Functions of mucin, as the major macromolecular component in saliva or gastric fluids, are drawing increasing attention in the context of understanding the oral processing or digestion of dairy foods at the molecular level. This study was designed to investigate the interactions between β-lactoglobulin (BLG)-lactose, mucin-lactose and BLG-lactose-mucin at the molecular level under different temperature and pH conditions using fluorescence spectroscopy in combination with scanning electron microscopes (sem). It is the first study of its kind. There was no lactose-dependent quenching on BLG fluorophore in the range of 0–10 mM lactose concentration. On the contrary, there was a continuous increase in the fluorescence intensity of the BLG protein when the lactose concentration increased, especially at 25°C. BLG-lactose complex became thermally unstable at 37 and 45°C. Moreover, BLG exhibited a pH dependent conformational change and had higher fluorescence intensity at pH 3 than pH 6.8. The fluorescence result was in correspondence with sem images where we observed lactose crystals gathering around and on the BLG molecule, but lactose molecules could not be seen in the presence of mucin. It was anticipated that mucin molecules interacted with BLG-lactose complex via electrostatic attraction and formed an extra protective layer around the BLG molecules to avoid solvent exposure.

Host mucins have crucial physical roles in preventing the parasitic establishment and maturation, and also in expelling the invading parasites. However, some parasites utilize mucinase enzymes to facilitate the infection. Recently, we have identified a mucinase enzyme of the liver fluke Opisthorchis viverrini, Ov-M60-like-1, which exhibits metallopeptidase activity against bovine submaxillary mucin substrate. Here, we aimed to study the localization of this enzyme in O. viverrini and the bile duct of hamsters using immunohistochemistry and functional analysis by mucin digestion in hamsters and mice tissues. The results showed that Ov-M60-like-1 was detected strongly in the tegument, tegumental cells, vitelline glands and mature eggs with miracidium. Expression in the gut, ovary and testis of the parasite was moderate while parenchyma showed slight colour intensity. In addition, the mucinase was also detected in the host biliary epithelial cells and goblet cells surrounding the worm. The mucinase assay revealed that the Ov-M60-like-1 could digest neutral mucin in the parenchyma, testis and seminal receptacle, but not the mucin in the tegument, tegumental cells and vitelline glands of the worm. The enzyme can also digest mucin in the cholangiocytes and modified the mixture type in the bile duct goblet cells of the infected hamsters, a susceptible host. In contrast, the enzyme was unable to digest neutral, acid and mixture mucin in the bile duct of the mice, a non-susceptible host. These findings indicate that Ov-M60-like-1 may have functions in both housekeeping tasks and host–parasite interactions, especially in modification of host susceptibility.

The objective of the current experiment was to determine the effects of high-concentration phytase (5000 FTU/kg) feeding to diverse lines of chickens fed phosphorus (P) adequate maize–soybean meal diets (4.5 g/kg non-phytate P) on the performance and intestinal immune function. Performance was measured for outbred broiler (Ross 308) and inbred Fayoumi lines over 0–21 days, and duodenum and ileum were harvested for the determination of mucin-2, interleukin (IL)-1β and IgA mRNA by quantitative reverse transcription polymerase chain reaction. Over the 0–7-day period, there was a significant line × diet interaction, as high phytase supplementation increased broiler average daily gain (ADG), but had no effect on Fayoumi ADG. Treatment of diets with phytase increased expression of the mucin-2 gene in the duodenum mucosa. There were significant interactions between line and age, and line, diet and age on duodenal expression of the IL-1β gene as phytase supplementation of the broiler line reduced IL-1β in comparison to control fed broilers without change in the Fayoumi line. Overall, the addition of a high concentration of phytase to broilers fed adequate concentrations of non-phytate P resulted in improved growth performance early with a reduction in this effect over time. Mucosal mucin-2 expression was increased with high-concentration phytase feeding across both lines, but IL-1β mRNA expression was reduced in the duodenum of broilers fed high concentrations of phytase, suggesting that the increased performance noted might be related to decreased inflammation.

Genome sequencing has greatly contributed to our understanding of parasitic protozoa. This is particularly the case for Cryptosporidium species (phylum Apicomplexa) which are difficult to propagate. Because of their polymorphic nature, simple sequence repeats have been used extensively as genotypic markers to differentiate between isolates, but no global analysis of amino acid repeats in Cryptosporidium genomes has been reported. Taking advantage of several newly sequenced Cryptosporidium genomes, a comparative analysis of single-amino-acid repeats (SAARs) in seven species was undertaken. This analysis revealed a striking difference between the SAAR profile of the gastric and intestinal species which infect mammals and one species which infects birds. In average, total SAAR length in gastric species is only 25% of the cumulative SAAR length in the genome of Cryptosporidium parvum, Cryptosporidium hominis and Cryptosporidium meleagridis, species infectious to humans. The SAAR profile in the avian parasite Cryptosporidium baileyi stands out due to the presence of long asparagine repeats. Cryptosporidium baileyi proteins with repeats ⩾20 residues are significantly enriched in regulatory functions. As postulated for the related apicomplexan species Plasmodium falciparum, these observations suggest that Cryptosporidium SAARs evolve in response to selective pressure. The putative selective mechanisms driving SAAR evolution in Cryptosporidium species are unknown.

Cryptosporidium host cell interaction remains fairly obscure compared with other apicomplexans such as Plasmodium or Toxoplasma. The reason for this is probably the inability of this parasite to complete its life cycle in vitro and the lack of a system to genetically modify Cryptosporidium. However, there is a substantial set of data about the molecules involved in attachment and invasion and about the host cell pathways involved in actin arrangement that are altered by the parasite. Here we summarize the recent advances in research on host cell infection regarding the excystation process, attachment and invasion, survival in the cell, egress and the available data on omics.

Immunoglobulins are major glycoproteins that modulate the immune response of gut-associated lymphoid tissue. In the present study, we sought to determine whether orally administered ovine serum immunoglobulins modulate selected indices of mucosal immune function and immune mediators in the growing rat challenged with Salmonella enteritidis. Rats were fed a casein-based basal control diet (BD; unchallenged). Three groups of rats were challenged orally with 1 × 107 viable S. enteritidis on day 15 of the study and were fed the BD, the BD containing freeze-dried ovine immunoglobulins (FDOI), or the BD containing autoclaved ovine immunoglobulins (AOI; negative control diet). The rats were randomly allocated to one of the four groups (n 15) and consumed their diet for 18 d. In all of the intestinal segments, the challenged rats fed either the BD or AOI diet produced higher (P< 0·05) mucosal levels of interferon-γ, TNFα, IgA and myeloperoxidase activity than the challenged rats fed the FDOI diet. In contrast, IL-4 and IL-10 levels were higher in the challenged FDOI-fed rats compared with the other challenged groups. The challenged FDOI-fed rats had higher (P< 0·05) mucosal anti-Salmonella IgA and IgG in all of the intestinal segments except the jejunum and ileum. Generally, the challenged rats receiving the FDOI diet had significantly (P< 0·05) higher mucosal mucin protein content compared with challenged rats receiving either the BD or AOI diet. In conclusion, an ovine immunoglobulin fraction positively modulated some selected indices of mucosal immune function and its mediators in growing rats challenged with S. enteritidis.

The effect of a dietary phytogenic feed additive (PFA) inclusion level in mucin monosaccharide composition, mucosal morphometry and mucus histochemistry along the broiler intestinal tract was studied. Cobb male broilers (n = 525) were allocated into five experimental treatments that, depending on the type of addition in the basal diet (BD), were labeled as follows: C (BD based on maize–soybean meal with no other additions), E1 (80 mg PFA/kg BD), E2 (125 mg PFA/kg BD), E3 (250 mg PFA/kg of BD) and A (2.5 mg avilamycin/kg BD). Samples from duodenum, ileum and cecum of 14- and 42-day-old broilers were collected and analyzed. In 14-day-old broilers, treatments E2 and E3 had higher (P < 0.01) duodenal mannose than treatments C, E1 and A. Ileal mannose was lower (P < 0.05) in treatment C compared with PFA treatments, and ileal galactose (Gal) was higher (P < 0.01) in treatments E2 and E3 compared with C and A. Polynomial contrast analysis with respect to PFA inclusion level showed that in 14-day-old broilers there was a linear increase (P = 0.001) in duodenal mannose and a quadratic effect (P = 0.038) in duodenal N-acetyl-galactosamine with increasing PFA level. Ileal Gal and mannose increased linearly (P = 0.002 and P = 0.012, respectively) with PFA inclusion level. There were no significant differences between treatments in mucin monosaccharide molar ratios of 42-day-old broilers. However, increasing PFA inclusion level resulted in a linear decrease of ileal fucose (P = 0.021) and cecal N-acetylgalactosamine (P = 0.036). Experimental treatments did not differ (P > 0.05) regarding duodenal villus height (Vh), crypt depth (Cd) and Vh/Cd ratio, irrespective of broiler age and the intestinal segment examined. However, increasing dietary PFA inclusion level showed a pattern of linear increase of duodenal Vh/Cd ratio in 14-day-old broilers and ileal Vh in 42-day-old broilers (P = 0.039 and P = 0.039, respectively). Alcian Blue–Periodic Acid-Schiff (pH 2.5) staining of neutral and acidic mucins showed that the staining intensity of mucus layer in villi was fragment (i.e. tip, midsection and base) dependent, whereas in crypts it was dependent both on intestinal segment (i.e. duodenum, ileum and cecum) and fragment. Finally, mucus layer thickness did not differ (P > 0.05) between treatments, yet a pattern of linear increase (P < 0.05) with PFA inclusion level was observed in the duodenum of 42-day-old broilers. In conclusion, the dietary inclusion level of PFA modulated broiler intestinal mucin composition and morphology. Further studies are required to elucidate the physiological implications of such changes in host–microflora interactions.

β-(1,3)-d-Glucan with β-(1,6) branches has been reported to have various pharmacological activities, such as anti-tumour and anti-infection activities, which result from its immunomodulating effects. Gastric lesions result from an imbalance between aggressive and defensive factors. In the present study, we examined the effect of β-(1,3)-d-glucan with β-(1,6) branches isolated from Aureobasidium pullulans on the gastric ulcerogenic response in mice. Oral administration of β-glucan ameliorated gastric lesions induced by ethanol (EtOH) or HCl. This administration of β-glucan also suppressed EtOH-induced inflammatory responses, such as infiltration of neutrophils and expression of pro-inflammatory cytokines, chemokines and cell adhesion molecules (CAM) at the gastric mucosa. Of the various defensive factors, the levels of heat shock protein (HSP) 70 and mucin but not PGE2 were increased by the administration of β-glucan. β-Glucan-dependent induction of the expression of HSP70 and mucin proteins and suppression of the expression of pro-inflammatory cytokines, chemokines and CAM were also observed in cultured cells in vitro. The results of the present study suggest that β-glucan protects the gastric mucosa from the formation of irritant-induced lesions by increasing the levels of defensive factors, such as HSP70 and mucin.

The aim of the present study was to establish the optimum inclusion level of laminarin derived from Laminaria digitata on selected microbial populations, intestinal fermentation, cytokine and mucin gene expression in the porcine ileum and colon. A total of twenty-one pigs (mean body weight 17·9 kg) were randomly assigned to one of three dietary treatments: T1 – basal (control) diet, T2 and T3 – basal diets supplemented with laminarin included at 300 and 600 parts per million (ppm), respectively. Selected intestinal bacterial populations and volatile fatty acid (VFA) concentrations were measured in the ileum and colon. Relative gene expression levels for specific cytokine and mucin genes were investigated in ileal and colonic tissue in the absence and presence of a lipopolysaccharide (LPS) challenge. There was an up-regulation of MUC2 gene expression at the 300 ppm inclusion level in the ileum. In the colon, there was a significant reduction in the enterobacteriaceae population at the 300 ppm inclusion level (P = 0·0421). Dietary supplementation of 600 ppm laminarin led to a significant increase in MUC2 (P = 0·0365) and MUC4 (P = 0·0401) expression in the colon, and in the total VFA concentration in the caecum (P = 0·0489). A significant increase was also recorded in IL-6 (P = 0·0289) and IL-8 gene expression (P = 0·0245) in LPS-challenged colonic tissue at both laminarin inclusion levels. In conclusion, dietary inclusion of 300 ppm laminarin appears to be the optimum dose in the present study due to the reduction in the enterobacteriaceae populations and enhanced IL-6 and IL-8 cytokine expression in response to an ex vivo LPS challenge.

Weaning of livestock mammals is often associated with digestive problems related to profound changes in the physiology of the gastrointestinal tract. This study was undertaken to study the developmental changes in the gastrointestinal tract of mink kits during the period of 34 to 59 days of age. Twenty-four mink kits from eight litters were included in the experiment. The dams and their litters were kept under standard farm conditions. The dams and the kits were fed a diet consisting of 48.1% protein, 40.7% fat and 11.1% carbohydrate of metabolizable energy. The mink kits were weaned at 42 days of age. At 34, 47 and 59 days of age, one male mink kit from each litter was euthanized. The activity of amylase, trypsin, chymotrypsin and lipase in the pancreatic tissue increased during the experimental period, whereas the activity of carboxyl ester hydrolase remained constant. The vitamin E concentration in plasma was stable from 34 to 59 days of age, whereas the concentration decreased in the liver. The stereochemical composition of α-tocopherol showed a steep decrease in the concentration of the biologically most active natural isomer in both plasma and liver through the whole weaning period, whereas the biologically less active 2S isomers showed a clear increase. The concentration of bile salts did not change during the experimental period. The villous height increased in the proximal part of the small intestine and decreased in the distal part, whereas the crypt depth was doubled in both the proximal and distal part of the small intestine. The mucin-staining area on the villi was markedly reduced during the experimental period but no change in the mucin-staining area in the crypts was observed.

Dietary protein might modulate mucin flow and intestinal mucin gene expression. Since unheated phaseolin from Phaseolus vulgaris bean is resistant to digestion and increases gut endogenous protein losses, we hypothesised that unheated phaseolin influences mucin flow and gene expression, and that phaseolin heat treatment reverses these effects. The hypothesis was tested using a control diet containing casein as the sole protein source and three other diets with casein being replaced by 33 and 67 % of unheated and 67 % of heated phaseolin. The rats were fed for 6 d and euthanised. Digesta and faeces were collected for determining digestibility and mucin flow. Gut tissues were collected for mucin (Muc1, Muc2, Muc3 and Muc4) and Trefoil factor 3 (Tff3) gene expressions. Colonic mucin flow decreased linearly with increasing the dietary level of unheated phaseolin (P < 0·05). Unheated phaseolin increased N flow in ileum, colon and faeces (P < 0·05), and reduced apparent N digestibility linearly (P < 0·01). Heat treatment reversed all these changes (P < 0·05 to < 0·001), except mucin flow. The expressions of Muc mRNA in gut tissues were influenced by dietary phaseolin level (ileum and colon: Muc3 and Muc4) and thermal treatment (ileum: Muc2; colon: Muc2, Muc3, Muc4 and Tff3) (P < 0·05 to 0·001). In conclusion, phaseolin modulates mucin flow and Muc gene expression along the intestines differentially.

The present experiment aimed to study the influence of six sources of non-digestible carbohydrates (NDC) on the mucous layer in the colon of rats. The NDC sources used were as follows: cellulose (C); pectin (P); inulin; resistant starch (RS); barley hulls. The diets contained 108–140 g NDC/kg DM. A fibre-free (FF) diet served as a control. The diets were fed to forty-eight rats for 34–41 d. The thickness of the total mucous layer in the colon was increased (P < 0·05) in rats fed C, P and RS when compared with rats fed a FF diet. In the colon, positive correlations were observed between the total thickness of the mucous layer and the area of neutral mucins, the pool of SCFA and the pool of acetic acid, while it was negatively correlated with the proportion of butyrate. The total thickness of the mucous layer was not correlated with the MUC gene transcription. The transcription of the gene MUC2 was negatively correlated (P = 0·04), whereas the transcription of MUC3 was positively correlated (P = 0·05) with the butyrate pool in the caecum. No correlations between the MUC2 or MUC3 transcription and SCFA were found in the colon. Hence, the regulation of the MUC genes differs between the compartments of the hindgut and, within compartments, the MUC genes may be regulated differently. In conclusion, a diet providing a large pool of SCFA with a low proportion of butyrate in the colon stimulates the formation of a thick mucous layer, which probably benefits intestinal health.

The influence of the form of phytic acid on the regulation of mucin and endogenous losses of amino acids, nitrogen and energy in chickens was investigated. Forty-eight 10-week-old male broilers were grouped by weight into eight blocks of six cages with one bird per cage. Birds received by intubation six dextrose-based combinations of phytic acid and phytase arranged in a 3 × 2 factorial consisting of phytic acid form (no phytic acid, 1·0 g free phytic acid or 1·3 g magnesium–potassium phytate) and phytase (0 or 1000 units). Each bird received the assigned combination added to 25 g dextrose at each of the two feedings on the first day of experimentation. All excreta were collected continuously for 54 h following feeding and frozen until analysed. Frozen excreta were thawed, pooled for each bird, lyophilised, ground, and analysed for DM, energy, nitrogen, amino acids, mucin, and sialic and uric acids. Chickens fed either magnesium–potassium phytate or free phytic acid showed increased (P < 0·05) loss of crude mucin and sialic acid. The amount of crude mucin lost was significantly greater (P < 0·05) with magnesium–potassium phytate than with free phytic acid treatment. Both phytic acid treatments also increased (P < 0·05) endogenous loss of threonine, proline and serine. In conclusion, the form of phytic acid fed to chickens affects the extent of mucin and endogenous amino acid losses from the gastrointestinal tract.

Infection and inflammation in the gastrointestinal (GI) tract induces a number of changes in the GI physiology of the host. Experimental infections with parasites represent valuable models to study the structural and physiological changes in the GI tract. This review addresses research on the interface between the immune system and GI physiology, dealing specifically with 2 major components of intestinal physiology, namely mucin production and muscle function in relation to host defence, primarily based on studies using the mouse-Trichinella spiralis system. These studies demonstrate that the infection-induced T helper 2 type immune response is critical in generating the alterations of infection-induced mucin production and muscle function, and that this immune-mediated alteration in gut physiology is associated with host defence mechanisms. In addition, by manipulating the host immune response, it is possible to modulate the accompanying physiological changes, which may have clinical relevance. In addition to enhancing our understanding of immunological control of GI physiological changes in the context of host defence against enteric infections, the data acquired using the mouse-T. spiralis model provide a basis for understanding the pathophysiology of a wide range of GI disorders associated with altered gut physiology.

Fructo-oligosaccharides (FOS) are widely used in commercial food products. Most studies on FOS concern the health benefits, but some negative effects were recently reported concerning thefaecal cytotoxicity and excretion of mucin-type oligosaccharides in combination with a Ca-restricted diet. The present study was performed to investigate whether these effects of FOS are observed in adults consuming a regular diet unrestricted in Ca. The study was a randomised, double-blind, placebo-controlled crossover trial, involving eleven healthy adults, who consumed 25–30g FOS or maltodextrin (control) in a random order for 2 weeks in addition to their regular diet. Stools were collected for analysis of pH and SCFA (as markers of fermentation), for the assessment of faecal water cytotoxicity, and for the analysis of alkaline phosphataseactivity (as a marker of epithelial cell turnover) andO-linked oligosaccharides (to estimate the excretion of mucin-type oligosaccharides). FOS consumption significantly altered bacterial fermentation (increased percentage of acetate, decreased percentage of butyrate) and tended to decrease stool pH. Furthermore, FOS consumption resulted in a significantly higher stool frequency and in significantly more complaints of flatulence. No significant differences between the control and FOS period were observed in the mean cytotoxicity of faecal water (37·5 (sem 6·9) % v. 18·5 (sem 6·9) % P=0·084), in mean alkaline phosphatase activity (27·7 (sem 2·9) v. 24·6 (sem 3·2) U/g dry faeces; P=0·496) or in the mean excretion of mucin-type oligosaccharides (49·9 (sem 4·0)v. 53·5 (sem 4·3) mg/g dry faeces; P=0·553). We conclude that dietary FOS in a dose up to 25–30g/d altered the bacterial fermentation pattern but did not affect faecal cytotoxicity or the faecal concentration of mucin-type oligosaccharides in human adults consuming a regular diet.

The aim of this study is to document a case of Extra Mammary Paget's Disease (EMPD), which was treated with radiotherapy at the Suffolk Oncology Centre. We have shown evidence, both in the reviewed literature and in this study, that radiotherapy can be used successfully as a primary form of treatment for this disease.

The patient discussed in this paper had EMPD in the perianal region. 40 Gy in 10# using a parallel-opposed pair field arrangement was prescribed. However due to mental and physical frailty only 90% of the dose could be delivered. The patient suffered only minor side effects and three years post-radiotherapy was still disease free. We can therefore say that radiotherapy was successful in this instance.

We concluded that there is a definite role for radiotherapy in the management of EMPD and that it can be effective as a primary treatment, where the only other option could be mutilating surgery.

Fasciola hepatica secretes proteolytic enzymes and other molecules that are essential for host penetration and migration. This mixture may include enzymes required for the degradation of supramucosal gels, which defend epithelial surfaces against pathogen entry. These contain hydrated mucins that are heavily glycosylated. Excretory-secretory products (ES) from F. hepatica were examined for a range of glycosidase activities, using synthetic 4-methylumbelliferyl glycosides as substrates. The ES product contained at least 8 different glycosidase activities, the most abundant of which were β-N-acetylhexosaminidase, β-galactosidase and β-glucosidase. Alpha-fucosidase, β-glucuronidase, α-galactosidase, α-mannosidase and neuraminidase were also present. β-N-acetylhexosaminidase and β-galactosidase were present in multiple isoforms (at least 4), whereas β-glucosidase appeared to exist as one isoenzyme with a pI <3·8. All three enzymes had acidic pH optima (4·5–5·0). Ovine small intestinal mucin was degraded by ES at pH 4·5 or 7·0, with or without active cathepsin L, the major protease found in F. hepatica ES. The ability of F. hepatica ES to degrade mucin in the presence or absence of active cathepsin L suggests that cathepsin L is not essential for mucin degradation. The abundance of β-galactosidase and β-hexosaminidase in ES supports a role for these enzymes in mucin degradation.

The effects of fructans in the diet on the mucosal morphometry (height of villi, depth of the crypts, number of goblet cells), the thickness of the epithelial mucus layer and the histochemical composition of intestinal mucosubstances in the distal jejunum and the distal colon were investigated by comparing germ-free (GF) rats, rats harbouring Bacteroides vulgatus and Bifidobacterium longum (diassociated (DA) rats), and rats with a human faecal flora (HFA). The rats were fed either a commercial standard diet (ST) or ST + (50 g oligofructose (OF)–long-chain inulin (lcIN))/kg. Changes in total bacteria, bifidobacteria and Bacteroides–Prevotella in response to feeding these diets were investigated by fluorescent in situ hybridization with 16S rRNA-targeted probes both in intestinal contents (lumen bacteria) and tissue sections (mucosa-associated bacteria). The OF–lcIN-containing diet resulted in higher villi and deeper crypts in bacteria-associated, but not in GF rats. In DA and HFA rats, the colonic epithelial mucus layer was thicker and the numbers of the goblet cells were greater than in GF rats. These effects were enhanced by the OF–lcIN-containing diet. In both dietary groups, bacterial colonization of GF rats caused an increase in neutral mucins in the distal jejunum and colon. Bacteria-associated rats had more acidic mucins in the colon than GF rats, and the OF–lcIN-containing diet stimulated sulfomucins as the predominant type of acidic mucins, while sialomucins dominated in the ST-fed groups. The number of mucosa-associated bifidobacteria detected in the colon of DA and HFA rats was greater with OF–lcIN than ST (4·9 and 5·4 v. 3·5 and 4·0 log10/mm2 mucosal surface respectively), whereas the number of luminal bifidobacteria was only affected by fructans in DA rats. Bacteroides did not differ between the groups. The stabilisation of the gut mucosal barrier, either by changes in the mucosal architecture itself, in released mucins or by stimulation of mucosal bifidobacteria with fructans, could become an important topic in the treatment and prophylaxis of gastrointestinal disorders and health maintenance.

Polymorphic epithelial mucin (PEM), the protein product of the gene muc-1, is a surface glycoprotein that is produced by a range of normal epithelial cells, but has been shown to be expressed at high levels in a range of adenocarcinomas. It has not been investigated extensively in head and neck related tissues, and not at all in head and neck squamous cell carcinomas (HNSCC). This immunohistochemical investigation using two monoclonal antibodies to muc-1 represents a baseline study of 18 HNSCC. In 13 cases, the glycoprotein was expressed at varying levels, usually in keratinizing foci. Although less prominent, expression was also present to some degree in nine of 23 control specimens of non-neoplastic mucosa, mostly at an epithelial level early in the parakeratinization process. Both antibodies showed a pattern of staining. The cellular basis for muc-1 expression is speculative at present and although it is at a lower level than in adenocarcinomas, it may help to provide further insight into epithelial cell differentiation in squamous cell carcinomas.