STUDIES ON THE ROLE OF HISTAMIINE AND 5 - HYDROXY TRYPTAMINE (5-HT) IN THE MEDIATION OF INFLAMMATORY RESPONSES IN THE NORMAL AND IMMUNOSUPPRESSED CHICKENS
Loading...
Date
2001
Authors
Shukla, Supriya
Journal Title
Journal ISSN
Volume Title
Publisher
AAU, Anand
Abstract
The present study was undertaken to know the basic differences in the mechanisms of acute inflammation induced in the normal and immunosuppressed (IS) chickens. IBDV-induced immunosuppression in chickens was used as a model in which bacterial (S.aureus), viral (ND LaSota), and chemical (Carrageenan and Turpentine) induced inflammatory studies were carried out. Pretreatment with anti-inflammatory drugs - promethazine and reserpine was followed to check the release of chemical mediators - histamine and 5-HT in the IS birds. The parameters evaluated were bursal histopathology, NDHI titre for immunosuppression and visual, quantitative assessment of the permeability response using the intravital dye - Evans blue technique as well as the qualitative and quantitative estimation of tissue leukocytosis for inflammatory studies. Both IVP and tissue leukocytosis were studied over five different intervals viz., 0 mt., 1, 3, 6 and 9 hrs. A partial immunosuppression of chickens was seen when infected with 10 per cent bursal suspension on the 14th, 15th and 16th day of life. Depletion of lymphoid follicles, bursal atrophy and a low NDHI titre were the hallmarks of IS. In normal birds, for the control, promethazine and reserpine pretreated groups, the permeability response was biphasic for bacteria, and monophasic for virus, carrageenan and turpentine. With the infectious agents - bacteria and virus, promethazine was found to be more effective, indicative of a more potent role of histamine in chemical mediation whereas with carrageenan and turpentine an almost equal involvement of 5-HT along with histamine was seen in the mediation of the acute inflammatory response after the 3 hr. interval. The permeability response was categorized as immediate-transient for bacteria and virus, immediate-sustained for carrageenan and delayed-prolonged type for turpentine. In contrast, in immunosuppressed birds, monophasic responses were seen even in the drug - pretreated bacterial groups, along with virus, carrageenan and turpentine. The dye exudation was overall quantitatively low as compared to the normal groups. Histamine proved to be a more effective mediator of permeability except in the turpentine group where a stronger action of 5-HT over histamine was noticed. In normal birds, the tissue leukocytosis was more or less stereotyped in nature. The initial emigration comprised heterophils and monocytoid cells, soon followed by a concurrent emigration of basophils. Almost similar mixed cellular exudate was observed with all four different stimuli with slight variations in the quantity (at 6 and 9 hrs.) and quality of exudate. In the bacterial group, heterophils dominated the picture till 9 hrs. Syncytia formation and phagocytosis of S.aureus organisms by macrophages was seen. However, giant cells were absent at the 9 hr. interval. There was an early formation of perivascular-lymphoid aggregates by 6 and 9 hrs. intervals following the degranulation of basophils. PVLA may have an analogous fiinction to mammalian lymph nodes. Their functional significance warrants further attention. Apart from similar findings in the viral injury groups, the appearance of lymphocytes and plasma cells as early as 1 hr. after injury, was the most significant observation. In normal birds with chemicals, the carrageenan-induced cellular response was the highest. The highest population of heterophils, monocytoid cells mainly lymphocytes, degenerated heterophils, necrosis and haemorrhage was noticed by 6 and 9 hr. in the oedematous interstitium. There was a marked absence of PVLA and syncytia formation compared to the infectious agents. Deposition of metachromatic carrageenan and its phagocytosis by monocytoids was distinguishing feature. In contrast, with turpentine a reduced level of cellular exudate with a highly oedematous interstitium till 9 hrs. was noticed, Maximal number and degranulation of basophils was observed at 3 hr. followed by PVLA formation, necrosis and syncytia formation in the 6 and 9 hr. intervals. In immunosuppressed birds, the carrageenan induced cellular inflammation was distinguished by a late basophilic and mast cell degranulation between 1 and 3 hr. and unusually high heterophilic and total cell count at 6 and 9 hrs. as compared to the normal groups. It is speculated that in immunosuppressed birds, heterophils are unable to phagocytose the non-infectious or kill the infectious agents. The accumulation of heterophils is most probably to wall off the foreign body as a part of defense. The significance of the presence of heterophils in immunosuppressed host needs to be explored in future. In addition, there was also marked absence of PVLA and syncytia formation with CGN injury. In comparison, although the turpentine-induced leukocytic response was quantitatively low, qualitatively after the 3 hr. interval, the heterophils were replaced by monocytoid cells. In all control and pretreated groups, appearance of PVLA and syncytia formation by macrophages was apparent between 6 and 9 hr. intervals. Thus, the overall permeability response was low and mostly cellular infiltration high with the infectious agents in the immunosuppressed birds. The exact reasons for these unusual differences are unknown. A prominent role of histamine with the infectious and also that of 5-HT to some extent with the chemicals has materialized. It is suggested that leukotrienes, prostaglandins, toxic oxygen and nitrogen radicals may be mediating the acute inflammatory responses in the immunosuppressed chickens. Generally a delayed start of the inflammatory mechanisms seems to take place. However, it was observed, as by the previous workers, that increased vascular permeability and leukocyte emigration occurred, chronologically, as dissociated phenomenon in both the normal and immunosuppressed chickens.
Description
Keywords
VETERINARY PATHOLOGY, A STUDY