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      Comparative Quantitative and Qualitative Attributes of the Surface Respiratory Macrophages in the Domestic Duck and the Rabbit Translated title: Atributos Cualitativos, Cuantitativos y Comparativos de los Macrófagos de la Superficie Respiratoria en el Pato Doméstico y el Conejo

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          Abstract

          In mammals, surface respiratory macrophages (SM) are known to play a foremost role in protecting the respiratory system by providing first line of defense through engulfing pathogens and particulate matter respired with air. It has been reported that the pulmonary cellular defense system of domestic birds is inadequate. In particular, low number of SM and even lack of the cells in a healthy avian respiratory system have been associated with susceptibility of domestic birds to respiratory diseases. In an endeavor to resolve the existing controversy, the quantitative and qualitative attributes of the surface respiratory macrophages of the domestic duck and of the domestic rabbit were compared under similar experimental conditions. Quantitatively, the rabbit SM were on average approximately fourteen times more than the duck SM. The SM were found to have comparable diameters measuring about 12 µm in the duck and 13 µm in the rabbit. Similarly, the duck and the rabbit SM were structurally similar. Typically, they were round granular cells possessing filopodial extensions and variable electron dense bodies in the cytoplasm. The phagocytic capacity measured using polystyrene particles revealed that the duck SM had a higher phagocytic capacity than the rabbit SM. The volume density of the engulfed polystyrene particles, i.e. the volume of the particles per unit volume of the cell was estimated at 20 % in the duck and 9 % in the rabbit. These results suggest that the comparatively low numbers of SM in domestic birds may contribute to susceptibility of the birds to diseases. However, given the high phagocytic capacity of the avian SM, susceptibility of the domestic birds may not be due to dearth of the SM alone but some other factor (s) such as persistent exposure of the birds to particulate matter which is known to reduce robustness of the SM may be involved.

          Translated abstract

          En los mamíferos, los macrófagos de la superficie respiratoria (SM) son conocidos por jugar el papel más importante en la protección del sistema respiratorio, proporcionando la primera línea de defensa en contra de agentes patógenos y envolviendo las partículas de aire respirado. Se ha informado que el sistema de defensa celular pulmonar de las aves domésticas es insuficiente. En particular, el bajo número de SM, e incluso las células del sistema respiratorio de las aves domésticas, en un ambiente sano, se ha asociado con susceptibilidad a enfermedades respiratorias. En un esfuerzo para resolver la controversia existente, los atributos cuantitativos y cualitativos de los macrófagos de la superficie respiratoria del pato doméstico y el conejo doméstico fueron comparados en las mismas condiciones experimentales. Cuantitativamente, los SM del conejo fueron en promedio aproximadamente catorce veces más que los SM en el pato. Los SM se encontraron con un diámetro comparable, al medir alrededor de 12 micras en el pato y 13 micras en el conejo. Del mismo modo, en el pato y el conejo los SM eran estructuralmente similares. Por lo general, correspondieron a células granulares con extensiones filopodiales y organismos electrodensos variables en el citoplasma. La capacidad fagocítica medida utilizando partículas de poliestireno reveló que los SM del pato tenían una mayor capacidad fagocítica que el conejo. La densidad de volumen de las partículas de poliestireno envueltas, es decir, el volumen de las partículas por unidad de volumen se estimó en 20% en el pato y 9% en el conejo. Estos resultados sugieren que el número comparativamente bajo de los SM en las aves domésticas puede contribuir a su susceptibilidad a enfermedades. Sin embargo, dada la alta capacidad fagocítica de los SM aviares, la susceptibilidad de las aves domésticas no puede deberse solamente a la escasez de SM, sino a algunos otros factores pueden estar involucrados, como la exposición persistente de las aves a partículas, las cuales se sabe reducen la robustez de los SM.

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          Human airway epithelial tight junctions.

          The flux of fluid, ions, macromolecules, and inflammatory cells across airway epithelium depends in part upon the integrity of its apico-lateral tight junctions. Without the correct balance of fluid and ions, the normal functioning of mucociliary clearance and the neural responsiveness of the airways cannot take place. Freeze-fracture electron microscopy has been used to investigate the structure of human airway tight junctions and their morphology comprehensively characterised at two airway levels (main and lobar bronchi). Further data is needed to establish if the fall in transepithelial electrical resistance found across progressively proximal disparate airway generations is correlated with an alteration in tight junction morphology. Altered epithelial permeability is associated with the development of the airway conditions: asthma, chronic bronchitis, and cystic fibrosis. However, few data have been published on the structure of tight junctions in asthma and chronic bronchitis. In patients with cystic fibrosis, airways obtained at transplantation and postmortem show a basal extension of the apico lateral tight junctional belt. This change is not unique to cystic fibrosis airways as it also occurs in non-respiratory systems postmortem. However the functional relevance of these changes remains uninvestigated and recently developed in vitro models may help answer this question. The data demonstrate that tight junctions are highly dynamic structures capable of rapid alterations in disease and in response to functional stress.
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            The avian lung-associated immune system: a review.

            The lung is a major target organ for numerous viral and bacterial diseases of poultry. To control this constant threat birds have developed a highly organized lung-associated immune system. In this review the basic features of this system are described and their functional properties discussed. Most prominent in the avian lung is the bronchus-associated lymphoid tissue (BALT) which is located at the junctions between the primary bronchus and the caudal secondary bronchi. BALT nodules are absent in newly hatched birds, but gradually developed into the mature structures found from 6-8 weeks onwards. They are organized into distinct B and T cell areas, frequently comprise germinal centres and are covered by a characteristic follicle-associated epithelium. The interstitial tissue of the parabronchial walls harbours large numbers of tissue macrophages and lymphocytes which are scattered throughout tissue. A striking feature of the avian lung is the low number of macrophages on the respiratory surface under non-inflammatory conditions. Stimulation of the lung by live bacteria but not by a variety of bacterial products elicits a significant efflux of activated macrophages and, depending on the pathogen, of heterophils. In addition to the cellular components humoral defence mechanisms are found on the lung surface including secretory IgA. The compartmentalisation of the immune system in the avian lung into BALT and non BALT-regions should be taken into account in studies on the host-pathogen interaction since these structures may have distinct functional properties during an immune response.
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              Ascites in poultry: recent investigations.

              In recent years, ascites research has centred on gaining an increased understanding of pulmonary hypertension syndrome together with the potential role of primary cardiac pathologies. The impact at a cellular level of factors which trigger ascites and substances that protect against it has also been documented. Primary pulmonary hypertension has been induced when birds are exposed to hypoxia during incubation. The conditions experienced during this phase of development may impact on the ability of the bird to regulate its basal metabolic rate through endocrine signals controlled by thyroid activity. The extent of ventilation in the lung influences the ability of the bird to oxygenate haemoglobin. Ventilation/ perfusion mismatches may occur prior to or post-hatching. This factor has been studied extensively using the pulmonary artery/bronchus clamp model. At high altitude, a decreased ventilation/perfusion ratio may occur following the effective increase in physiological dead space due to the lowered oxygen tension at the level of the parabronchi. This explains the mechanism by which ascites is triggered by hypoxia in this particular situation. The effects of ascites are ameliorated by the use of beta agonists and dietary arginine, which act by increasing ventilation and blood flow in the lungs and thus correcting a ventilation/perfusion mismatch. Transient bacterial and viral infections may also influence the induction of pulmonary hypertension. The increases in blood viscosity associated with ascites are most probably a consequence of the condition rather than a cause. A bird may alleviate the effects of pulmonary hypertension by decreasing blood viscosity through inhibition of platelet function, increased erythrocyte deformability and the production of coronary relaxants. Evidence is accumulating that primary cardiac pathology may be associated with a number of ascites cases. Broilers that subsequently develop ascites, exhibit lower heart rates than their normal flock mates. Furthermore, during ascites, hypoxic broilers exhibit bradycardia as opposed to the expected tachycardia. In these cases, a tachycardia induced by feed restriction may protect the bird by raising its cardiac output. Right atrio-ventricular regurgitant flow velocities in chickens are relatively slow compared with similar regurgitant flows induced by pulmonary hypertension in other species. The conduction system in the avian heart is specialized and contains a recurrent bundle branch that innervates the right atrio-ventricular valve, thus initiating active valve closure before right ventricular systole. This predisposes the heart to right ventricular volume overload through a valvular incompetance following a failure of valvular innervation. The resultant elevated diastolic wall stress can trigger the production of angiotensin II and its converting enzyme, which mediate ventricular hypertrophy. Subclinical myocardial damage, irrespective of its cause, can be detected by the presence of troponin T in the blood. Reactive oxygen species may damage cell membranes compromising cellular function in a number of body systems. A positive correlation exists between oxidized glutathione concentrations and right ventricular weight ratio. This indicates a failure to cope with oxidative stress at the level of the respiratory membrane. It is not known if it is possible to modulate levels of antioxidants at this location and hence protect the bird. The final description of the ascites aetiology may lie in the concept of a circuit of events between the cardiac, pulmonary and vascular systems that satisfy the metabolic requirements of the bird. A deficit in one of these systems, at a level that prevents adequate compensation from other components, triggers the pathological cascade that results in the end point of clinical ascites.
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                Author and article information

                Contributors
                Role: ND
                Role: ND
                Role: ND
                Role: ND
                Journal
                ijmorphol
                International Journal of Morphology
                Int. J. Morphol.
                Sociedad Chilena de Anatomía (Temuco )
                0717-9502
                June 2011
                : 29
                : 2
                : 353-362
                Affiliations
                [1 ] Kenyatta University Kenya
                [2 ] Kenyatta University Kenya
                Article
                S0717-95022011000200008
                10.4067/S0717-95022011000200008
                0725af06-a597-4cb0-a807-594c114724b0

                http://creativecommons.org/licenses/by/4.0/

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                SciELO Chile

                Self URI (journal page): http://www.scielo.cl/scielo.php?script=sci_serial&pid=0717-9502&lng=en
                Categories
                ANATOMY & MORPHOLOGY

                Anatomy & Physiology
                Avian,Cellular defense,Lung,Phagocytosis,Rabbit,Surface macrophages,Aviar,Defensa celular,Pulmón,Fagocitosis,Conejo,Macrófagos de superficie

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