Table 2.
Expression and implications of MUC5AC in benign pathologies
| Benign conditions | Pathologies | MUC5AC status |
|---|---|---|
| Allergic rhinitis | Disorders of nasopharyngeal mucosa with goblet cell hyperplasia, mast cell infiltration and lymphocytes (66) | MUC5AC is differentially overexpressed during allergic rhinitis, causing airway obstruction and infection (67) |
| Chronic rhinosinusitis | Goblet cell and submucosal gland cell hyperplasia resulting in mucus production and hypersecretion with defective mucociliary clearance of nasopharyngeal mucosa (68) | MUC5AC mRNA and protein levels are observed to be significantly increased in goblet cells of the epithelium in chronic rhinosinusitis compared with those in normal sinus mucosa (68–70) |
| Otitis media | Uncontrolled, excessive mucus production in the eustachian tube and middle ear contributing significantly to conductive hearing loss (71) | Post-transcriptionally modified longer length of MUC5AC mucin results in the higher viscosity of mucin, leading to abnormal mucociliary clearance, middle ear fluid stasis and ultimately chronic disease condition (72) |
| Chronic airway diseases (CADs) | CADs (asthma, cystic fibrosis and chronic obstructive pulmonary disease) are associated with mucous cell metaplasia, resulting in mucus hypersecretory phenotype (15) that involves increased expression, production and release of mucins | A marked increase in MUC5AC mRNA and protein expression is observed in CADs (73). Expression of MUC5AC is also found to be elevated in the cystic fibrosis sputum (74). A 6.4 kb VNTR in the MUC5AC gene has been significantly associated with the severity of cystic fibrosis lung disease (75) |
| Barrett’s esophagus | Premalignant condition of the esophagus consisting of mucosa with a metaplastic columnar epithelium (76) | MUC5AC expression and secretion during Barrett’s esophagus can be attributed to the conjugated bile acids present in the refluxate (77) |
| Helicobacter pylori infections | Helicobacter pylori (H.pylori) colonizes the gastric mucosa to induce chronic inflammation and intestinal metaplasia through genetic and epigenetic changes (78) | H.pylori colonize by its adhesion via BabA and SabA adhesins to the blood group antigens LeB and Sialyl LeX present on gastric mucin MUC5AC (79). The reduced MUC5AC expression might be associated with H.pylori mediated gastric carcinogenesis and the progression to GC (80). Among H.pylori virulence factors, urease virulence factor downregulate MUC5AC mucin expression in cell-specific manner and independent of NF-kB (81) |
| Pancreatitis | Inflammation of the pancreas that may progress to necrosis of the pancreas or surrounding fatty tissue. The two main types include acute and chronic pancreatitis (82) | In a case of autoimmune pancreatitis, the atypical cells were tested positive for the MUC5AC overexpression (83). In case of mouse models, chronic pancreatic injury results in hyperplastic PDGs along with de novo expression of mouse Muc5ac (84) |
| Inflammatory bowel disease | Dysfunctional mucus barrier caused by host immune, microbial, genetic or environmental | MUC5AC expression was detected in the mucus of 70% ulcerative colitis cases and associated with gastric metaplasia during long-standing inflammation to exhibit foveolar differentiation in intestinal mucosa. MUC5AC expression was observed predominantly in columnar cells of the significantly distorted crypts and positively correlated with disease activity and goblet cell depletion (85,86) |