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PubMed1994

The development of effective vaccine adjuvants employing natural regulators of T-cell lymphokine production in vivo.

Steroid hormones are important regulators of gene function in vivo. A number of naturally occurring species of steroid hormones are able to qualitatively and quantitatively influence the production of lymphokines by activated T cells in vitro. Similar mechanisms are probably also occurring naturally in vivo and could explain why mucosal and nonmucosal lymphoid organs harbor T cells having unique potentials for lymphokine production. It was established that the topical application of 1,25 dihydroxyvitamin D3 (1,25(OH)2D3) to normal mice changed the pattern of lymphokines produced by activated T cells isolated from the draining peripheral lymph nodes. The hormone-treated T cells produced a pattern of lymphokines similar to that normally found in Peyer's patches. Subcutaneous vaccination with a protein antigen, in a site afferent to 1,25(OH)2D3-manipulated lymph nodes, resulted in an enhanced serum antibody response and was uniquely capable of also stimulating a common mucosal immune response to the antigen as well. Common mucosal immunity was confirmed by demonstrating the presence of antigen-specific IgA and IgG responses in a number of mucosal secretions and by further establishing that antibody-secreting plasma cells had migrated to the lungs and small intestines of the hormone-treated and vaccinated animals. Additional experiments established that common mucosal immunity could also be induced in aged animals as long as the immune system of the vaccinated animals was functioning normally. This was accomplished by providing the aged animals with a dietary supplement of dehydroepiandrosterone sulfate (DHEAS). Previous studies by us have documented that aged animals provided with replacement levels of DHEAS, a natural steroid hormone whose endogenous production declines with advancing age, are able to mount normal systemic humoral and cellular immune response following subcutaneous vaccination with a variety of protein and polysaccharide antigens. The combination of supplemental DHEAS therapy with topical 1,25(OH)2D3 treatment at the time of vaccination provided the conditions needed to generate mucosal and systemic immune responses to inactivated influenza virus antigen by old animals.

Adjuvants, Immunologic↗
PubMed2002

The immunology of inflammatory bowel disease.

The dogma of systemic immunity can be ignored in relation to mucosal immunity. These distinct immune systems evolved based on specific environmental realities. Given the potentially hostile environment encountered by the mucosal immune system, it is a necessary adaptation that the overall tone is one of suppression. Breaches in this tone may lead to chronic inflammation. Understanding how specific components and processes of the mucosal immune system interact with the environment will elucidate the pathogenesis of IBD and lead to novel therapeutic approaches.

Epithelial Cells↗
PubMed2005

A predictive model for the level of sIgA based on IgG levels following the oral administration of antigens expressed in Saccharomyces cerevisiae.

Oral vaccination may be the most efficient way of inducing an immune response at the remote mucosal site through the common mucosal immune network. Antigen-specific secretory IgA (sIgA) is the major immunoglobulin type generally detected in the secretions of experimental animals following an effective oral immunization. Actinobacillus pleuropneumoniae causing disease in the lung of pig initially interacts, colonizes, and infects the host tissues at the mucosal surface of the respiratory tract. Also, importantly for A. pleuropneumoniae protection, the quantity of sIgA in the lung had merits associated with the mucosal immunity. However, there is no simple method to monitor the level of sIgA as an indicator for the induction of local immune responses by an oral vaccination in the target tissue. Therefore, the relationship between sIgA and IgG was analyzed to evaluate the induction of local immune responses by an oral immunization with Saccharomyces cerevisiae expressing the apxIA and apxIIA genes of A. pleuropneumoniae in this study. The correlation coefficient of determination (r2 x 100) for paired samples in both vaccinated and control groups showed a significant positive-relationship between IgG in sera and sIgA in the lung or intestine. These results indicated that IgG antibody titers in sera could be useful to indirectly predict local immune response, and sIgA, in the lung or intestine to evaluate the efficacy of an oral vaccination.

Actinobacillus pleuropneumoniae↗
PubMed2002

Tracking the tissue distribution of marker dye following intranasal delivery in mice and chinchillas: a multifactorial analysis of parameters affecting nasal retention.

The combined mucosal surface area is vast and represents the primary site of entry of most pathogens to the respiratory, gastrointestinal (GI), and urogenital tracts. It is recognized that vaccines delivered parenterally typically only induce weak mucosal immune responses and that by targeting the mucosal immune system protective antibodies and effector lymphocytes could be induced at the primary site of infection. In the present study, we have evaluated an extensive set of conditions required to ensure maximum retention of intranasally administered substances within the nasal cavity in the chinchilla and murine hosts. We report here that many parameters, such as anaesthesia, position of animal during and post delivery, and dosing schedule, must be optimized in concert with each other and that results from one species cannot be extrapolated directly to another animal model.

Administration, Intranasal↗
PubMed2002

Humans immunized with Streptococcus mutans antigens by mucosal routes.

Strategies aimed at the prevention of Streptococcus mutans infection and dental caries include mucosal immunization, which results in salivary anti-S. mutans responses. The purpose of this study was to evaluate the effectiveness of nasal vs. tonsillar immunization with S. mutans antigens in inducing salivary immune responses. Twenty-one adult subjects were immunized twice, within a seven-day interval, with a glucosyltransferase-enriched preparation (E-GTF) administered by nasal or tonsillar topical spray. Parotid saliva, nasal wash, and serum were collected prior to and at one- to two-week intervals for 3 months following immunization and were assayed by ELISA for anti-E-GTF activity. Results were analyzed by means of the mixed-models procedure with p < 0.05 level of significance. Significantly higher anti-E-GTF responses were detected in saliva and nasal wash samples from the group immunized by the nasal compared with the tonsillar route, indicating that nasal immunization was more effective in inducing mucosal responses in adults.

Administration, Intranasal↗
PubMed2005

Mucosal innate immune response to intragastric infection by Salmonella enterica serovar Choleraesuis.

The innate immune response is critical to enteric disease resistance and the induction of mucosal adaptive immunity. In mucosae of the small intestine, Peyer's patches play a central role in immune surveillance and sampling of bacteria by specialized M cells. The innate immune response to Salmonella enterica serovar Choleraesuis, an enteric pathogen of swine, involves IL-1beta and IL-8 mRNA induction but not that of IL-6 and TNFalpha, in contrast to Salmonella serovar Typhimurium infection of murine small intestine. We investigated in vivo responses to Salmonella and potential effects of animal variation since the gut environment is highly dynamic and constantly changing physiologically. Salmonella serovar Choleraesuis induced an early proinflammatory cytokine response at 6h after infection, which was characterized by a 4-fold increase in production of CXCL2 mRNA by jejunal Peyer's patches (JPP), and a 12-fold increase in IL-1beta and 4-fold increase in IL-8 (CXCL8) mRNAs by distal ileal Peyer's patches (IPP). Levels of IL-1beta and IL-8 mRNA were positively correlated with numbers of mucosal neutrophils in the distal IPP. Salmonella DNA was also detected in ileal tissues, including Peyer's patches, absorptive epithelium and mesenteric lymph nodes, in 33-83% of infected animals, compared to the jejunal tissues, which were positive in 0-33% of infected pigs. Notwithstanding substantial animal-to-animal variation, IL-1beta was increased in both proximal and distal IPP, IL-8 was increased in the distal IPP, and calprotectin was associated with both by cluster analysis. These data indicate that IL-1beta and IL-8 expression in the IPP plays a key role early in the interaction between Salmonella serovar Choleraesuis and the small intestine.

Animals↗
PubMed1992

A study of mucosal gut immunity in infants who develop Hirschsprung's-associated enterocolitis.

The aim of this study was twofold. First, to establish quantitatively the distribution of the immunoglobulin-containing (plasma) cells, T and B lymphocytes in the lamina propria of the rectal mucosa of normal neonates and neonates with Hirschsprung's disease (HD). Second, to review the neonates with HD to determine any differences in these cell populations between those who subsequently developed Hirschsprung's enterocolitis (HEC) and those who did not. Two conclusions can be drawn from the results of our study of rectal mucosal immune defenses. First, neonates with HD have no deficiencies in these defenses when compared with normal neonates. Second, neonates with HD who subsequently develop HEC have no premorbid deficiency in these defenses. It was noted that the pan-T cell count in the infants who went on to develop HEC appeared to be increased, although this did not reach statistical significance. The use of fresh or frozen material would permit a more detailed analysis of the separate T cell subsets.

Child, Preschool↗
PubMed1998

IFN-gamma is required for IL-12 responsiveness in mice with Candida albicans infection.

To elucidate the role of IFN-gamma in antifungal CD4+ Th-dependent immunity, 129/Sv/Ev mice deficient for IFN-gamma receptor (IFN-gammaR(-/-)) were assessed for susceptibility to gastrointestinal or systemic Candida albicans infection and for parameters of innate and adaptive T helper immunity. IFN-gammaR(-/-) mice failed to mount protective Th1-mediated acquired immunity upon mucosal immunization or in response to a live vaccine strain of the yeast. The impaired Th1-mediated resistance correlated with defective IL-12 responsiveness, but not IL-12 production, and occurred in the presence of an increased innate antifungal resistance. The development of nonprotective Th2 responses was observed in IFN-gammaR(-/-) mice upon mucosal infection and subsequent reinfection. However, under experimental conditions of Th2 cell activation, the occurrence of Th2 cell responses was similar in IFN-gammaR(-/-) and in IFN-gammaR(+/+) mice. These results indicate the complex immunoregulatory role of IFN-gamma in the induction of mucosal and nonmucosal anticandidal Th cell responses; IFN-gamma is not essential for the occurrence of Th2 responses but is required for development of IL-12-dependent protective Th1-dependent immunity.

Animals↗
PubMed2006

Mucosal innate immune factors in the female genital tract are associated with vaginal HIV-1 shedding independent of plasma viral load.

Recent studies indicate that mucosal innate immune factors modulate HIV-1 infection in vitro. Our interest was to examine the levels of innate mucosal factors for their potential association with HIV-1 shedding in the female genital tract. Vaginal lavages were collected from HIV-1-infected women who had vaginal viral loads (VVL) that were below, within, or above the 90% confidence interval (CI) predicted by their matched plasma viral loads. Innate immune factors [cathepsin D, lactoferrin (Lf), myeloid related protein (MRP)-8, MRP-8/14, secretory leukocyte protease inhibitor, and gp340], cytokines (IL-1beta and TNF-alpha), and chemokines (MIP-1alpha, MIP-1beta, RANTES, and SDF-1alpha) were quantified by ELISA. Leukocyte levels were determined using a leukocyte reagent strip for urinalysis. Lf, MRP-8/14, gp340, and IL-1beta levels were significantly higher in vaginal lavages above the 90% CI and generally correlated with each other and with VVL. Leukocyte levels were significantly higher in the lavages that had virus shedding above the 90% CI and correlated strongly with Lf levels and VVL. In this group of women, these results suggest that the levels of certain innate immune factors are more closely associated with HIV-1 shedding in the genital mucosa than plasma virus concentrations.

Adolescent↗
PubMed2000

Immunostimulatory sequence oligodeoxynucleotide: A novel mucosal adjuvant.

The majority of infectious agents enter the body via mucosal surfaces. Therefore, there is great interest in developing vaccination strategies that lead to mucosal immunity. However, to generate strong mucosal immune responses to nonreplicating immunogens, mucosal delivery with an adjuvant is required, and no safe and effective mucosal adjuvants are presently available for use in humans. Recently, immunostimulatory sequence oligodeoxynucleotide (ISS-ODN) has been shown to be a potent mucosal adjuvant. Intranasal (i.n.) delivery of antigen with ISS-ODN elicits a secretory IgA response both locally in respiratory secretions and distally in intestinal and vaginal secretions. In this regard, ISS-ODN has been shown to be as effective as cholera toxin (CT), but unlike CT, ISS-ODN has not been shown to have significant toxicity. Furthermore, i.n. antigen/ISS-ODN coimmunization induces a strong Th(1)-biased systemic immune response with cytotoxic T lymphocyte activity. These observations suggest that ISS-ODN would be an ideal mucosal adjuvant for development of vaccines against mucosal pathogens.

Adjuvants, Immunologic↗
PubMedDate not supplied

Gut as the largest immunologic tissue.

The host is continuously exposed to the environment via the mucosal surface. To this end, a large number of infectious agents, allergens and foreign proteins enter the inside of our bodies via the oral region, nasal and upper respiratory tracts, intestine and reproductive tract. The total area of these mucosal surfaces, which cover these tube-like tissues are at least two hundred times larger than those of skin. To provide an optimal first line of defense for these large surface areas, the mucosal immune system including secretory immunoglobulin A (S-IgA), mucosal alphabeta and gammadelta T-cells and epithelium play an essential role. The goal of our research is aimed at understanding the molecular and cellular aspects of the mucosal immune system and their defense against infectious diseases, inflammation and immunological disorders. Further, it is important to quickly apply our fundamental findings of the mucosal immune system to the development of mucosal vaccines.

Cytokines↗
PubMed2001

Modulation of immunity against herpes simplex virus infection via mucosal genetic transfer of plasmid DNA encoding chemokines.

In this study, we examined the effects of murine chemokine DNA, as genetic adjuvants given mucosally, on the systemic and distal mucosal immune responses to plasmid DNA encoding gB of herpes simplex virus (HSV) by using the mouse model. The CC chemokines macrophage inflammatory protein 1beta (MIP-1beta) and monocyte chemotactic protein 1 (MCP-1) biased the immunity to the Th2-type pattern as judged by the ratio of immunoglobulin isotypes and interleukin-4 cytokine levels produced by CD4(+) T cells. The CXC chemokine MIP-2 and the CC chemokine MIP-1alpha, however, mounted immune responses of the Th1-type pattern, and such a response rendered recipients more resistant to HSV vaginal infection. In addition, MIP-1alpha appeared to act via the upregulation of antigen-presenting cell (APC) function and the expression of costimulatory molecules (B7-1 and B7-2), whereas MIP-2 enhanced Th1-type CD4(+) T-cell-mediated adaptive immunity by increasing gamma interferon secretion from activated NK cells. Our results emphasize the value of using the mucosal route to administer DNA modulators such as chemokines that function as adjuvants by regulating the activity of innate immunity. Our findings provide new insight into the value of CXC and CC chemokines, which act on different innate cellular components as the linkage signals between innate and adaptive immunity in mucosal DNA vaccination.

Animals↗
PubMed2005

Biologic therapy for inflammatory bowel disease.

Despite all of the advances in our understanding of the pathophysiology of inflammatory bowel disease (IBD), we still do not know its cause. Some of the most recently available data are discussed in this review; however, this field is changing rapidly and it is increasingly becoming accepted that immunogenetics play an important role in the predisposition, modulation and perpetuation of IBD. The role of intestinal milieu, and enteric flora in particular, appears to be of greater significance than previously thought. This complex interplay of genetic, microbial and environmental factors culminates in a sustained activation of the mucosal immune and non-immune response, probably facilitated by defects in the intestinal epithelial barrier and mucosal immune system, resulting in active inflammation and tissue destruction. Under normal situations, the intestinal mucosa is in a state of 'controlled' inflammation regulated by a delicate balance of proinflammatory (tumour necrosis factor [TNF]-alpha, interferon [IFN]-gamma, interleukin [IL]-1, IL-6, IL-12) and anti-inflammatory cytokines (IL-4, IL-10, IL-11). The mucosal immune system is the central effector of intestinal inflammation and injury, with cytokines playing a central role in modulating inflammation. Cytokines may, therefore, be a logical target for IBD therapy using specific cytokine inhibitors. Biotechnology agents targeted against TNF, leukocyte adhesion, T-helper cell (T(h))-1 polarisation, T-cell activation or nuclear factor (NF)-kappaB, and other miscellaneous therapies are being evaluated as potential therapies for IBD. In this context, infliximab is currently the only biologic agent approved for the treatment of inflammatory and fistulising Crohn's disease. Other anti-TNF biologic agents have emerged, including CDP 571, certolizumab pegol (CDP 870), etanercept, onercept and adalimumab. However, ongoing research continues to generate new biologic agents targeted at specific pathogenic mechanisms involved in the inflammatory process. Lymphocyte-endothelial interactions mediated by adhesion molecules are important in leukocyte migration and recruitment to sites of inflammation, and selective blockade of these adhesion molecules is a novel and promising strategy to treat Crohn's disease. Therapeutic agents that inhibit leukocyte trafficking include natalizumab, MLN-02 and alicaforsen (ISIS 2302). Other agents being investigated for the treatment of Crohn's disease include inhibitors of T-cell activation, peroxisome proliferator-activated receptors, proinflammatory cytokine receptors and T(h)1 polarisation, and growth hormone and growth factors. Agents being investigated for treatment of ulcerative colitis include many of those mentioned for Crohn's disease. More controlled clinical trials are currently being conducted, exploring the safety and efficacy of old and new biologic agents, and the search certainly will open new and exciting perspectives on the development of therapies for IBD.

Animals↗
PubMed2005

Iron chelator induces MIP-alpha/CCL20 in human intestinal epithelial cells: implication for triggering mucosal adaptive immunity.

A previous report by this laboratory demonstrated that bacterial iron chelator (siderophore) triggers inflammatory signals, including the production of CXC chemokine IL-8, in human intestinal epithelial cells (IECs). Microarray-based gene expression profiling revealed that iron chelator also induces macrophage inflammatory protein 3 alpha (MIP-3alpha)/CC chemokine-ligand 20 (CCL20). As CCL20 is chemotactic for the cells involved in host adaptive immunity, this suggests that iron chelator may stimulate IECs to have the capacity to link mucosal innate and adaptive immunity. The basal medium from iron chelator deferoxamine (DFO)-treated HT-29 monolayers was as chemotactic as recombinant human CCL20 at equivalent concentrations to attract CCR6(+) cells. The increase of CCL20 protein secretion appeared to correspond to that of CCL20 mRNA levels, as determined by real-time quantitative RT-PCR. The efficacy of DFO at inducing CCL20 mRNA was also observed in human PBMCs and in THP-1 cells, but not in human umbilical vein endothelial cells. Interestingly, unlike other proinflammatory cytokines, such as TNF-alpha and IL-1beta, a time-dependent experiment revealed that DFO slowly induces CCL20, suggesting a novel mechanism of action. A pharmacologic study also revealed that multiple signaling pathways are differentially involved in CCL20 production by DFO, while some of those pathways are not involved in TNF-alpha-induced CCL20 production. Collectively, these results demonstrate that, in addition to some bacterial products known to induce host adaptive immune responses, direct chelation of host iron by infected bacteria may also contribute to the initiation of host adaptive immunity in the intestinal mucosa.

Calcium↗
PubMed1986

[Humoral aspects of mucous membrane immunity--perspectives for the female genital tract].

Mucosal immunity of the female genital tract is a part of the "Common mucosal immunity". It is possible to induce local antibodies in the female genital tract by means of oral immunization. From these investigations new perspectives in terms of immunoprophylaxis against bacterial, viral an parasitic infections come into consideration for clinical use. In the case of bacterial infections IgA blocks the attachment of pathogens to relevant mucosal tissues and cells. Predominant among the immune mechanisms is the occurrence of secretory antibodies in the fluids that bath mucosal membranes. Secretory IgA (S-IgA) is an 11S molecule (MW 390,000) consisting of two IgA monomers covalently bonded by joining chain (J chain) and complexed to one molecule of SC.S-IgA ist the main immunoglobulin of mucosal surface. A medically important group of bacterial pathogens produce IgA1 protease cleaving only IgA1 proteins. S-IgA is resistant to protease hydrolysis. The secretory component (SC) is an epithelial cell receptor for the transport of IgA dimers, polymers and IgM polymers. Systemic suppression after oral antigen application has been demonstrated with a variety of thymic-dependent antigens, including heterologous erythrocytes, haptens, and various soluble proteins. Tolerance is mediated by antigen specific T suppressor cells (Ts). Suppressor cells first appear in the gut associated lymphoid tissue and subsequently migrate to systemic sites. At present immunoglobulin estimations in secretions are of clinical importance regarding supporting diagnostic tool of mucosal infections.(ABSTRACT TRUNCATED AT 250 WORDS)

Antibody Formation↗
PubMed1998

IgG antibody levels in the sinus, ear, and airway in a rabbit model of sinusitis with Bacteroides.

OBJECTIVE: To evaluate distribution of IgG antibodies (Ab) in the airway, ear, and sinuses in association with inflammatory changes in a rabbit sinusitis model. DESIGN: We measured IgG Ab and lactate dehydrogenase levels in solutions from sinus, airway, and middle ear lavage and in serum, and determined interferon y messenger RNA expression in sinus and ear mucosa at 1, 2, 3, and 4 weeks after inoculation with Bacteroides fragilis. SUBJECTS: Six rabbits at each time point; controls were untreated (n=5) and sham-operated rabbits at 2 and 4 weeks (n=4-5). INTERVENTION: Bacteroides fragilis was inoculated into the left maxillary sinus with ostium closed. RESULTS: IgG Ab was undetectable in all controls. IgG Ab (>50 microg/g protein) was present at 2, 3, and 4 weeks in most bilateral sinus lavage samples and in 2 of 6, 5 of 6, and 6 of 10 ear lavage samples at 2, 3, and 4 weeks, respectively, following inoculation. Inflammatory changes (histological and lactate dehydrogenase) were much greater in the inflamed sinus. IgG Ab (>50 microg/g protein) was also detected in most bronchoalveolar lavage samples after 2 weeks. Interferon gamma mRNA was undetectable in all untreated and most sham-operated controls but was detected in the bilateral sinus mucosa at 1 to 2 weeks, and remained detectable up to 4 weeks in most rabbits. Serum IgG Ab levels positively correlated with those in lavage samples, with highest correlation with right sinus lavage IgG Ab levels (r=0.56, P<.001). CONCLUSION: IgG Ab levels in the upper airway mucosa likely increase within 2 weeks following bacterial inoculation as a part of mucosal immune responses independent of tissue necrosis.

Animals↗
PubMed2006

Up-regulation of chemokine ligand 20 in chronic rhinosinusitis.

OBJECTIVES: To investigate the up-regulation of chemokine ligand 20 (CCL20) in chronic rhinosinusitis mucosa and to localize the distribution of CCL20 in the human paranasal sinus mucosa. DESIGN: Prospective study. SETTING: Tertiary academic institution. PATIENTS: Ten patients who underwent functional endoscopic sinus surgery for chronic rhinosinusitis without nasal polyps and 10 normal control subjects. INTERVENTIONS: Messenger RNA was extracted from the sinus mucosa, and semiquantitative reverse transcriptase-polymerase chain reaction was performed. Immunohistochemical staining was used to localize the CCL20 protein. RESULTS: The expression levels of CCL20 messenger RNA level in chronic rhinosinusitis without nasal polyps were significantly increased compared with those in normal sinus mucosa. The expression of CCL20 protein was greater in chronic rhinosinusitis without nasal polyps mucosa and was localized to the epithelial and submucosal glandular cells. CONCLUSION: CCL20 is an inducible product of human paranasal sinus epithelium that may play a role in modulating mucosal immunity of the sinus mucosa.

Adult↗
PubMed2003

CRP-ductin, the mouse homologue of gp-340/deleted in malignant brain tumors 1 (DMBT1), binds gram-positive and gram-negative bacteria and interacts with lung surfactant protein D.

CRP-ductin is a protein expressed mainly by mucosal epithelial cells in the mouse. Sequence homologies indicate that CRP-ductin is the mouse homologue of human gp-340, a glycoprotein that agglutinates microorganisms and binds the lung mucosal collectin surfactant protein-D (SP-D). Here we report that purified CRP-ductin binds human SP-D in a calcium-dependent manner and that the binding is not inhibited by maltose. The same properties have previously been observed for gp-340 binding of SP-D. CRP-ductin also showed calcium-dependent binding to both gram-positive and -negative bacteria. A polyclonal antibody raised against gp-340 reacted specifically with CRP-ductin in Western blots. Immunoreactivity to CRP-ductin was found in the exocrine pancreas, in epithelial cells throughout the gastrointestinal tract and in the parotid ducts. A panel of RNA preparations from mouse tissues was screened for CRP-ductin and SP-D expression by reverse transcription-PCR. The pancreas was the main site of synthesis of CRP-ductin, but transcripts were also readily amplified from salivary gland, the gastrointestinal tract, liver, testis, uterus and lung. Lung was the main site of synthesis of SP-D, but transcripts were also amplified from uterus, salivary gland, thymus, thyroid gland, pancreas and testis. We conclude that CRP-ductin is the mouse homologue of human gp-340 and that its capacity to bind SP-D as well as gram-negative and gram-positive bacteria suggests a role in mucosal immune defense.

Agglutinins↗