Antigen Absorption Research Articles

Dietary wheat germ agglutinin modulates ovalbumin-induced immune responses in Brown Norway rats.

The trend towards an increased consumption of minimally processed plant food results in a higher intake of non-nutritive compounds such as lectins. Lectins are typically globular proteins that are resistant to digestion in the gastrointestinal tract. They affect the integrity of the intestinal epithelium and the absorption of dietary antigens, and induce the release of allergic mediators from mast cells in vitro. Based on this information we have studied whether dietary wheat germ agglutinin (WGA) could be involved in triggering food allergies. Brown Norway rats were immunized intraperitoneally using ovalbumin (OVA; 10 microg/rat) and 10 d later treated for five consecutive days with WGA (10 mg/rat per d) administered intragastrically. Rats were then orally challenged with OVA (100 microg/rat) 1 h after the last WGA application, and blood was collected 4 h later. Immunological responses (anti-OVA immunoglobulins E and G, rat mast cell protease II, interferon-gamma and lymphocyte proliferation) were measured and lymphocyte subpopulations were determined. In immunized rats WGA treatment resulted in increased serum rat mast cell protease II concentrations (pre-challenge 0.26 (SE 0.08) microg/ml, post-challenge 0.49 (SE 0.09) microg/ml; P < 0.01) 4 h after the OVA challenge. After 5 d serum concentrations of anti-OVA immunoglobulin E were significantly increased only in the immunized controls (absorbance at 405 nm on days 14 and 19 was 0.09 (SE 0.008) and 0.24 (SE 0.046) respectively; P = 0.02), while in WGA-treated rats no significant increase was seen (0.08 (SE 0.004) and 0.15 (SE 0.037 respectively; P = 0.14). CD4+ : CD8+ T lymphocytes in the spleen was significantly increased at this time (OVA 1.1 (SD 0.2), 1.4 (sd 0.1), P < 0.05). The treatment did not impair the proliferation and interferon-gamma production of mesenteric lymphocytes. In conclusion, these data suggest that high dietary intake of lectins such as WGA may affect the allergic response towards oral antigens in the gut-associated lymphoid tissue.

Cyclooxygenase (COX) 1 and 2 in normal, inflamed, and ulcerated human gastric mucosa

BACKGROUND AND AIMSConstitutive cyclooxygenase (COX) 1 is believed to mediate prostaglandin dependent gastric protection. However, gastric mucosa contains cells capable of expressing inducible COX-2. We therefore investigated COX-1 and COX-2...

Expression of a neu/c-erbB-2-like product in neuroendocrine cells of mammals.

The neu/c-erbB-2 oncogene encodes a 185 kDa protein closely homologous to the epidermal growth factor receptor. The protein product (p185) is a glycoprotein with an external domain and an internal domain with tyrosine kinase activity. Amplification and/or overexpression of p185 is related to several human adenocarcinomas. Subsequent studies demonstrated its presence in certain neuroendocrine (NE) neoplasms, including phaeochromocytomas, insulinomas and medullary thyroid carcinomas. However, relatively little is known about its role in normal cell growth regulation and development. Therefore, our objective was to determine whether neu/c-erbB-2 was expressed in normal NE tissues of different mammals, specially in humans, as it was in their neoplasms. We have examined by immunohistochemistry different endocrine glands (thyroid, pancreas, suprarrenal and hypophysis) and the small intestine of human beings, rats and guinea pigs, using two polyclonal antibodies raised against the intracytoplasmic part of the protein, and specific antigen absorption controls. We have found that a neu/c-erbB-2-like product occurs in all normal NE tissues examined: C cells of the thyroid gland, chromaffin cells of the adrenal medulla, pancreatic islets, enteroendocrine cells of the small intestine and, finally, scattered cells of the adenohypophysis, according to a typical granular immunohistochemical pattern. Our results indicate that normal NE cells share a new common antigen in their cytoplasms, a neu/c-erbB-2-like product, with a similar immunostaining pattern to that presented by the neoplasms derived from them.

Effect of diesel exhaust on guinea pig nasal mucosa.

In this study using guinea pigs, we investigated the effects of diesel exhaust (DE) containing diesel exhaust particulate (DEP) on 1) vascular permeability induced by histamine, 2) nasal mucosal permeability to horseradish peroxidase (HRP), and 3) eosinophilic epithelial infiltration. The vascular permeability induced by histamine was enhanced significantly and dose-dependently in DE-exposed guinea pigs. The HRP reaction products in epithelial cells and intercellular spaces were significantly and dose-dependently increased in those guinea pigs. Eosinophil infiltration into the epithelial layer was significantly increased in guinea pigs exposed to DE containing 3.2 mg/m3 DEP, and the reactivity of the nasal mucosa to histamine solution applied on the nasal mucosa was significantly enhanced in those guinea pigs. These findings suggest that DE may play an important role not only in promoting nasal hyperreactivity induced by the enhancement of absorption of antigen through the nasal epithelium, but also in inducing eosinophil infiltration in nasal mucosa and enhancing nasal mucosal reactivity.

Sensitisation through breast milk?

The benefit of breast feeding to prevent or delay the development of food allergy in infants is somewhat controversial. Although prolonged breast feeding has widely been recommended for infants at high risk of allergy, studies concerning the composition of human milk in atopic mothers are scarce. Human breast milk is not a stabile concept. We have previously found that the cellular composition of human milk is significantly different in mothers with a food allergic infant than in those with a healthy child. The number of monocytes, lymphocytes or eosinophils, was greatly elevated whereas the number of activated macrophages was decreased in the breast milk of mothers with a severely allergic infant. The high numbers of eosinophils could easily increase the permeability of the gut thereby increasing the absorption of dietary antigens, and thus enhance the development of food allergies. Breast feeding provide many advantages to the suckling infant. However, infants developing food allergic symptoms on exclusive breast feeding may benefit from changing to formula feeding to protect adequate growth and to prevent the development of a more severe allergic symptomatology.

Prospective study of Entamoeba dispar infection in a cohort of mothers and their infants: relationship to serum antibody response.

The sera of cohorts of newborn infants and their mothers, characterized as cyst passers of Entamoeba with nonpathogenic zymodemes (E. dispar) and seropositive for amoebic antigens, were analyzed. Both cohorts were followed for a period of 12 months by microscopic examination of feces and determination of serum anti-amoebic antibody titers using the indirect hemagglutination assay. Control groups (noncyst passer mothers and their infants) were included and followed. To characterize antigens involved in the induction of IgG and IgA antibody responses, Western blots of serum from all participants were tested and immunoplots of the frequency of antigenic recognition were constructed. Results of clinical follow-up and microscopic examination of feces showed that during the 12-month period none of the cyst passer mothers had episodes of diarrhea attributable to E. histolytica invasion; five of 21 children of cyst passer mothers became infected during the study, five of five infected children developed serum antiamebic antibodies (titers 1:64-1:128); none of the cohort of children from cyst passer mothers had diarrhea due to E. histolytica. Western blot analysis showed that there are antigenic fractions that induce serum antibodies of the IgG and IgA classes against E. dispar very early in the host-parasite relationship. Our results suggest that mechanisms of antibody induction different from intestinal invasion may be operating in amebic infection. Intestinal absorption of antigen, systemic reflection of secretory antibody response, and priming of newborns by maternal anti-idiotypic antibody transfer are discussed.

Breast milk and the prevention of neonatal and preterm gastrointestinal disease states: a new perspective.

In this review of the protective properties of human breast milk, a new perspective is taken to underscore the passive and active protection properties of breast milk in providing specific protection against selective gastrointestinal disease affecting the neonate and preterm infant. The normal protective properties of the gastrointestinal epithelial barrier (immunologic and nonimmunologic) are considered as is the development of barriers to antigen absorption in the immature infant human intestine as a background for considering three accelerated gastrointestinal diseases-necrotizing enterocolitis, intestinal allergy, and bacterial gastroenteritis. In each of these conditions, the developmental protective defect is considered and the role of breast milk plays in filling the protective void discussed. Besides considering passive protection of breast milk including the new roles assigned to nutrients such as lactoferrin and nucleotides, and importance of active substances in breast milk such as growth factors, cytokines and hormones are discussed in the context of actively stimulating the infant's own intestinal defenses to function as a protective barrier. Future studies at the cellular and molecular level should be helpful in designing both preventative and treatment strategies to deal with these diseases.

Outer periarteriolar lymphoid sheath arrest and subsequent differentiation of both naive and tolerant immunoglobulin transgenic B cells is determined by B cell receptor occupancy.

T-dependent B cell responses in the spleen are initiated in the outer periarteriolar lymphoid sheath (PALS) and culminate in the generation of proliferative foci and germinal center reactions. By pulsing anti-hen egg lysozyme (HEL) immunoglobulin transgenic (IgTg) B cells with various concentrations of HEL in vitro before adoptive transfer into normal recipients, it was shown that a critical number of B cell receptors (BCRs) must be ligated for B cells to undergo arrest in the outer PALS. T cell help was manipulated independently of the BCR stimulus by incubating B cells expressing the appropriate major histocompatibility complex class II antigen with a peptide recognized by CD4(+) TCR Tg T cells. B cells which either failed to arrest in the outer PALS due to a subthreshold BCR stimulus, or arrested only transiently due to the brevity of the BCR stimulus, underwent an abortive response within the follicles when provided with T cell help. In contrast, naive B cells stimulated by a sustained, suprathreshold concentration of either foreign or self-antigen and given T cell help, proliferated in the outer PALS and then differentiated. Outer PALS arrest was not influenced by the nature of the B cells occupying the follicle, but appeared to be determined solely by the magnitude of BCR stimulation. Thus antigen-pulsed B cells arrested in the outer PALS in an identical manner irrespective of whether the follicles comprised a population of normal B cells with multiple specificities, a monoclonal naive population, or a monoclonal population of tolerant B cells. In addition, tolerant B cells were found to relocate from the follicles to the outer PALS of HEL/anti-HEL double Tg mice in which the concentration of soluble self-antigen had been increased by zinc feeding. Similarly, when anti-HEL Tg mice were crossed with a second HEL Tg strain expressing a higher concentration of soluble HEL, the tolerant anti-HEL Tg B cells were located constitutively in the outer PALS. Thus, subtle variations in antigen concentration resulted in dramatic changes in positioning of B cells within the spleen. A series of mixed bone marrow chimeras in which the effective antigen concentration was inversely related to the number of self-reactive B cells due to absorption of antigen by transgene-encoded membrane and secreted Ig, was used to confirm that alteration in B cell position previously attributed to changes in follicular composition could be explained on the basis of available antigen concentration, rather than the diversity of the repertoire.

Pharmacokinetics of allergens after local administration.

The authors review the status of knowledge on absorption and kinetic of allergens administered on nasal mucosa. Intranasal administration is well known in pharmacology, and has been used for a long time for peptide drugs, mainly hormones. The immunological response to intranasally administered antigens have been studied in some experimental models: bovine Rnase, dextran, KLH, tetanus toxoid. These studies showed in atopic people a greater absorption of antigens by nasal mucosa compared to normal individuals, a difference that might be of importance in the pathogenesis of atopic diseases. The absorption rate of peptides through nasal mucosa has been studied biologically by PK-test with Rnase and peanut allergen, and a consistent passage of intact molecules has been observed. Using as tracer 125I-labelled human albumin, transport across the nasal mucosa has been demonstrated in 3/9 normal subjects, 1/9 patients with extrinsic asthma and 9/10 patients with atopic rhinitis. In experimental animals (rabbits) the passage of allergens through the nasal mucosa has been confirmed using 125I-labelled Parietaria allergens that showed a peak in the bloodstream 60 min after administration. It is concluded that peptide molecules such as allergens can be absorbed through the nasal mucosa and reach the bloodstream, and that in atopic patients nasal permeability is enhanced.

Probiotics: A novel approach in the management of food allergy

Background: The gastrointestinal microflora is an important constituent of the gut mucosal defense barrier. We have previously shown that a human intestinal floral strain, Lactobacillus GG (ATCC 53103), promotes local antigen-specific immune responses (particularly in the IgA class), prevents permeability defects, and confers controlled antigen absorption. Objective: The aim of this study was to evaluate the clinical and immunologic effects of cow's milk elimination without ( n = 14) and with ( n = 13) the addition of Lactobacillus GG (5 × 10 8 colony-forming units/gm formula) in an extensively hydrolyzed whey formula in infants with atopic eczema and cow's milk allergy. The second part of the study involved 10 breast-fed infants who had atopic eczema and cow's milk allergy. In this group Lactobacillus GG was given to nursing mothers. Methods: The severity of atopic eczema was assessed by clinical scoring. The concentrations of fecal α 1-antitrypsin, tumor necrosis factor-α, and eosinophil cationic protein were determined as markers of intestinal inflammation before and after dietary intervention. Results: The clinical score of atopic dermatitis improved significantly during the 1-month study period in infants treated with the extensively hydrolyzed whey formula fortified with Lactobacillus GG. The concentration of α 1-antitrypsin decreased significantly in this group ( p = 0.03) but not in the group receiving the whey formula without Lactobacillus GG ( p = 0.68). In parallel, the median (lower quartile to upper quartile) concentration of fecal tumor necrosis factor-α decreased significantly in this group, from 709 pg/gm (91 to 1131 pg/gm) to 34 pg/gm (19 to 103 pg/gm) ( p = 0.003), but not in those receiving the extensively hydrolyzed whey formula only ( p= 0.38). The concentration of fecal eosinophil cationic protein remained unaltered during therapy. Conclusion: These results suggest that probiotic bacteria may promote endogenous barrier mechanisms in patients with atopic dermatitis and food allergy, and by alleviating intestinal inflammation, may act as a useful tool in the treatment of food allergy. (J Allergy Clin Immunol 1997;99:179-85.)

Impaired gut barrier function in malnourished patients

The gastrointestinal tract is essential to host defence, acting as a barrier to absorption and translocation of gut antigens, including bacteria. In experimental models, protein malnutrition is permissive to gut barrier failure and endogenous infection. A clinical correlate has not been described. Intestinal morphology and barrier function to food protein antigens was studied in malnourished patients. Thirty-five individuals were evaluated, 20 malnourished patients and 15 well nourished hospital controls. Morphology was assessed from endoscopic biopsies of the second part of the duodenum, and serum immunoglobulin (Ig) G antibodies to gliadin and beta-lactoglobulin were measured. No antibody to food proteins was evident in the control group. In contrast, serum IgG antibodies to at least one antigen were present in 15 malnourished patients and to both antigens in ten (P < 0.0001 versus controls). Severely malnourished patients were more likely to have both antibodies present than those with mild or moderate malnutrition (P < 0.05). Antibody-positive malnourished patients had significantly better nutritional status than antibody-negative patients with malnutrition (P < 0.05). In no group of patients was there morphological evidence of abnormal mucosa or an immunological infiltrate. Gut barrier function is compromised in malnourished patients which suggests a mechanism that may facilitate gut-derived infection and sepsis.

Evaluation of suprapubic bladder aspiration for detection of group B streptococcal antigen by latex agglutination in neonatal urine.

Our objective was to determine whether urine collection by suprapubic bladder aspiration (SBA) improves the specificity of the group B streptococcal (GBS) latex agglutination (LA) test by avoiding contamination of urine with GBS from perineal and rectal colonization that can result in a positive LA test in an uninfected infant when the urine is collected by bag. Part 1 consists of a retrospective review of the medical records of 113 infants who had urine collected by SBA for GBS LA testing as part of evaluation for possible sepsis. The sensitivity and specificity of the urine LA test was assessed by comparing it with blood culture results. In part 2, a prospective analysis was performed of 19 newborns who had rectal and vaginal/penile cultures as well as urine by SBA and bag for GBS cultures and LA. Results of LA testing on urine collected by both of these methods were compared with results of urine, perineal, and rectal cultures. In the retrospective review of GBS LA testing performed on 113 consecutive urine specimens collected by SBA from neonates being evaluated for suspected sepsis, the sensitivity and specificity were 67% and 89%, respectively, when compared with blood culture results. Twelve infants who had a positive LA test result but a sterile blood culture (BC-,LA+) were compared with 95 infants with both blood cultures and urine LA tests negative for GBS (BC-, LA-). BC-, LA+ infants were more likely than those with BC-, LA- to have an immature to total neutrophil (I/T) ratio > or = 0.16 at 12 and 24 hours (p = 0.04 and 0.02, respectively). In the prospective study, we found that a positive GBS LA test can be due to perineal contamination and possibly to gastrointestinal absorption of GBS antigen. No false positive LA test results occurred on urine obtained by SBA; however, use of this method failed to detect the one infant with GBS bacteremia. Because of suboptimal sensitivity and specificity, use of the GBS LA test on urine obtained either by SBA or bag cannot be recommended for diagnosis of early onset GBS disease.

Induction by chronic autoimmune arthritis in DBA/1 mice by oral administration of type II collagen and Escherichia coli lipopolysaccharide.

We have developed a new model of autoimmune arthritis in DBA/1 mice by feeding chick type II collagen (CII) for 2-3 week intervals over a 15 week period. Clinically evident arthritis occurred in 8/10 mice receiving native CII (nCII; 100 micrograms/mouse) alone at 9-13 weeks. Arthritis was aggravated by the further ingestion of CII, while remission occurred after withdrawal of the CII. Heat-denatured CII (dCII; 200 micrograms/mouse) was also arthritogenic if co-administered with ovoinhibitor (OVI; 2 mg/mouse), a proteinase inhibitor. Co-oral administration of lipopolysaccharide (LPS; 10 micrograms/mouse) with CII enhanced the antibody production and T-cell responses to CII, and induced a more chronic arthritis that progressed spontaneously without further administration of CII or LPS. Long-term oral administration of LPS alone also induced a mild arthritis characterized by destruction of bone rather than cartilage. These observations suggest that abnormal gastrointestinal absorption of dietary mimic antigens and intestinal bacterial toxins can potentially disrupt self-tolerance mechanisms, thereby precipitating or exacerbating autoimmune disease in genetically susceptible individuals.

Dietary Fiber in Weaning Foods of Young Children

An evaluation of the opportunity to introduce fiber in the diet of weaning infants. A descriptive review of the literature to assess the role of fiber in the following dietary interventions: (1) definition of the nutrient amounts that meet the weaning infant's physiologic needs; (2) modulation of digestive and absorption processes; and (3) improving the nutritional balance between the 6th and the 12th months of life and setting habitual dietary patterns for subsequent years. Whole cereals, nonstarchy vegetables, fruits, and legumes lower the caloric and proteic density of meals, modulate nutrient and antigen absorption, and provide bulk material. They supply proteins of low biological value, minimal amounts of lipids (mostly essential polyunsaturated), complex carbohydrates, and soluble fiber, which are fermented into short-chain fatty acids by the colonic flora, and insoluble fiber that modulates intestinal function. Minerals, trace elements, and vitamins add to the value of fiber-containing foods in the diet. Recent nutritional surveys indicate that the diets of 12-month-old infants tend to include too much animal proteins and to be too protein-dense, which could be corrected with an increase of fiber-containing foods. Fiber-containing foods share unique characteristics with nutritional and metabolic implications for the weaning infant. Whole cereals, green vegetables, and legumes should be routinely introduced during the weaning process to achieve a better nutritional balance and to accustom children to diets with fiber content. The daily intake of fiber should be gradually increased to 5 g/d during the second semester of life.

Absorption and presentation of antigens by epithelial cells of the small intestine: Hypotheses and predictions relating to the pathogenesis of coeliac disease

Effects of the route of antigen absorption and presentation in the small intestine are discussed in relation to outcomes from antigen exposure. It is proposed that antigens presented by epithelial cells to intrinsic T cell populations in the mucosa induce anti-inflammatory immune responses, while antigens presented to conventional T cells by lamina propria APC predisposes to inflammation. The pathogenesis of coeliac disease is attributed to three factors: a defect in antigen processing by epithelial cells; the intrinsic properties of the gliadins; and the HLA-D haplotype of the individual. It is suggested that MHC class II molecules play a role in antigen uptake by enterocytes, in addition to their function in antigen presentation to T cells.

In vivo tolerization of Th1 lymphocytes following a single feeding with ovalbumin: Anergy in the absence of suppression

Oral tolerance is a biologically relevant pathway for inducing peripheral tolerance to foreign antigens. The mechanisms responsible for the tolerant state following feeding with antigen have been shown to involve both anergy and suppression. The demonstration of anergic T lymphocytes following oral tolerance has so far been limited in in vitro systems, and a primary objective of the present study was to provide evidence, in vivo, for the existence of a state of anergy in mice orally fed with ovalbumin (OVA). In addition, it has been shown that peripheral anergy following the intravenous administration of antigen is selectively induced in Th1 lymphocytes. Thus, a second objective of this study was to investigate whether tolerance induced by a feeding regimen known to cause anergy could be selectively limited to Th1 lymphocytes, and whether tolerance induction could be explained by antigen absorption from the gut into the circulation. Oral tolerance was induced by a single feeding with OVA, and was demonstrated by diminished antibody production in vivo, and by reduced cytokine secretion or proliferation in vitro. Anergy, as a mechanism for tolerance, was demonstrated by the ability to reverse the tolerant state after culturing tolerant cells in recombinant interleukin-2 (rIL-2). Reversal of the tolerant state in vivo was established by antibody production in irradiated mice adoptively transferred with cells cultured in the presence of rIL-2. The possibility that suppression was also an in vivo mechanism for tolerance was studied by adoptive transfer experiments. Our results show: 1) that a single dose of orally administered OVA leads to the selective tolerization of Th1 responses (diminished IgG2a, IL-2 and interferon-gamma production) with intact Th2 responses (IgG1, and IL-4), 2) that tolerance in vivo is explained by anergy in the absence of active suppression, 3) that exposure of tolerant cells to rIL-2 in vitro abrogates the anergic state both in vitro (proliferation and cytokine secretion) and in vivo (IgG2a production), and 4) that the induction of oral tolerance is inhibited by the presence of antibodies specific for the tolerizing antigen. These findings indicate that the induction of anergy via the oral route might depend on the dissemination of antigen absorbed from the gut. It is suggested that tolerance is guaranteed by the fact that this absorbed antigen is presented to Th1 lymphocytes in the absence of inflammatory and co-stimulatory molecules; these foreign antigens are thus not different from self antigens.

Production and localization of mammary-derived growth factor 1 in the normal and malignant mammary gland

Previously, we have detected a human milk and breast cancer-derived, acidic, 62 kDa, N-glycosylated growth factor named mammary-derived growth factor 1 (MDGF1). The N-terminal amino acid sequence of MDGF1 showed it to be a new growth factor. The factor stimulated collagen synthesis by fibroblasts and proliferation in normal and malignant mammary epithelial cells. Polyclonal antisera raised against the N-terminal synthetic peptide has been used to demonstrate that some human breast cancer and normal mammary epithelial cell strains and cell lines secrete the factor into their conditioned media. The antibody could adsorb the biological activity of the factor present in conditioned media. The objective of the present study was to utilize this high titre polyclonal anti-MDGF1 antisera to establish the presence and distribution of the factor in benign and malignant human breast tissues as determined by immunohistochemical analysis and enzymelinked immunosorbent assay (ELISA) assays. Frozen sections of normal and malignant breast tissue were used for immunostaining, while homogenized soluble fractions were used for ELISA testing. Antigen absorption confirmed the antibody staining to be specific. MDGF1 is localized in the duct and lobular epithelial cells of the mammary gland. Staining was nuclear and cytoplasmic in tumour and normal specimens. All of the breast tumour specimens demonstrated intense staining of the tumour cells. Localization of MDGF1 in benign and malignant human breast tissue suggests that it is universally present in breast epithelial derived cells. Study of MDGF1 could eventually provide new insights into breast development and/or tumour formation and progression.

The effects of different adjuvants on intestinal antigen absorption and subsequent immune responses of the tilapian Oreochromis mossambicus

The effects of three potential adjuvants, cholera toxin β-subunit (CTB); aluminium hydroxide [Al(0H)3] and ammonium chloride (NH4Cl) on the absorption of human gamma globulin (HGG) from the gastrointestinal tract of the tilapian Oreochromis mossambicus, and subsequent antibody generation were investigated utilising specific ELISA assays. CTB increased the levels of HGG transcytosed into the plasma over levels observed after HGG delivery alone or delivery of HGG with either Al(OH)3 or NH4Cl. The enteric immunisation with HGG plus CTB or Al(OH)3 resulted in antibody titres that were raised above those observed after the enteric immunisation with the antigen on its own or with NH4Cl. Parenteral immunisation with each of the three adjuvants resulted in levels of specific antibodies similar to those achieved after immunisation with HGG alone.

A three-tiered view of the role of IgA in mucosal defense

Mucosal IgA has generally been viewed as an immune barrier to prevent the adherence and absorption of antigens. Recent studies employing polarized epithelial monolayers have suggested two additional functions for mucosal IgA. One is to neutralize intracellular microbial pathogens, such as viruses, directly within epithelial cells. The second is to bind antigens in the mucosal lamina propria and excrete them through the adjacent epithelium into the lumen, thereby ridding the body of locally formed immune complexes and decreasing their access to the systemic circulation.

Allergic Contact Dermatitis in Children

Definition Allergic contact dermatitis (ACD) is an inflammatory reaction of the skin that follows percutaneous absorption of antigen from the skin surface and recruitment of previously sensitized, antigen-specific T lymphocytes into the skin. Epidemiology In the pediatric age group, ACD can involve either sex and manifest as early as the first week of life. A recent review of several European and US studies found that ACD may account for up to 20% of cases of dermatitis in the 0- to 14-year-old age group. Although the incidence and prevalence of the disease in the general pediatric population is unknown, epicutaneous patch testing of randomly selected and otherwise healthy children revealed that 13% to 20% were allergic to one or more common antigens, suggesting that at least 20% of children in the general population theoretically are at risk of developing ACD. When one considers poison ivy or poison oak as contact allergens prevalent in certain areas of North America, the likelihood of allergic contact dermatitis may be much higher. Pediatricians should recognize that children are sensitized to contact allergens early in life, with most children being sensitized by age 5 years. The allergens most commonly responsible for allergic contact dermatitis in North American children are listed in Table 1.