P Brandtzaeg

University of Oslo, Kristiania (historical), Oslo County, Norway

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Publications (414)1892.41 Total impact

  • P Brandtzaeg
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    ABSTRACT: There is currently a major focus on the role of the gut barrier function in balancing mucosal immune responses. Increased epithelial permeability for exogenous antigens is a crucial primary or secondary event in the pathogenesis of several disorders affecting body surfaces and beyond. The epithelial gate-keeper function is determined by the individual's age (e.g. preterm vs. term infant), diet, genetics, mucus composition, interactions between mast cells, nerves and neuropeptides, concurrent infection, the commensal microbiota and the epithelium-shielding effect of secretory IgA (SIgA) antibodies provided by breast milk or produced in the individual's gut. The integrity of the epithelial barrier furthermore depends on homeostatic regulatory mechanisms, including mucosal induction of regulatory T cells, where commensal microbiota-host interactions apparently play decisive roles. Thus, both extrinsic and intrinsic factors have been identified that may have an impact on the dynamics of the epithelial cell-cell junctions in the gut and thereby increase or reduce paracellular permeability. Experiments have shown that SIgA normally cooperates with innate defence factors to protect the epithelium and reinforce its barrier function. In the absence of SIgA commensal gut bacteria overstimulate innate epithelial immunity at the expense of expression of genes that regulate fat and carbohydrate metabolism, resulting in an epithelial gene signature that correlates with the development of lipid malabsorption. This shows that the intestinal epithelial barrier is a cross-road between defence and nutrition, and that SIgA is essential to keep the balance between these two functions.
    Beneficial Microbes 12/2012; 4(1):1-16. DOI:10.3920/BM2012.0024 · 1.50 Impact Factor
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    Scandinavian Journal of Immunology 09/2012; 76(3):344. DOI:10.1111/j.1365-3083.2012.02742.x · 1.88 Impact Factor
  • P. Brandtzaeg
    European Journal of Pharmacology 09/2011; 668. DOI:10.1016/j.ejphar.2011.09.192 · 2.68 Impact Factor
  • P Brandtzaeg
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    ABSTRACT: In the process of evolution, the mucosal immune system has generated two layers of anti-inflammatory defence: (1) immune exclusion performed by secretory IgA (and secretory IgM) antibodies to modulate or inhibit surface colonisation of microorganisms and dampen penetration of potentially dangerous antigens; and (2) suppressive mechanisms to avoid local and peripheral hypersensitivity to innocuous antigens, particularly food proteins and components of commensal bacteria. When induced via the gut, the latter phenomenon is called 'oral tolerance', which mainly depends on the development of regulatory T (Treg) cells in mesenteric lymph nodes to which mucosal dendritic cells (DCs) carry exogenous antigens and become conditioned for induction of Treg cells. Mucosally induced tolerance appears to be a rather robust adaptive immune function in view of the fact that large amounts of food proteins pass through the gut, while overt and persistent food allergy is not so common. DCs are 'decision makers' in the immune system when they perform their antigen-presenting function, thus linking innate and adaptive immunity by sensing the exogenous mucosal impact (e.g. conserved microbial molecular patterns). A balanced indigenous microbiota is required to drive the normal development of both mucosa-associated lymphoid tissue, the epithelial barrier with its secretory IgA (and IgM) system, and mucosally induced tolerance mechanisms including the generation of Treg cells. Notably, polymeric Ig receptor (pIgR/SC) knock-out mice that lack secretory IgA and IgM antibodies show reduced epithelial barrier function and increased uptake of antigens from food and commensal bacteria. They therefore have a hyper-reactive immune system and show predisposition for systemic anaphylaxis after sensitisation; but this development is counteracted by enhanced oral tolerance induction as a homeostatic back-up mechanism.
    Beneficial Microbes 09/2010; 1(3):211-27. DOI:10.3920/BM2010.0009 · 1.50 Impact Factor
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    P Brandtzaeg
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    ABSTRACT: Prevention of infections by vaccination remains a compelling goal to improve public health. Most infections involve the mucosae, but the development of vaccines against many of these pathogens has yet to be successful. Mucosal vaccines would make immunization procedures easier, be better suited for mass administration, and most efficiently induce immune exclusion - a term coined for non-inflammatory antibody shielding of internal body surfaces - mediated principally by secretory immunoglobulin A (SIgA). The exported antibodies are polymeric, mainly IgA dimers (pIgA) - produced by local plasma cells stimulated by antigens that target the mucosae. SIgA was early shown to be complexed with an epithelial glycoprotein - the secretory component (SC). In 1974, a common SC-dependent transport of pIgA and pentameric IgM was proposed. From the basolateral surface, pIg-SC complexes are taken up by endocytosis and finally extruded into the lumen. Membrane SC is now referred to as polymeric Ig receptor (pIgR). In 1980, it was shown to be synthesized as a larger transmembrane protein - first cloned from rabbit and then from human. Mice deficient for pIgR showed that this is the only receptor responsible for epithelial transport of IgA and IgM. In the gut, induction of B cells occurs in gut-associated lymphoid tissue, particularly the Peyer's patches, but also in mesenteric lymph nodes. Plasma cell differentiation is accomplished in the lamina propria to which the memory/effector cells home. The airways also receive such cells from nasopharynx-associated lymphoid tissue - but by different homing receptors. Such compartmentalization is a challenge for development of mucosal vaccines.
    Scandinavian Journal of Immunology 12/2009; 70(6):505-15. DOI:10.1111/j.1365-3083.2009.02319.x · 1.88 Impact Factor
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    ABSTRACT: Mucosal immunity protects the epithelial barrier by immune exclusion of foreign antigens and by anti-inflammatory tolerance mechanisms, but there is a continuing debate about the role of secretory immunoglobulins (SIgs), particularly SIgA, in the protection against allergy and other inflammatory diseases. Lack of secretory antibodies may cause immune dysfunction and affect mucosally induced (oral) tolerance against food antigens. We used polymeric Ig receptor (pIgR) knockout (KO) mice, which cannot export SIgA or SIgM, to study oral tolerance induction by ovalbumin (OVA) feeding and for parenteral antigen sensitization in the same animal. Remarkable systemic hyperreactivity was observed in pIgR KO mice, as 50% died after intradermal OVA challenge, which was not seen in similarly sensitized and challenged wild-type (WT) mice. Oral tolerance induced by OVA completely protected the sensitized pIgR KO mice against anaphylaxis and suppressed antibody levels (particularly IgG1) as well as delayed-type hypersensitivity (DTH) to OVA. Delayed-type hypersensitivity to a bystander antigen, human serum albumin, was also suppressed and T-cell proliferation against OVA in vitro was reduced in tolerized compared with non-tolerized pIgR KO mice. This effect was largely mediated by CD25+ T cells. Adoptive transfer of splenic putative regulatory T cells (CD4+ CD25+) obtained from OVA-fed pIgR KO mice to naïve WT mice mediated suppression of DTH against OVA after sensitization of the recipients. Compensatory regulatory T-cell function becomes critical in pIgR-deficient mice to avoid the potentially catastrophic effects of systemic immune hyperreactivity, presumably resulting from defective secretory antibody-mediated immune exclusion of microbial components.
    Allergy 11/2009; 65(5):561-70. DOI:10.1111/j.1398-9995.2009.02225.x · 6.00 Impact Factor
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    ABSTRACT: Among patients with recurrent, protracted or chronic infections of the respiratory tract involving the middle ear, 18 were found to have immunodeficiencies. In 10 of the patients, deficiency of immunoglobulins belonging to the IgG, IgA and IgM classes was found. Seven patients had an isolated IgA deficiency. One patient had a combined immunodeficiency with defects of the T-cell system and the B-cell system. One patient had an isolated T-cell deficiency.
    Acta Oto-Laryngologica 07/2009; 82(3-4):185-92. DOI:10.3109/00016487609120879 · 0.99 Impact Factor
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    ABSTRACT: Expression of the γ/δ T cell receptor (TCR) on CD3+ intracpithclial lymphocytes (IELs) was studied by two-colour immunofluorescence in duodenal tissue sections from healthy (n= 6) or infection-prone (n = 7) subjects with selective IgA deficiency (IgAD), and subjects (n= 4) with combined IgAD and IgG subclass deficiency. TCRγ/δ+ IEL proportions in selective IgAD subjects (median 6.3%, range 1.0–41%) and in those with combined deficiency (median 4.5%, range 1±2.33%) were well within the range (0.3.38%) for histologically normal controls (n= 11), but the healthy IgAD subgroup tended to show raised TCRγ/δ+ IEL proportions (median 13.6%) compared with the other two subgroups. Also the number of TCRγ/δ+ IELs per intestinal length unit was relatively high (median 13.9/mm) in the healthy IgAD subjects, and significantly raised (P < 0.03) compared with controls (median 3.2/mm). Paired staining revealed that most TCRγ/δ+ IELs in both selective IgAD (98%) and combined deficiency (99%) were CD8, and a large fraction (median 84% and 63%, respectively) expressed the Vδ1/Jδ1-encoded epitope. The total number of CD3’ IELs (mostly CD8+) was similar to controls. IgAD subjects, and especially the healthy subgroup, had significantly increased serum concentrations of soluble CD8 (P < 0.0002), neopterin (P < 0.005), and β2-microglobulin (P < 0.007). which was similar to our previous observations in common variable immunodeficiency, and probably reflected stimulation of cell-mediated immunity. In addition, the increased TCRγ/δ+ IELs might reflect a component of compensatory surface protection in the healthy IgAD subgroup.
    Clinical & Experimental Immunology 10/2008; 94(1):91-98. DOI:10.1111/j.1365-2249.1993.tb05983.x · 3.28 Impact Factor
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    ABSTRACT: Regulatory T cells (T(regs)) may inhibit immunity against cancer. Induction and expansion of T(regs) in the immunosuppressive microenvironment created by a growing tumour appear to be one of the mechanisms by which it can evade host defence. We studied the impact of CD25+ T(regs) in a B cell lymphoma model in which Rag2-/- mice received adoptive transfer of wild-type spleen cells with or without CD25+ cells, and concurrently subcutaneous inoculation of the B cell lymphoma cell line A20. We also examined the effect of engaging the glucocorticoid-induced tumour necrosis factor receptor (GITR) - an approach reported previously to abrogate the suppressive effects of T(regs). Mice that received spleen cells depleted of CD25+ T(regs) showed significantly slower tumour growth and increased survival compared with mice that received unsorted spleen cells. The T(reg)-depleted group also had significantly more CD8+ T cells infiltrating the tumours and higher levels of serum immunoglobulin G subclasses. The anti-GITR treatment had no significant effect on tumour growth, survival or immunoglobulin production. In the CD25-depleted group four of 10 mice developed clinical signs of autoimmunity, in contrast to none in the non-depleted group. Forkhead box P3+ T cells were found in tumour-draining lymph nodes in mice in the CD25-depleted group, suggesting an in vivo induction or expansion of rare transferred donor T(regs). Thus, our study showed that removal of CD25+ T(regs) enhanced anti-tumour immunity against local growth of a B cell lymphoma and that induction or expansion of T(regs) could be one mechanism by which the growing tumour evades immune surveillance.
    Clinical & Experimental Immunology 06/2008; 152(2):381-7. DOI:10.1111/j.1365-2249.2008.03642.x · 3.28 Impact Factor
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    ABSTRACT: In early childhood, the ability to mount protective immune responses in the airways is impaired, with increased risk of allergic sensitisation to inhaled allergens. Antigen presenting cells (APC) and regulatory T cells (Treg) are important modifiers of T cell immunity but little is known about their distribution in bronchial mucosa at this age. Here the subset distribution of APC and the appearance of Foxp3(+) Treg and bronchus associated lymphoid tissue (BALT) were examined immunohistochemically in children less than 2 years of age with chronic asthma-like symptoms of the lower airways. Immunophenotyping was performed in situ on bronchial biopsy specimens obtained from 45 infants, 4-23 months of age, under investigation for airway disease. A well developed HLA-DR(+) network of APC was present in all samples, approximately 50% of the cells being CD68(+) macrophages and the remainder various subsets of dendritic cells. The density of HLA-DR(+) cells increased significantly with age but was not related to atopy, clinical symptoms or lung function. Comparing the density of APC subsets and clinical parameters, only the number of intraepithelial CD1a(+) dendritic cells was significantly increased in infants who had recently suffered a respiratory infection. BALT structures were identified in 22 children, with no relation to lung function, atopic status or human rhinovirus positivity. Plasmacytoid dendritic cells and Foxp3(+) Treg were located primarily within these isolated lymphoid follicles. A bronchial network of dendritic cells and macrophages develops quite rapidly after birth, apparently independent of clinical symptoms or atopy. The high frequency of BALT structures containing putative tolerogenic dendritic cells and Treg suggests that these lymphoid follicles play an important role in bronchial immune homeostasis during infancy.
    Thorax 03/2008; 63(8):703-9. DOI:10.1136/thx.2007.082974 · 8.56 Impact Factor
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    P Brandtzaeg, H Kiyono, R Pabst, M W Russell
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    ABSTRACT: Stimulation of mucosal immunity has great potential in vaccinology and immunotherapy. However, the mucosal immune system is more complex than the systemic counterpart, both in terms of anatomy (inductive and effector tissues) and effectors (cells and molecules). Therefore, immunologists entering this field need a precise terminology as a crucial means of communication. Abbreviations for mucosal immune-function molecules related to the secretory immunoglobulin A system were defined by the Society for Mucosal Immunolgy Nomenclature Committee in 1997, and are briefly recapitulated in this article. In addition, we recommend and justify standard nomenclature and abbreviations for discrete mucosal immune-cell compartments, belonging to, and beyond, mucosa-associated lymphoid tissue.
    Mucosal Immunology 02/2008; 1(1):31-7. DOI:10.1038/mi.2007.9 · 7.54 Impact Factor
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    ABSTRACT: The production of immunoglobulin A (IgA) in mammals exceeds all other isotypes, and it is mostly exported across mucous membranes. The discovery of IgA and the realization that it dominates humoral mucosal immunity, in contrast to the IgG dominance of the systemic immune system, was early evidence for the distinct nature of mucosal immunology. It is now clear that IgA can function in high-affinity modes for neutralization of toxins and pathogenic microbes, and as a low-affinity system to contain the dense commensal microbiota within the intestinal lumen. The basic map of induction of IgA B cells in the Peyer's patches, which then circulate through the lymph and bloodstream to seed the mucosa with precursors of plasma cells that produce dimeric IgA for export through the intestinal epithelium, has been known for more than 30 years. In this review, we discuss the mechanisms underlying selective IgA induction of mucosal B cells for IgA production and the immune geography of their homing characteristics. We also review the functionality of secretory IgA directed against both commensal organisms and pathogens.
    Mucosal Immunology 02/2008; 1(1):11-22. DOI:10.1038/mi.2007.6 · 7.54 Impact Factor
  • U Haddeland, P Brandtzaeg, B Nakstad
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    ABSTRACT: Elevated proliferative response to allergen in cord blood mononuclear cells (CBMCs) is related to subsequent allergy development of the neonate and has been suggested as a screening marker for high allergy risk. To characterize the proliferating cells in CBMCs from a neonatal group influenced by maternal allergy compared with a control group without known allergic heredity. CBMCs were stimulated with bovine beta-lactoglobulin (beta-LG) and proliferation was analysed by radioactive thymidine incorporation and expressed both as the traditional stimulation index (SI) and SI corrected by eliminating non-specific proliferation. After beta-LG combined with endotoxin stimulation, cellular expression of IL-4 and IFN-gamma mRNA was determined by quantitative RT-PCR and adhesion as well as chemokine receptors were analysed by three-colour flow cytometry in proliferating T cells (CD3+ Ki-67+). The percentage of CCR4+ cells correlated weakly with concurrent IL-4 expression (r(S)=0.5, P<0.05), while CXCR3 correlated strongly with IFN-gamma expression (r(S)=0.83, P<0.001). In the allergy risk group, the percentage of proliferating T cells expressing CCR4 or integrin alphaE (CD103) was significantly reduced compared with the control group, while CXCR5 and the corrected SI were relatively increased (CCR4: P=0.01; integrin alphaE: P=0.03; CXCR5: P=0.04; SI: P=0.04). Our results implied delayed maturation of immune functions involved in cellular migration, cell-cell interaction and immunoregulatory functions in neonates with hereditary allergy risk. The alterations observed in this subject group suggested that the corrected SI as well as proliferation of CCR4+, CXCR5+ or CD103+ T cells in allergen-stimulated CBMCs might serve as early screening markers for allergy risk.
    Clinical & Experimental Allergy 07/2007; 37(6):856-64. DOI:10.1111/j.1365-2222.2007.02728.x · 4.32 Impact Factor
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    M Hvatum, L Kanerud, R Hällgren, P Brandtzaeg
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    ABSTRACT: Patients with rheumatoid arthritis (RA) often feel there is an association between food intake and rheumatoid disease severity. To investigate a putative immunological link between gut immunity and RA, food antibodies were measured in serum and perfusion fluid from the jejunum of RA patients and healthy controls to determine the systemic and mucosal immune response. IgG, IgA, and IgM antibodies to dietary antigens were measured in serum and jejunal perfusion fluid from 14 RA patients and 20 healthy subjects. The antigens originated from cow's milk (alpha-lactalbumin, beta-lactoglobulin, casein), cereals, hen's egg (ovalbumin), cod fish, and pork meat. In intestinal fluid of many RA patients, all three immunoglobulin classes showed increased food specific activities. Except for IgM activity against beta-lactoglobulin, all other IgM activities were significantly increased irrespective of the total IgM level. The RA associated serum IgM antibody responses were relatively much less pronounced. Compared with IgM, the intestinal IgA activities were less consistently raised, with no significant increase against gliadin and casein. Considerable cross reactivity of IgM and IgA antibodies was documented by absorption tests. Although intestinal IgG activity to food was quite low, it was nevertheless significantly increased against many antigens in RA patients. Three of the five RA patients treated with sulfasalazine for 16 weeks had initially raised levels of intestinal food antibodies; these became normalised after treatment, but clinical improvement was better reflected in a reduced erythrocyte sedimentation rate. The production of cross reactive antibodies is strikingly increased in the gut of many RA patients. Their food related problems might reflect an adverse additive effect of multiple modest hypersensitivity reactions mediated, for instance, by immune complexes promoting autoimmune reactions in the joints.
    Gut 10/2006; 55(9):1240-7. DOI:10.1136/gut.2005.076901 · 13.32 Impact Factor
  • T. S. HALSTENSEN, H. SCOTT, P. BRANDTZAEG
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    ABSTRACT: Expression of the /δ T-Cell receptor (TcR) for antigen on CD3+ intraepithelial lymphocytes (IEL) was studied in situ by two-colour immunofluorescence on jejunal tissue secretions from 24 patients with coeliac disease and 17 controls. The proportion of intraepithelial TcR/δ+ cells was significantly increased (P<0.002) in untreated (median 20%, range 11–53%) as well in treated (gluten-free diet) coeliac disease (median 23%, range 16–55%) compared with controls (median 2%, range 0–39%). Although TcR/β+ IEL dominated both in controls and coeliac disease. T cells expressing the TcR/δ were preferentially located within the epithelium rather than in the lamina propria. Paired staining for TcR/δ and CD8 revealed that most (∼90%) intraepithelial TcR/δ+ lymphocytes in coeliac disease were CD8−. A remarkably large fraction (median 67%, range 58–94%) of intraepithelial TcR/δ+ cells expressed the Vδ1/Jδ1-encoded epitope revealed by monoclonal antibody δTCS1. Our results suggested that increase of the intraepithelial TcR/δ+ CD8− subset of T cells is particularly related to coeliac disease.
    Scandinavian Journal of Immunology 06/2006; 30(6):665 - 672. DOI:10.1111/j.1365-3083.1989.tb02474.x · 1.88 Impact Factor
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    ABSTRACT: Reduced microbial exposure in early life may contribute to the increase of atopic diseases in 'westernized' societies but the underlying mechanisms remain elusive. The objective of this study was to examine how exposure to bacterial lipopolysaccharide (LPS) during early antigen encounter might influence the maturation of neonatal lymphoid cells, and to define possible differences in this respect between neonates with high risk of allergy due to a family history (FH(+)) and controls with no apparent hereditary risk (FH(-)). Cord blood mononuclear cells from the FH(+) or FH(-) group were stimulated with pure LPS or beta-lactoglobulin (beta-LG) in the presence of LPS. T cell expression of chemokine receptors CCR4 and CXCR3 was determined by flow cytometry and reverse transcription-polymerase chain reaction (RT-PCR). Cellular expression of interleukin (IL)-4 was analysed by quantitative RT-PCR, whereas interferon (IFN)-gamma was analysed by both quantitative RT-PCR and immunoassay. Stimulation with LPS, or beta-LG together with LPS, induced up-regulation of CCR4 (P < 0.05) and CXCR3 (P < 0.05). For CCR4, such up-regulation was related to the level of IL-4 produced by the same T cells (r(S) = 0.49, P = 0.03), while CXCR3 expression was negatively correlated with the IL-4 levels (r(S) = -0.56, P = 0.02). Compared with the FH(-) group, the FH(+) group showed a significantly lower capacity for generation of CCR4(+) T cells (mean percentage of total T cells: FH(+), 2.42%versus FH(-), 5.74%; P < 0.01), whereas induction of CXCR3 and IFN-gamma did not differ significantly between the two groups. When the immune system in early life encounters antigen together with LPS, the T cell potential for compartmentalized interaction with other immune cells might be increased by elevated CCR4- and CXCR3-expression levels. In neonates at hereditary allergy risk, this putative homeostatic mechanism could theoretically be jeopardized due to decreased up-regulation of CCR4. Conversely, Th1 responses to antigen in the presence of LPS did not appear to be reduced compared with controls.
    Clinical & Experimental Immunology 03/2005; 139(2):314-22. DOI:10.1111/j.1365-2249.2005.02706.x · 3.28 Impact Factor
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    U Haddeland, P Brandtzaeg, B Nakstad
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    ABSTRACT: Background: The hygiene hypothesis suggests that the increasing prevalence of allergy in “westernised” countries is due to reduced bacterial exposure in early life, but the underlying mechanism remains elusive.
    Pediatric Research 09/2004; 56(3). DOI:10.1203/00006450-200409000-00221 · 2.84 Impact Factor
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    ABSTRACT: Background: Reduced microbial exposure in early life may be partly responsible for an increase in atopic diseases in ‘westernised' societies but the underlying mechanisms remain elusive. Objective To examine how exposure to bacterial lipopolysaccharide (LPS) during the first antigen encounter might influence the maturation of neonatal lymphoid cells, and to analyse possible differences in this respect between neonates with a high risk of allergy due to family history (FH−) and controls with no apparent risk (FH-).
    Pediatric Research 09/2004; 56(3). DOI:10.1203/00006450-200409000-00220 · 2.84 Impact Factor
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    D E Nilssen, O Øktedalen, P Brandtzaeg
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    ABSTRACT: It is well documented that highly active antiretroviral therapy (HAART) restores systemic immunity to human immunodeficiency virus (HIV) but the effect of this treatment on the mucosal immune system is less clear. Because future preventive or therapeutic vaccines against HIV may be administered by the mucosal route, we wished to evaluate the effect of HAART on the activation level and homeostasis of the intestinal B cell system. Duodenal biopsy specimens were collected consecutively from infection prone HIV positive adults (n = 31), mostly with advanced AIDS. In situ two colour immunofluorescence staining was performed to quantify mucosal immunoglobulin (Ig) class and subclass producing immunocytes (plasmablasts and plasma cells). HIV positive patients had, on average, duodenal proportions of IgA (74.6%), IgM (19.5%), and IgG (3.4%) immunocytes similar to median values recorded in 11 HIV seronegative healthy controls but the total immunocyte number per mucosal section length unit (500 microm) was significantly increased in patients (median 175 v 120 cells/unit; p<0.008), mainly comprised of IgA (p<0.02) and IgG1 (median 81.8% of total IgG; p<0.02) isotypes. Patients receiving a successful HAART regimen tended to normalise their IgG1 proportion and showed significantly lower total duodenal IgA immunocyte number than those receiving no or insufficient antiretroviral treatment (p<0.005). Our study demonstrated that advanced AIDS patients hyperactivate their intestinal B cell system. HAART could significantly reverse this perturbation, suggesting restored ability of the mucosal immune system to control intestinal infections.
    Gut 04/2004; 53(4):487-93. · 13.32 Impact Factor
  • P Brandtzaeg

Publication Stats

17k Citations
1,892.41 Total Impact Points

Institutions

  • 1971–2012
    • University of Oslo
      • • Department of Pathology (PAT)
      • • Department of Chemistry
      • • Division of Medicine
      • • Department of Biochemistry
      • • Department of Microbiology (MIC)
      Kristiania (historical), Oslo County, Norway
  • 1976–2011
    • Oslo University Hospital
      • • Department of Pathology
      • • Department of Medical Biochemistry
      • • Department of Infectious Diseases
      Kristiania (historical), Oslo County, Norway
  • 2004
    • Akershus universitetssykehus
      Kristiania (historical), Oslo County, Norway
  • 2001
    • Radboud University Medical Centre (Radboudumc)
      • Department of Human Genetics
      Nymegen, Gelderland, Netherlands
  • 1994
    • Nordlandssykehuset Bodoe
      Bodø, Nordland, Norway
  • 1992
    • Cancer Registry of Norway
      Kristiania (historical), Oslo, Norway
  • 1988
    • University of Pécs
      Fuenfkirchen, Baranya county, Hungary