization and aerosol challenge with ovalbumin (OVA), Gob-5 knockout mice exhibit significantly increased bronchoalveolar lavage (BAL) inflammation as compared with wild-type controls. The augmented inflammation in BAL consisted predominantly of neutrophils. Examination of perivascular inflammation revealed that tissue inflammation was decreased in OVA-challenged Gob-5-/- mice. OVA-challenged Gob-5 knockout mice also had decreased goblet cell hyperplasia as well as decreased mucus production. These mice also had decreased airway hypersensitivity after cholinergic provocation with methacholine. Gob-5 knockout mice were also challenged via intranasal LPS, a TLR-4 agonist. Gob-5-/- mice responded with increased neutrophilic BAL inflammation and decreased perivascular tissue inflammation as compared with wild-type controls. There was little effect on goblet cell hyperplasia and mucus production after LPS challenge. These observations reinforce findings that associate Gob-5 with goblet cell hyperplasia and mucus production in the allergic immune response, but also implicate Gob-5 in the regulation of tissue inflammation in the innate immune response.

Pubmed ID: 16645179


  • Long AJ
  • Sypek JP
  • Askew R
  • Fish SC
  • Mason LE
  • Williams CM
  • Goldman SJ


American journal of respiratory cell and molecular biology

Publication Data

September 18, 2006

Associated Grants


Mesh Terms

  • Airway Resistance
  • Animals
  • Antigens
  • Bronchoalveolar Lavage Fluid
  • Chemokines
  • Chloride Channels
  • Disease Models, Animal
  • Epithelial Cells
  • Goblet Cells
  • Hyperplasia
  • Lipopolysaccharides
  • Mice
  • Mice, Knockout
  • Mucoproteins
  • Mucus
  • Ovalbumin
  • Pneumonia