This cross-sectional study examined neurobiologic correlates of depression in ischemic stroke patients. Depression severity was measured with a standardized scale (Center for Epidemiologic Studies Depression Scale; CES-D). Eighty-two patients (53.1% male, mean (± SD) age 71.9 ± 14.2 years, mean (± SD) National Institutes of Health Stroke Scale (NIHSS) score 4.6±4.7, mean (± SD) CES-D score 12.6 ± 10.8) were recruited. A linear regression controlling for age and stroke severity (NIHSS) determined that the kynurenine to tryptophan ratio (β= -0.105, p=0.369) was not significantly associated with CES-D (primary hypothesis) (overall model R2=0.069, F3,73=1.805, p=0.154). Secondary analyses suggested one instance of cytokines favouring inflammatory states in mild depressive symptomatology; IFN-Ɣ/IL-10 (OR, 2.17; 95% CI, 1.02-4.64, p=0.045). For the most part however, inclusion of cytokines and neuroimaging correlates such as atrophy, lesion location and white matter changes were non-significant. Longitudinal studies are necessary to identify the possible neurobiologic correlates of depressive symptoms post-stroke.

This cross-sectional study examined neurobiologic correlates of depression in ischemic stroke patients. Depression severity was measured with a standardized scale (Center for Epidemiologic Studies Depression Scale; CES-D). Eighty-two patients (53.1% male, mean (± SD) age 71.9 ± 14.2 years, mean (± SD) National Institutes of Health Stroke Scale (NIHSS) score 4.6±4.7, mean (± SD) CES-D score 12.6 ± 10.8) were recruited. A linear regression controlling for age and stroke severity (NIHSS) determined that the kynurenine to tryptophan ratio (β= -0.105, p=0.369) was not significantly associated with CES-D (primary hypothesis) (overall model R2=0.069, F3,73=1.805, p=0.154). Secondary analyses suggested one instance of cytokines favouring inflammatory states in mild depressive symptomatology; IFN-Ɣ/IL-10 (OR, 2.17; 95% CI, 1.02-4.64, p=0.045). For the most part however, inclusion of cytokines and neuroimaging correlates such as atrophy, lesion location and white matter changes were non-significant. Longitudinal studies are necessary to identify the possible neurobiologic correlates of depressive symptoms post-stroke.

Hemocytes (blood cells) play an important role in the immune response in invertebrates, and thus the regulation of hemocyte homeostasis (hematopoiesis) is essential for the host survival against pathogens. Astakine 1, a homologue to vertebrate prokineticins, was first identified in the freshwater crayfish Pacifastacus leniusculus as a cytokine, and was found to be necessary for new hemocyte synthesis and release in vivo, and also to induce spreading and proliferation of Hematopoietic tissue cells (Hpt cells, precursor of hemocytes) in vitro. The work of this thesis is aimed to further our understanding of the molecular mechanisms involved in astakine 1 induced hematopoiesis. Crayfish transglutaminase (Tgase) has been identified in the hemocytes, and is essential for the coagulation reaction. Interestingly this enzyme is exceedingly abundant in the Hpt cells, and the spreading of Hpt cells induced by astakine 1 was accompanied by sequential loss of TGase activity from the surface of these cells. This loss of TGase activity may be an important effect of astakine 1, resulting in recruiting new hemocytes into the circulatory system. Although astakine 1 contain a prokineticin domain, it lacks the conserved N-terminal AVIT motif present in its vertebrate homologues. This motif is important for vertebrate prokineticins to interact with their receptors, indicating a different receptor interaction for crayfish astakine 1. Astakine 1 was indeed found to interact with a completely different receptor, the β-subunit of ATP synthase, on a portion of Hpt cells, and subsequently block its extracellular ATP formation. Surface ATP synthase has been reported on numerous mammalian cells, but now for the first time in an invertebrate. The activity of ATP synthase on the Hpt cells may be important for the survival and proliferation of Hpt cells, but the underlying mechanisms remain further study. With the finding of a second type of astakine in crayfish, invertebrate astakines can be divided into two groups: astakine 1 and astakine 2. The properties of astakine 2 are different from those of astakine 1 both in structure and function. In primary cell culture of Hpt cells, only astakine 1 can promote proliferation as well as differentiation into semigranular cells, whereas astakine 2 may play a potential role in the maturation of granular cells. Moreover, a novel cysteine rich protein, Pacifastacus hematopoiesis factor (PHF), was found to be one target gene of astakine 1 in Hpt cells. Down regulation of PHF results in increased apoptosis in Hpt cells in vitro, and in vivo silencing PHF leads to a severe loss of hemocytes in the animal. Therefore astakine 1 acquires the anti-apoptosis ability by inducing its downstream gene PHF in the Hpt cells. With its ability to promote the survival, proliferation and differentiation of Hpt cells, astakine 1 is proven to be an important hematopoietic growth factor.

The depression of immune cell function that is typically observed after prolonged exercise is thought to be largely mediated by increased plasma concentrations of stress hormones and cytokines and possibly oxidative stress. The aims of this thesis were to determine the effects of acute and longer term oral antioxidant supplementation on immunoendocrine responses following prolonged exercise. In study 1 (Chapter 3) it was shown that vitamin C ingested acutely before and during prolonged exercise has little or no effect on immunoendocrine responses. Furthermore, the combined ingestion of vitamin C with carbohydrate provides no additional effects compared with carbohydrate alone. However, when vitamin C was supplemented acutely, 2 h prior to, and during prolonged exercise in addition to on the night before (14 h prior) exercise this limited the fall in neutrophil oxidative burst activity (study 2, Chapter 4). This was probably a result of reduced direct oxidative damage to neutrophils with vitamin C supplementation since there were no effects on the cortisol, interleukin-6, leukocytosis or neutrophilia responses. Longer periods of antioxidant supplementation (2 - 4 weeks) may be effective at blunting the cortisol, leukocytosis and neutrophilia responses to prolonged exercise (Chapters 5 and 6) but this had no effect on in vitro measures of neutrophil function. In study 5 (Chapter 7) it was shown that acute pre-exercise dark chocolate (which contains polyphenols) ingestion has some effects on plasma oxidative stress markers and circulating insulin and glucose responses but not the immunoendocrine responses to prolonged exercise.

Normal wound healing is a complex process that occurs in overlapping phases and depends upon interactions of the patient, environment and a large number of cells, growth factors, cytokines, chemokines, and other biochemical mediators. Psychological stress has been shown to adversely affect the normal wound healing process through its impact on cellular immunity. Cellular immunity impacts wound healing through the production and regulation of many of the above biochemical mediators of wound healing. The purpose of this pilot study was to examine the relationships among pre- and post-operative psychological stress experienced by women who were undergoing either immediate or delayed breast reconstruction following mastectomy for breast cancer and influence of that stress on wound healing, specifically the biochemical mediators of wound healing in the local wound environment. An integration of Lazarus and Folkman’s cognitive appraisal model of stress and coping and the psychoneuroimmunology model proposed by McCain, Gray, Walter and Robins (2005) served as the theoretical framework for the research. A descriptive non-experimental design was used, with samples collected over time to describe biochemical patterns in surgical wounds of women undergoing autologous breast reconstruction. Biochemical data were collected preoperatively, as well as at 24, 48, 72 and 96 hours postoperatively. Psychological stress instruments were administered pre-operatively and 48 hours post-operatively. Although subjects overall displayed low levels of psychological stress, meaningful wound fluid biochemical mediator patterns were detected. This study adds to our knowledge concerning wound fluid chemical mediators present in the local wound environment over time.

Rheumatoid arthritis (RA) is a chronic autoimmune disease that is associated with formation of autoantibodies, activation of inflammatory cascade and up-regulation of several cytokines. These processes lead to persistent synovial inflammation, joint damage and systemic manifestations. The aim of this diploma thesis is to characterize the role of a novel cytokine interleukin-20 (IL-20) in the pathogenesis of RA and to investigate its involvement in different stages of the disease as a potential surrogate biomarker. In this work, several methods including Enzyme-Linked Immunosorbent Assay (ELISA), Immunohistochemistry and Real-Time quantitative Polymerase Chain Reaction (RT-qPCR) have been employed. We demonstrated increased expression of IL-20 in the synovial tissue of RA compared with control osteoarthritis (OA) patients. Along with the up-regulation at sites of inflammation, concentrations of IL-20 were higher in the synovial fluid compared with circulating levels of IL-20. Furthermore, serum and synovial fluid IL-20 levels significantly correlated with RA disease activity. Synthesis of IL-20 was significantly increased in peripheral blood mononuclear cells (PBMCs) and synovial fibroblasts upon stimulation with some TLR ligands and pro-inflammatory cytokines. Although not regulating PBMCs functions in...

Der Einsatz der Vitamin B 1 Vorstufe Benfotiamin hat sich im Tiermodell durch Verhinderung oder gar Aufhebung typischer diabetischer Folgeschäden wie Ne- phropathie, Retinopathie und Neuropathie ausgezeichnet. Diese Wirkung wird unter anderem der Aktivitätssteigerung des Enzyms Transketolase zugeschrie- ben, welches auch bei Dialysepatienten ohne diabetische Grunderkrankung sup- primiert ist. Das Ziel der vorliegenden Arbeit war, die Auswirkungen einer ora- len Benfotiaminsubstitution auf den Stoffwechsel von Langzeithämodialysepati- enten zu untersuchen. Die 15 rekrutierten Patienten mit und ohne Diabetes mel- litus erhielten über einen Zeitraum von 2 Monaten eine Dosis von 300 mg/d Benfotiamin, die in den folgenden 2 Monaten bis maximal 450 mg/d gesteigert wurde. Um einen Eindruck über den Verlauf der Entzündungssituation und des oxidativen Stresses zu gewinnen, wurden im Patientenvollblut AGEs und pro- inflammatorische Zytokine gemessen. Außerdem wurden peripheren Lympho- zyten mit Hilfe des alkaline Comet-Assay und des Mikrokerntestes auf DNA- Schädigungen analysiert. In beiden Patientengruppen lässt die Senkung der Mi- krokernraten den Schluss zu, dass Benfotiamin DNA-Schäden und somit eventu- ell das Krebsrisiko reduziert. Dieses vielversprechende Ergebnis korreliert jedoch nicht mit dem Resultat des Comet-Assay. Da hier der relative DNA-Schaden ten- dentiell ansteigt, sollte es Ziel weiterer Studien sein, diesen Sachverhalt an ei- nem größeren Patientenkollektiv mit Kontrollgruppen zu überprüfen. Eventuell ist letzteres Testsystem wegen seiner hohen Sensitivität in diesem Fall nicht op- timal geeignet. Außerdem sollte gezielt auf die beobachtete schnellere und stär- kere Mikrokernsenkung der diabetischen Patienten eingegangen werden, da die- se in der vorliegenden Studie zahlenmäßig unterrepräsentiert waren. Positiv zu bewerten ist der leichte CRP-Abfall sowie der Anstieg des Gesamtproteins und Albumin im Serum, was auf eine Reduktion der Mikroinflammation und oder eine verbesserte Ernährungssituation hinweist. Andererseits spricht der Anstieg des Neopterin- und Interleukin 6-Spiegels gegen die Veränderung des Inflamma- tionsstatus. Entgegen der Erwartung ließ sich in dieser Studie keine Reduktion der zirkulierenden AGEs und AOPPs im Serum erzielen. Um eine Reduktion des oxidativen Stresses besser beurteilen zu können, sollten in Folgestudien direkte und leicht veränderliche Marker wie der Glutathionspiegel verwendet werden. Zusammenfassend reduzierte Benfotiamin bei Hämodialysepatienten mit und ohne Diabetes mellitus DNA-Schäden in peripheren Lymphozyten bei unver- änderter Inflammationssituation und steigerte die Plasmaproteinkonzentration. Dies wurde eventuell durch Reduktion von oxidativem Stress und oder Beein- flussung seiner Ursachen wie Reduktion von Urämietoxinen erreicht.Weitere kli- nische Studien sind notwendig, um dieses vielversprechende Medikament in der täglichen Praxis einsetzen zu können. Besonders vorteilhaft ist seine gute Verträg- lichkeit auch in hoher Dosierung. Darüber hinaus soll das Präparat auch neuro- patische Schmerzen reduzieren, die sich bei Dialysepatienten häufig manifestie- ren, und wirkt somit multikausal. / It has been shown in animal models, that Benfotiamine, a precursor of the vitamine B1, prevents typical complications of diabets, like nephropathy, retinopathy and neuropathy. This effect is attributed to the increased activity of the enzyme trankelotase. The latter is also suppressed in patients of the hemodialysis program who are not diabetic. The goal of this thesis was to show the effects of an oral administration of benfotiamine on longterm hemodialysis patients. Fifteen patients were treated with 300 mg per day of benfotiamine which was increased in the following two months to 450 mg per day. The patient group consisted of a sub-group of diabetic and non-diabetic individuals. Advanced glycation endproducts (AGEs) and proinflammatory cytocines were measured in patients full-blood to show the impact on the inflammation and the oxidative stress situation. The DNA-damage in peripheral lymphocytes was determined using the alkaline comet-assay and the micronucleus-assay. The rate of micronuclei was diminished in both patient groups which could be attributed to the reduction of DNA-damage by benfotiamine and so eventually to a reduced risk of cancer. However, this result does not agree with the comet-assay experiments. The relative DNA-damage increased in the course of the study and so seems to be unaffected by the benfotiamine therapy. This may be attributed to the high sensitivity of the comet-assay technique. Therefore, further investigations with a bigger patient group in a double-blind study are necessary. Additionally, there should be a greater focus on diabetic patients that showed a faster and increased reduction of micronuclei which were underrepresentated in this study. The slight reduction of CRP and the increased protein and serum-albumine concentration correlates to a better nutritional status. On the other hand, the increasing neopterine and interleukine 6 level do not agree to the changes in the inflammatory situation. Against all expectations there was no reduction of AGEs and AOPPs in patients serum. Following studies should focus on rapidly changing direct markers like the glutathione level. In summary, benfotiamine reduces DNA-damage in peripheral lymphocytes in hemodialysis patients with or without diabetes. The plasma protein concentration was increased but unexpectedly the inflammatory situation was stable. These effects may be due to a reduction of oxidative stress or its causes like diminished ureamic toxines. One of Benfotiamines advantages is its good tolerance, even in increased dosages. Furthermore it seems to diminish neuropathic pain which is frequent in hemodialysis patients. However, more clinical studies are neccessary for a use in daily practice.

Das Ziel der Arbeit war, die Einflüsse verschiedener Zytokine bzw. Wachstumsfaktoren (unter anderem Stammzellfaktor (SCF), Thrombopoetin (TPO), Flt3-Ligand (FL-3), Interleukin-3 (IL-3), Tumornekrosefaktor-a (TNF-a) und Granulozyten-Makrophagen-Stimulierender-Faktor (GM-CSF)) auf humane hämatopoetische, CD34-positive Stammzellen (HSZ) zu evaluieren. Eine relativ hohe Zellamplifikation bei gleichzeitig geringer Differenzierungsinduktion ermöglichte eine Kombination der Zytokine TSF, SCF und FL-3. Eine gezielte Differenzierung von CD14-positiven, monozytären Zellen gelang am besten mit einer Kombination der Zytokine TSF, SCF, FL-3 und IL-3. Für die Generierung von dendritischen Zellen eignete sich eine Zytokinkombination aus IL-4, TNF-a und GM-CSF. Im zweiten Teil der Arbeit wurde das Verhalten von Philadelphiachromosom-positiven CML-Stammzellen (CML = chronisch myeloische Leukämie) im Vergleich zu benignen HSZ, analog zu den obigen Gesichtspunkten, evaluiert. Die CML-Stammzellen zeigten bei Inkubation mit Zwei- und Mehrfachzytokinkombinationen eine z.T. deutlich höhere Amplifikation als die Vergleichsansätze mit benignen Zellen. In den Mehrfachzytokinansätzen fand sich im zeitlichen Verlauf darüberhinaus eine größere, verbleibende CD34-positive Zell-Population als in den benignen Vergleichsansätzen. Bei der zielgerichteten dendritischen Zelldifferenzierung verhielten sich die CML-Stammzellen ähnlich wie die benigen Zellen, wobei die Differenzierung in den Kulturen zu einem späteren Zeitpunkt auftrat. Ein Unterschied gegenüber den benignen Ansätzen zeigte sich bei den CML-Stammzellen in einer nahezu fehlenden Differenzierungsfähigkeit in CD14-positive, monozytäre Zellen. Dieser Differenzierungsblock ließ sich jedoch durch eine Kombination der verwendeten Zytokine mit Vitamin D3 überwinden. / the intention of our studies was, to explore the cytokine-influence on humane hematopoetic stem cells (amongst others there were used stem-cell-factor (SCF), thrombopoetine (TPO), Flt3-Ligand (FL-3), Interleukine-3 (IL-3), Tumornecrosisfactor-a (TNF-a) und Granulocyte-Makrophage-stimulating-Factor (GM-CSF). A relatively high cell-amplification combined with a low induction of cell-differentiation was found in a cytokine cocktail made up of SCF, TPO and FL-3. A selective differentiation of CD14-positive, monocytic cells was found in presence of TSF, SCF, FL-3 und IL-3. The generation of dendritic cells succeeded with a combination of IL-4, TNF-a and GM-CSF. The intention of the second part of the studies was, to analyze the characteristics of Philadelphia-chromosome-positive CML-Stem (cml = chronic myeloic leukemia) cells compared to benign stem cells. The CML-stem cells were featured by a very high cell-amplification. Furthermore we found a very high persistent CD34-positive Population in the Cytokine Cultures containing two or more cytokines (compared to benign stem cells). Looking at the selective differentiation of dendritic cells, the findings are assimilable with the results found with benign stem cells, though the cml-stem cells differentiated at a later date. A main difference between benign and cml-stem cells was found in the differentiation in CD14-positive, monocytic cells. We found a lack of monocytic differentiation in the cml stem cells. However, this effect could be overcome by a incubation of the CML cells with a combination of cytokines and vitamine D3.

Le vitiligo est une dermatose inflammatoire caractérisée par une perte progressive des mélanocytes de la lame basale de l’épiderme. Cette pathologie reste à ce jour orpheline de traitement efficace. Toutefois, les mécanismes qui sont liés à la perte des mélanocytes restent débattus et impliquent un détachement des mélanocytes de la lame basale ou leur mort cellulaire par apoptose. Nous avons montré au sein de notre équipe l’implication des lymphocytes T CD8+ effecteurs mémoires dans la pathogénie du vitiligo. Ces populations produisent des niveaux élevés de deux cytokines inflammatoires qui sont, le TNF-α (tumor necrosis factor) et l’IFN-γ (interféron γ), suggérant ainsi un rôle majeur de ces deux cytokines dans la pathogénie du vitiligo. L’objectif de mon projet de thèse est d’étudier les mécanismes immunologiques impliqués dans la perte du mélanocyte au cours du vitiligo. Ainsi, nous avons observé dans les zones péri-lésionnelles de vitiligo ou lésionnelles de psoriasis, une localisation suprabasale des mélanocytes et une anomalie de l’expression de la E-cadhérine dans l’épiderme, protéine majeure impliquée dans l’attachement des mélanocytes. Nous avons également montré l’absence de la mort cellulaire par apoptose des mélanocytes au niveau cutané chez les patients atteints de vitiligo et/ou de psoriasis. En se basant sur ces observations, nous nous sommes donc intéressés à évaluer les effets combinés du TNF-α et de l’IFN-γ sur l’adhésion des mélanocytes. Nos résultats ont montré que les deux cytokines combinés diminuent l’expression du gène codant la Ecadhérine et entrainent probablement la redistribution de cette protéine. De plus, nous avons observé que ces deux cytokines en combinaison altèrent l’expression de la E-cadhérine dans un modèle d’épidermes reconstruits pigmentés in vitro. Cette altération était associée à une augmentation des niveaux de la E-cadhérine soluble (sE-cad) au niveau des surnageants de culture. D’une manière intéressante, nous avons montré que ces deux cytokines induisent l’expression kératinocytaire de la métalloprotéase 9 (MMP9) dont l’action est connue pour cliver la E-cadhérine sous sa forme soluble, participant ainsi au détachement des mélanocytes. Des taux élevés de MMP9, mais également de la sE-cad sont retrouvés dans le sérum des patients atteints de vitiligo. L’inhibition de la MMP9 dans des modèles in vitro et in vivo empêche les effets combinés du TNF- α et de l’IFN-γ sur le détachement des mélanocytes permettant leur stabilisation à la lame basale. Par ailleurs, comme nous avons montré que la survie des mélanocytes n’était pas altérée dans le vitiligo, nous nous sommes intéressés à évaluer l’action combinée du TNF-α et de l’IFN-γ sur la fonction, le phénotype des mélanocytes et leur production des médiateurs inflammatoires. Nous avons montré que ces deux cytokines en combinaison inhibent l’expression des gènes mélanocytaires (MITF, TYR, DCT) et favorisent l’induction des chimiokines CXCL9 et CXCL10, de la cytokine inflammatoire TNF-α et de la molécule d’adhésion ICAM-1, suggérant un rôle majeur des mélanocytes dans la promotion de l’inflammation. Enfin, considérant que la voie de signalisation du récepteur de l’IFN-γ est dépendante de la voie JAK/STAT, nous avons étudié l’impact de l’inhibition de cette voie dans les effets induits dans nos modèles, et avons montré au niveau de l’expression des gènes, une amélioration des gènes associés à la fonction mélanocytaire et une inhibition de ceux associés à l’inflammation. L’ensemble de nos résultats mettent en évidence un nouveau mécanisme pour expliquer la perte des mélanocytes et identifie MMP9 ainsi que les inhibiteurs de JAK comme des cibles thérapeutiques prometteuses permettant ainsi de mieux comprendre les mécanismes physiopathologiques au cours du vitiligo et d’établir un lien direct entre immunité, facteurs solubles inflammatoires et perte des mélanocytes au cours du vitiligo. / Vitiligo is a chronic inflammatory skin disorder characterized by a progressive loss of melanocytes. This stigmatizing disease has a major social impact and no real effective therapies have been reported so far. However, the mechanisms leading to melanocyte disappearance remain debated and include melanocyte detachment and/or death. The role of the immune response has now been well described, implying CD8+ effector memory T cells that produce high levels of inflammatory cytokines as TNF-α (tumor necrosis factor) and IFN-γ(interferon γ), suggesting the involvement of these two cytokines in the pathogenesis of vitiligo. Thus, the aim of this project is to study the interplay between the inflammatory response characterizing vitiligo disease and melanocyte loss. We first observed that melanocytes are located in suprabasal layers of the epidermis in perilesional skin of vitiligo and lesional skin of psoriasis patients, which was associated with an altered expression of E-cadherin, a major protein involved in melanocyte attachment to the basal membrane. Such suprabasal melanocytes did not undergo apoptosis. Based on these observations, we next investigated the combined effects of TNF-α and IFN-γ on melanocyte adhesion. We showed that these two cytokines decrease E cadherin gene expression and probably induce a redistribution of E-cadherin. In addition, these two cytokines in combination altered the expression of E-cadherin in reconstructed human pigmented epidermis in vitro. This finding was associated with increased levels of soluble E-cadherin in culture supernatants. Furthermore, TNF-α and IFN-γ induced the production of matrix metalloproteinase 9 (MMP9) by keratinocytes, leading to the cleavage of the E-cadherin. Inhibition of MMP9 prevents the combined effects of TNF-α and IFN-γ on melanocyte detachment and led to their stabilization to the basal membrane of epidermis in vitro and in vivo models. Since we demonstrated that melanocyte survival is not impaired in vitiligo, we assessed the impact of these two cytokines on melanocyte function, phenotype and inflammation. We demonstrate that the combination of TNF-α and IFN-γ inhibits the expression of genes involved in melanocyte function (MITF, TYR, DCT) and promote the induction of the chemokine ligands CXCL9 and CXCL10, the inflammatory cytokine TNF-α and adhesion molecule ICAM-1, suggesting an important role of melanocytes in the promotion of inflammation. Lastly, considering that the signaling pathway of IFN-γ involves activation of the JAK / STAT pathway, we studied the impact of the inhibition of that pathway in our models. Our results show that the JAK inhibition suppressed the effects of TNF-α and IFN-γ on melanocyte function, on the release of pro-inflammatory mediators and led to the melanocyte stabilization to the basal membrane of epidermis. All of our results highlight a new mechanism to explain the loss of melanocytes and identify MMP9 and JAKs as promising therapeutic targets to better understand the physiopathological mechanisms during vitiligo and establish a direct link between immunity, soluble factors. Inflammation and loss of melanocytes during vitiligo.

A Asma vem apresentando taxas de prevalência crescentes em todo o mundo. Os objetivos deste trabalho são avaliar a presença de elementos celulares e humorais indicativos em sangue e colostro de mães asmáticas e saudáveis e no sangue de cordão umbilical de seus recém-nascidos (RN). Observamos menor produção de IgG pelas mães asmáticas. Células dendríticas de mães asmáticas possuem maior expressão de CD80 e CD86. Mães asmáticas possuem mais células de memória central. Linfócitos T CD4+ de mães asmáticas produzem níveis maiores IFN-g. Células CD3+ e CD4+ de mães asmáticas produziram mais IL-13. Mães saudáveis produziram maiores quantidades de IL-10. Concluímos que mães asmáticas possuem menores níveis de IgG e IgM, o que parece aumentar dos níveis de IgE, mães asmáticas possuem mais células de memória central, linfócitos T CD4+ produzem maiores quantidades de citocinas como IL-13 e IFN-g, células dendríticas de mães asmáticas possuem maior expressão das moléculas co-estimulatórias, assim como seus RNs possuem maior expressão de CD80. Células de mães asmáticas produzem níveis menores de IL-10, o colostro de mães atópicas não possui diferenças entre os parâmetros aqui estudados. O aleitamento materno deve ser indicado para mães asmáticas e seus filhos. / Asthma has been presenting higher prevalence rates worldwide. The objective of this work is to evaluate the presence of cellular elements and humoral indicative in blood and colostrums of healthy and asthmatic mothers and in cord umbilical blood of their newborn (NB). Lower production of IgG from asthmatic mothers was observed. Dendritic cells of asthmatic mothers have higher CD80 and CD86 expression. Asthmatic mothers have more central memory cells. TCD4+ lymphocyte of asthmatic mothers produce higher levels of IFN-g. CD3+ and CD4+ cells of asthmatic mothers produce higher quantity of IL-13. Healthy mothers produce higher quantity of IL-10. We conclude that asthmatic mothers have lower levels of IgG and IgM, and this seems to raise the IgE levels, asthmatic mothers have more central memory cells, CD4+ T lymphocyte and produce higher quantities of cytokines such as Il-13 and IFN-g. Dendritic cells of asthmatic mothers have higher expression of costimulatory molecules, as well as their NBs have higher expression CD80. Cells of asthmatic mothers produce lower levels of IL-10, the colostrums of atopic mothers does not have differences in the parameters here studied. The maternal breastfeeding must be indicated for asthmatic mothers and their of spring.