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Burns often leads to infection, due to damage to the skin's protective barrier. Burn injury has been repeatedly shown to induce considerable inflammatory and immune dysfunction. The innate immune system is a universal and ancient form of host defense against infection. Activation of innate immunity constitutes the first line of host defense against infection. Neutrophils are white blood cells and part of the immune system. They are the most common PMN (polymorphonuclear neutrophils) and accounted for 70% of all leukocytes. Neutrophils provided the first line of defense of the innate immune system by phagocytosing, killing, and digesting bacteria and fungi. Priming means a process whereby the response of neutrophils to an activating stimulus is potentiated, sometimes greatly, by prior to exposure to priming agents such as tumor necrosis factor-alpha(TNF-alpha), platelet-activating factor (PAF). Neutrophil priming causes a dramatic increase in the response of these cells to an activating agent; this process has been shown to be critical for neutrophil-mediated tissue injury both in vitro and in vivo. However, the intracellular signaling pathways used by neutrophil in response to pro-inflammatory stimuli have not been elucidated. The discovery of TLRs has made us understanding of the mechanisms of innate immune recognition. The innate immune system detectes the invasion of microorganism through TLRs, which recognize microbial components and trigger inflammatory responses. Severe burn injury produces shock and induces acute gastrointestinal derangement that may disrupt gastrointestinal mucosa integrity and facilitate the bacterial translocation (BT) to Mesenteric lymph node (MLN), liver, and spleen. Hypertonic saline (HTS) has been advocated in thermal injury resuscitation because of the possibility of giving less total volume of resuscitation fluid, with a resulting decrease in edema and the need for escharotomy. In this study, I found that priming effect of BM neutrophils is TNF-alpha and p38 dependent and TLRs play a critical role to the innate immunity by recognizing bacteria and HTS enhance host response to bacterial challenge by increasing TLRs of inflammatory cells.

Background and Objectives: The pathophysiology of post-operative pneumonia following lung resection is poorly understood despite it being the most common complication which may lead to death. The role of the acute inflammatory response following lung resection, in particular innate immune cells, was investigated and used to identify biomarkers for post-operative pneumonia. Comparison of inflammatory responses to resection undertaken by video-assisted thorascopic surgery (VATS) and thoracotomy was also evaluated. Methods: Patients undergoing lung resection for suspected bronchogenic carcinoma were recruited. Objective pre-defined criteria were used to diagnose pneumonia. Bronchoalveolar lavage (BAL) was conducted in the contra-lateral lung pre- and postoperatively to measure cellular composition and cytokines. Blood was sampled preoperatively and 6-, 24- and 48-hours post-operatively primarily to assess neutrophil phagocytic capacity, monocyte subsets, monocyte cytokine responses to lipopolysaccharide (LPS) stimulation and serum cytokine responses. Exhaled nitric oxide (eNO) was also measured at these time points. Patient groups were compared using paired or student t-tests together with ANOVA/ANCOVA modelling. The predictive strength of the biomarkers identified was tested. Results: 40 patients were recruited. 26 patients (65%) underwent major lung resection using VATS and 14 (35%) thoracotomy. There was a post-operative blood monocytosis (p<0.0005) with an absolute expansion of classical and intermediate monocytes (p=0.001) and a relative fall in non-classical monocytes (p<0.005). Post-operatively blood monocytes became more pro-inflammatory with an overall significant increase in IL-8 (p=0.034) and TNF-α (p=0.028) together with an increase in IL-6 (p=0.028) and IL-10 by 48 hours (p=0.010). VATS was associated with a smaller release of IL-10 only (p=0.011). There was a general trend towards post-operative reduction in neutrophil phagocytosis of zymosan (in suspension) on ANOVA modelling (p=0.047). Lung resection led to an increase in serum cytokines IL-6, IL-8 and IL-10 which peaked at 24hrs before falling (p<0.0005). ANOVA modelling confirmed significantly lower levels of serum cytokines in VATS patients compared with thoracotomy (p=0.026 for IL-6, p=0.018 for IL-8 p=0.047 for IL-10). No significant post-operative change was found for IL-1β, TNF-α and IL-12p70 (p>0.05). Bronchoalveolar lavage fluid (BALF) and blood samples demonstrated a relative post-operative leucocytosis due principally to neutrophilia. A relative blood lymphopenia and thrombocytopenia developed postoperatively (p<0.0005). VATS was associated with a lower fall in serum albumin (p=0.001). BALF from the non-operated lung became more pro-inflammatory immediately post-operatively with an increase in IL-6 (p<0.0005), IL-8 (p=0.017), IL- 10 (p=0.018) and IL-1β (p=0.002). eNO tended to fall post-operatively which reached significance at 48 hrs (p=0.029). 14 patients developed pneumonia. Pre-operatively, a blood neutrophil count above 5.04x109/L had a relative risk (RR) for pneumonia of 3.3 (95% confidence interval (CI95) 1.1-10.1), and a BAL cell count of greater than 1.04x105/ml had a RR of 3.4 (CI95 1.3-9.0), whilst LPS-stimulated monocyte secretion of IL-12 of less than 0.15 pg/ml/μg protein had a RR of 3.0 (CI95 1.2-7.3). At 24 hours post-operatively, LPS-stimulated release from monocytes of IL-10 greater than 1.99 pg/ml/μg protein (RR 4.1, CI95 1.3- 12.3) and IL-6 greater than 414 pg/ml/μg protein (RR 3.1, CI95 1.2-8.1) were predictive of pneumonia. Conclusion: Lung resection is associated with significant early pro- and antiinflammatory responses. VATS resection invoked significantly lower levels of serum cytokines and albumin changes compared with thoracotomy suggesting VATS lobectomy should be the surgical treatment strategy of choice for early stage lung cancer. No difference in neutrophil function or monocyte function was however observed between the surgical groups. Clinical benefits of this reduced inflammation need to be evaluated in a larger cohort of patients. Relative pre-operative leucocytosis in blood and BAL together with monocyte hyper-responsiveness in the early postoperative period is associated with the development of pneumonia. These findings warrant further investigation for their predictive power in accurately identifying postoperative pneumonia. Ultimately, they may be incorporated into a risk stratification model enabling targeted prophylactic or earlier therapeutic intervention.

Long-term survival of implanted cells requires oxygen and nutrients, the need for which is met by vasculari- zation of the implant. The use of scaffolds with surface-attached heparin as anchoring points for angiogenic growth factors has been reported to improve this process. We examined the potential role of surface modification of gelatin scaffolds in promoting endothelial cell infiltration by using a unique macromolecular conjugate of heparin as a coating. Compared to other heparin coatings, this surface modification provides flexible heparin chains, representing a new concept in heparin conjugation. In vitro cell infiltration of scaffolds was assessed using a three-dimensional model in which the novel heparin surface, without growth factors, showed a 2.5-fold increase in the number of infiltrating endothelial cells when compared to control scaffolds. No additional improvement was achieved by adding growth factors (vascular endothelial growth factor and/or fibroblast growth factor-2) to the scaffold. In vivo experiments confirmed these results and also showed that the addition of angiogenic growth factors did not significantly increase the endothelial cell infiltration but increased the number of inflammatory cells in the implanted scaffolds. The endothelial cell-stimulating ability of the heparin surface alone, combined with its growth factor-binding capacity, renders it an interesting candidate surface treatment to create a prevascularized site prepared for implantation of cells and tissues, in particular those sensitive to inflammation but in need of supportive revascularization, such as pancreatic islets of Langerhans. / <p>De två sista författarna delar sistaförfattarskapet.</p>

Im Rahmen der Routinediagnostik von Endometriumbioptaten der Stute fielen regel-mäßig periglanduläre mononukleäre Entzündungszellinfiltrate (PAME) auf. Ziel der vorliegenden Studie war die histomorphologische und immunhistologische Charakterisierung der PAME im klinisch-gynäkologischen, jahreszeitlichen und endometrialen Kontext. Insbesondere sollte geklärt werden, ob das Phänomen der periglandulären Entzündungszellakkumulation Ausdruck eines physiologischen endometrialen Befundes, Frühstadium (Trigger) der Endometrose oder Begleitsymptom einer Endometritis ist. Zu diesem Zweck wurden alle im Jahr 2009 mittels einer Übersichtsfärbung (H.-E.-Färbung) im Institut für Veterinär-Pathologie der Universität Leipzig untersuchten Endometriumbioptate von Stuten (n = 754) hinsichtlich des Vorkommens einer PAME überprüft. Es konnten 133 Bioptate von 131 Stuten identifiziert werden, die ausführlich histopathologisch ausgewertet wurden. 72 Bioptate wurden zusätzlich anhand einer Methylgrün-Pyronin-Färbung (MGP) und immunhistologischer Verfahren beurteilt: Neben der Differenzierung der an der PAME beteiligten Zellpopulationen (CD3, CD79 A, MAC 387, MGP), wurde das Vorkommen der Intermediärfilamente Vimentin und Desmin sowie von α-GMA in den beteiligten Epithel- und Stromazellen untersucht. Die glanduläre Basallamina wurde anhand der Basallaminakomponente Laminin dargestellt und charakterisiert. PAME kamen in 18 % aller im Jahr 2009 untersuchten Bioptate vor, bevorzugt (96 %) in entzündlich und/oder fibrotisch alterierten Endometrien. Der Entzündungszellcharakter der begleitenden Endometritis stimmte in 29 % der Fälle nicht mit dem Entzündungszellbild der PAME (mononukleär) überein. Während im übrigen Endometrium häufig (95 %) eine gering- bis mittelgradige Endometrose nachweisbar war, wiesen die PAME-Drüsen mehrheitlich (71 %) keine periglanduläre Fibrose auf. Bei der Endometrose um Drüsen mit einer PAME handelt es sich überwiegend (67 %) um die destruierende und zu 50 % um die aktive/gemischte Form. In 48 % der PAME-Lokalisationen wurde eine Infiltration der periglandulären Entzündungszellen zwischen die Drüsenepithelzellen beobachtet. Die PAME bestanden hauptsächlich aus T-Lymphozyten (CD3-positiv). Daneben fanden sich, in geringerer und variierender Anzahl, Plasmazellen (MGP), B-Zellen (CD79A-positiv) und Makrophagen (MAC 387-positiv). Anhand der Expression der Basallaminakomponente Laminin wurden in allen untersuchten PAME-Lokalisationen Alterationen der Basallamina nachgewiesen. Die Läsionen der Basallamina waren bei mittel- und hochgradigen PAME graduell stärker ausgeprägt und standen häufig (43 %) mit einer intraepithelialen Infiltration der Entzündungszellen im Zusammenhang. Vimentin wurde vereinzelt (4 %) in intraläsionalen Drüsenepithelzellen nachgewiesen. Periläsionale Stromazellen exprimieren zu 60 % Vimentin, zu 17 % Desmin und zu 28 % α-GMA. Bei der PAME handelt es sich sehr wahrscheinlich nicht ausschließlich um ein „histopathologisches Symptom“ einer chronischen nicht-eitrigen Endometritis. Die Interpretation der PAME als physiologischer Bestandteil eines Schleimhaut-assoziierten lymphatischen Gewebes (MALT) im equinen Endometrium hingegen ist denkbar und bedarf in Folgeuntersuchungen der Klärung. Hinsichtlich der Strukturfilamente wurden in den involvierten Epithel- und Stromazellen immunhistologische Expressionsmuster nachgewiesen, die mit denen in frühen Stadien der equinen Endometrose vergleichbar sind. Darüber hinaus wiesen die periläsionalen Stromazellen Differenzierungsmerkmale von Myofibroblasten auf. PAME waren eng mit dem Vorliegen von Basallaminaalterationen verknüpft, die im Entstehungsprozess der equinen Endometrose eine zentrale Bedeutung besitzen. Es ist vorstellbar, dass es sich bei der PAME möglicherweise um einen auslösenden Faktor der Endometrose handelt. Außerdem ist eine intrinsische Aufrechterhaltung im Rahmen der zytokinvermittelten Interaktion (IL-4, IL-13, MCP-1), zwischen den periglandulären Entzündungszellen und den an einer Fibrose beteiligten Stromazellen, mit daraus resultierender progredienter Fibrose denkbar. Zukünftig sollte in weiteren Untersuchungen eine diesbezügliche Analyse der potentiellen Regelkreise erfolgen.

Ο καρκίνος αποτελεί μια από τις μεγαλύτερες μάστιγες της σύγχρονης ζωής. Η ιστολογική εξέταση των νεοπλασμάτων (τόσο στις πρωτοπαθείς εστίες όσο και στις δευτεροπαθείς εναποθέσεις) αποκαλύπτει ότι οι όγκοι αποτελούν ένα ετερογενές σύνολο άμορφων και έμμορφων στοιχείων. Η νεοπλασματική μάζα εκτός από τα καρκινικά κύτταρα, περιλαμβάνει ποικίλα κύτταρα (ινοβλάστες, κύτταρα αγγείων, μακροφάγα, φλεγμονώδη κύτταρα, λιποκύτταρα) και στοιχεία της εξωκυτταρίου ουσίας (κολλαγόνο, ελαστικές ίνες, πρωτεΐνες της εξωκυττάριας ουσίας) τα οποία στη μεγάλη πλειοψηφία τους προσελκύονται, άμεσα ή έμμεσα, από τα κακοήθη κύτταρα. Τα κύτταρα του καρκινικού μικροπεριβάλλοντος δεν αποτελούν αδρανείς παρατηρητές της καρκινικής διεργασίας αλλά συμμετέχουν ενεργά σε αυτή καθώς αυξάνουν τον πολλαπλασιασμό, καταστέλλουν την απόπτωση, ευνοούν την επιβίωση, διευκολύνουν τη μετανάστευση και εξασφαλίζουν την επαρκή θρέψη και οξυγόνωση των καρκινικών κυττάρων. Επιπλέον προστατεύουν τα καρκινικά κύτταρα από το ανοσοποιητικό σύστημα του ξενιστή. Η μελέτη των ποικίλων αλληλεπιδράσεων που αναπτύσσονται στο καρκινικό μικροπεριβάλλον ανάμεσα στα καρκινικά κύτταρα και τα στοιχεία του ξενιστή αποκαλύπτει καινούργιους θεραπευτικούς στόχους στην αντικαρκινική θεραπεία και βοηθάει στην κατανόηση του μηχανισμού των μεταστάσεων, δημιουργώντας την ελπίδα της αποτελεσματικότερης αντιμετώπισης του καρκίνου. Στην παρούσα εργασία γίνεται μια συνολική αναφορά της συμμετοχής όλων των στοιχείων του καρκινικού μικροπεριβάλλοντος στη νεοπλασματική εξεργασία. Επίσης καταβάλλεται προσπάθεια να τονιστούν οι σύνθετες αλληλεπιδράσεις ανάμεσα στα καρκινικά κύτταρα και το μικροπεριβάλλον. / Cancer is a devastating disease. Histologic examination of neoplasms (in the primary sites and their metastases as well) reveals that tumors are composed of a heterogeneous population of cells (fibroblast, vascular cells, macrophages, inflammatory cells, lipocytes) and extracellular matrix proteins (ECM) (collagen, elastin fibers, other ECM proteins). Recruitment of non-neoplastic tissue (stromal cells and ECM) to the tumor microenvironment is mostly mediated, directly or indirectly, by the malignant cells. Stromal cells are not quiescent bystanders of the neoplastic process. Instead they have an active role since they promote the proliferation, growth and migration of the tumor cells, inhibit their apoptosis and support tumor supply of oxygen and nourishment. In addition, stromal cells and ECM network protect cancer cells from the host defense. Research on the evolving crosstalk between the different cell types and ECM molecules within the tumor mass can disclose new therapeutic targets and help elucidate the pathogenetic mechanisms underlying metastasis, thus leading to a more effective anticancer therapy. This study discusses the potential role of the different stromal compartments in cancer initiation and progression and emphasizes the complex crosstalk between cancer cells and their microenvironment.

Lėtinė obstrukcinė plaučių liga (LOPL) – šiuo metu pasaulyje viena svarbiausių didelį sergamumą ir mirtingumą sąlygojančių ligų. Pacientams, kuriems pasunkėja kasdieniai LOPL simptomai pasireiškia LOPL paūmėjimas. Šio tyrimo tikslas – įvertinti nespecifinį uždegimą paūmėjus lėtinei obstruk¬cinei plaučių ligai. Nustatyti periferinio kraujo ir indukuotų skreplių ląstelių sudėties skirtumai ir įvertintos sąsajos su plaučių funkcijos rodikliais bakterinio ir nebakterinio lėtinės obstrukcinės plaučių ligos paūmėji¬mo metu. Tirtos sergančiųjų bakterinės kilmės lėtinės obstrukcinės plaučių li¬gos paūmėjimo indukuotų skreplių neutrofilų ir makrofagų funkcijos (apoptozė, fagocitozė ir reaktyvių deguonies formų susidarymas) bei palygintos su nebakteriniu paūmėjimu. Įvertinti sergančiųjų bakterinės ir nebakterinės kilmės lėtinės obs¬trukcinės plaučių ligos paūmėjimo periferinio kraujo neutrofilų ir monocitų apoptozė ir chemotaksis, bei periferinio kraujo neutrofilų fagocitozė ir reaktyvių deguonies formų susidarymas. Ištirta sergančiųjų bakterinės ir nebakterinės kilmės lėtinės obstruk¬cinės plaučių ligos paūmėjimu interleukino-8 koncentracija ir sąsajos su periferinio kraujo neutrofilų chemotaksiu bei C reaktyviojo baltymo koncentracijos periferinio kraujo serume sąsajos su plaučių funkcija ir rūkymo intensyvumu. / Chronic obstructive pulmonary disease (COPD) – a common preventable and treatable disease, is characterized by persistent airflow limitation that is usually progressive and associated with an enhanced chronic inflammatory response in the airways and the lung to noxious particles or gases. An acute exacerbation of COPD (AECOPD) is an acute event characterized by a worsening of the patient’s respiratory symptoms that is beyond normal day-to-day variations and leads to a change in medication. The aim of this study was to evaluate the non-specific inflammation during acute exacerbation of COPD to investigate change of cellular activity (apoptosis, chemotaxis, phagocytosis and production of reactive oxygen species) during AECOPD depending on infection agent. Subjects with AECOPD and the same in remission were investigated. Increased count of induced sputum neutrophils and macrophages as well peripheral blood neutrophils and monocytes during bacterial and non-bacterial AECOPD was related with impaired pulmonary function and smoking history. Induced sputum neutrophils and macrophage apoptosis and phagocytosis were weaker, but production of reactive oxygen species was strongly activated during bacterial acute exacerbation of chronic obstructive pulmonary disease than non-bacterial AECOPD. This study showed differences of peripheral blood neutrophil and monocyte apoptosis, chemotaxis, as well as peripheral blood neutrophil phagocytosis and the production of reactive oxygen species... [to full text]

Submitted by Ana Maria Fiscina Sampaio (fiscina@bahia.fiocruz.br) on 2013-04-19T16:30:30Z No. of bitstreams: 1 Marina Loyola Dantas Aspectos comparativos....pdf: 35265598 bytes, checksum: c8a29ec5c8fd370f04c04a980fb43507 (MD5) / Made available in DSpace on 2013-04-19T16:30:30Z (GMT). No. of bitstreams: 1 Marina Loyola Dantas Aspectos comparativos....pdf: 35265598 bytes, checksum: c8a29ec5c8fd370f04c04a980fb43507 (MD5) Previous issue date: 2012 / Universidade Federal da Bahia. Fundação Oswaldo Cruz. Centro de Pesquisas Gonçalo Moniz / A forma clínica mais frequente das leishmanioses é a leishmaniose cutânea, que acomete somente a pele e constitui um importante problema de saúde no Brasil. A leishmaniose cutânea caracteriza-se por lesão cutânea ulcerada única: leishmaniose cutânea localizada, que pode regredir espontaneamente ou se disseminar com múltiplas úlceras e pápulas e que aparecem em diferentes locais. A presença de disseminação caracteriza a leishmaniose cutânea disseminada. Investigar, no tecido, células que compõem o infiltrado inflamatório em lesões de pele na leishmaniose e caracterizar a resposta imune e sua correlação com a extensão total da inflamação in situ pode contribuir para aprofundar o entendimento da leishmaniose cutânea. Neste estudo, através da imunomarcação e quantificação de células por imunoistoquímica e HE, e análise da extensão da inflamação, foi comparado a histopatologia e presença de células inflamatórias CD4+, CD8+, CD68+, CD20+, plasmócitos e neutrófilos, e células granzima B+ em biópsias de pacientes com leishmaniose cutânea tardia (úlcera tardia e úlcera recente) e leishmaniose disseminada (úlcera e pápula). A análise dos padrões histomorfológicos mostrou semelhança entre os quatro grupos de biópsias analisados. Avaliando o número e tipo de células presentes, o predomínio foi de macrófagos e linfócitos. As úlceras da leishmaniose cutânea clássica e disseminada apresentaram média maior de inflamação, maior frequência de linfócitos T CD4+, T CD8+, macrófagos, linfócitos B CD20+ e plasmócitos que úlceras recentes e pápulas. Estas, por sua vez, ao contrário das úlceras tardias de ambas formas clínicas, tiveram correlação positiva entre o aumento do infiltrado inflamatório e T CD4+ e T CD8+, e não correlação com granzima B e neutrófilos. Os plasmócitos se mostraram elementos quase constantes no infiltrado das lesões em todos os grupos, e sua frequência foi maior que de linfócitos B. Seguindo o mesmo padrão descrito nos linfócitos B, os plasmócitos não apresentam correlação com o influxo de infiltrado inflamatório entre os grupos. A frequência de macrófagos é vista nos dois estágios avaliados da doença e nas duas formas clínicas de forma semelhante, porém com uma tendência para maior presença em lesões de LD. A análise de neutrófilos revelou semelhança da frequência dessas células em todos os tipos de lesões em ambas formas clínicas, com as pápulas tendendo para uma menor quantidade. Portanto, o desenvolvimento das lesões ocorrem com o influxo de células inflamatórias, como linfócitos T CD4+ e T CD8+ e a resposta imune celular é mais intensa em lesões crônicas da leishmaniose cutânea localizada e disseminada do que em lesões localizadas recentes e pápulas da leishmaniose disseminada. Diferenças in situ na resposta inflamatória destas duas formas clínicas e quatro espectros de lesão da leishmaniose humana podem elucidar o papel de células no local da lesão e contribuir para o entendimento da patogênese da leishmaniose. / Cutaneous leishmaniasis is the most frequent clinical form of leishmaniasis, which affects only the skin and is an important health problem in Brazil. Cutaneous leishmaniasis is characterized by single ulcerated skin lesion: localized cutaneous leishmaniasis, which may regress spontaneously or spread with multiple ulcers and papules that appear in different parts of the body. The presence of dissemination features disseminated leishmaniasis. Investigate tissue cells from inflammatory infiltrate in skin lesions in leishmaniasis and characterize the immune response and its correlation with the total extent of inflammation in situ may contribute to deepen the understanding of cutaneous leishmaniasis. In this study, immunostaining and cells quantification by immunohistochemistry and HE and analysis of inflammation extention was compared with histopathology and CD4+, CD8+, CD68+, CD20+, plasma cells, neutrophils and granzyme B+ cells in biopsies of patients with localized cutaneous leishmaniasis (late ulcer and recent ulcer) and disseminated leishmaniasis (ulcers and papules). The histopathological patterns analysis was similar among the four biopsies groups analyzed. Macrophages and lymphocytes were the predominant cells. The ulcers of localized cutaneous leishmaniasis and disseminated leishmaniasis presented higher mean inflammation, increased frequency of CD4+ and CD8+ T cells, macrophages, B lymphocytes CD20+ and plasma cells than recent ulcers and papules. These, in turn, unlike late ulcers of both clinical forms, had positive correlation between the increase in inflammatory infiltrate and CD4+ and CD8+ T cells, differing in Granzyme B and neutrophils. Plasma cells were almost constant in lesion infiltrate in all groups and was higher than the frequency of B lymphocytes. Following the same pattern described in B lymphocytes, plasma cells did not show an association with the influx of inflammatory infiltrate between groups. The frequency of macrophages is seen in both stages of the disease and in the two clinical forms similarly, but with a tendency to be increased in disseminated lesihmaniasis lesions. The analysis revealed similarity of neutrophils frequency in all types of lesions, with papules tending to a lesser extent. Therefore, the development of lesions occur with the influx of inflammatory cells such as CD4+ and CD8+ T cells and cellular immune response is more intense in chronic lesions of localized cutaneous leishmaniasis and disseminated leishmaniasis than recent localized lesions and papules from disseminated leishmaniasis. Differences of inflammatory response in situ in these two clinical forms and four spectra of human leishmaniasis lesions may elucidate the role of cells at the lesion site and contribute to the understanding of leishmaniasis pathogenesis.

Orientador: Wilma Aparecida Starke Buzetti / Banca: Solange Maria Gennari / Banca: Maria de Lurdes de Azevedo Rodrigues / Banca: Rosangela Zacarias Machado / Banca: Gervasio Henrique Bechara / Resumo: Para estudar a cinética populacional de células imune/inflamatórias na infecção natural por Toxocara vitulorum em bezerros búfalos, realizou-se a quantificação de mastócitos, eosinófilos, linfócitos intraepiteliais (LIE) e células caliciformes na camada intraepitelial e de macrófagos na parede do intestino delgado. Para isto, amostras de tecidos foram retiradas do duodeno, jejuno e íleo de seis grupos de animais, de acordo com o resultado do exame coprológico, ou seja: animais que estavam no início ou ascensão (1), no pico (2) do parasitismo, durante as fases de declínio ou expulsão (3), e de pós-expulsão dos parasitas (4), além de dois grupos controles de animais não parasitados por T. vitulorum com idades médias entre 30 (C30) e 50 (C50) dias. Pelo estudo morfológico, feito através de mensurações de todas as camadas da parede do intestino delgado, constatou-se somente uma significativa atrofia vilosa no duodeno, durante as fases de ascensão, de pico e de expulsão do parasita, mas a hipertrofia muscular não foi observada. Concluiu-se que a infecção pelo nematódeo T. vitulorum em bezerros búfalos foi responsável pela hiperplasia celular (LIEs, células caliciformes, eosinófilos e mastócitos) na camada intraepitelial e pela interação entre mastócitos e processos nervosos na mucosa, nos plexos submucoso e mioentérico. Como estas alterações celulares predomindando no pico da infecção normalizaram-se após a expulsão, concluiu-se também que elastiveram participação no mecanismo imunológico celular de controle e expulsão do parasita pelo hospedeiro. O macrófago presente em maior quantidade na fase da pós-expulsão sugeriu uma importante participação destas células na recuperação das lesões inflamatórias nesta infecção. / Abstract: The populational kinetics of immune/inflammatory cells was studied in the wall of the small intestine from buffalo calves naturally infected with Toxocara vitulorum. Samples of tissues were removed from duodenum, jejunum and ileum of four groups of animals during the beginning of the infection, at the peak of egg output, during the period of expulsion and post-expulsion of the worms, as well as from uninfected calves. Cells (mast cells, eosinophils, intraepithelial lymphocytes - IEL and goblet cells) present in the epithelial layer (intraepithelial) of the small intestine were counted. In the duodenum, jejunum and ileum, the population of mast cells, eosinophils and lymphocytes increased significantly during the peak of the infection. Goblet cell numbers increased also during the beginning and at the peak of the infection. The decline of the number of these cells occurred during the periods of expulsion of the worms reaching to uninfected control counts at the post-expulsion period indicated a role of these cells in the process of expulsion of T. vitulorum by the buffalo calves. Morphological examinations showed a significant vilar atrophy, particularly in the duodenum during the beginning, peak and during the phase of expulsion of the worms, but smooth muscle hypertrophy or other alteration was not observed in any phase of the infection. In conclusion, the infection by T. vitulorum in buffalo calves elicited cellular hyperplasy of LIEs, goblet cells, eosinophils and mast cells in the intraepithelial layer of the small intestines and association between mast cells and nervous process in the mucosa and in the submucosal and mioentérico plexa, these cellular changes might be important for the worm expulsion. The macrophages presents in high numbers in the post-expulsion phase might have important role in the recovery of the infection. / Doutor