IL-4 mRNA expression levels were variable while IL-13 again showed a sustained up-regulation. focused to find new strategies against the disease, resulting in the development of an efficacious live-attenuated vaccine. In addition to efficacy and safety several studies were performed to obtain a deeper understanding of the immune response of the host against which was much pronounced in the ceca. Furthermore, expression profiles of various cytokines revealed that RU 24969 chickens mounted an effective cecal innate immune response during histomonosis compared to turkeys. Studying the cellular immune response following contamination and/or vaccination of host birds showed a limitation of pronounced changes of B cells and T-cell subsets in vaccinated birds in comparison to non-protected birds. Additionally, numbers of lymphocytes including cytotoxic T cells increased in the ceca of diseased turkeys compared to infected chickens suggesting an immunopathological impact on disease pathogenesis. The identification of type 1 and type 2 T-helper (Th) cells in infected and lymphoid organs by hybridization did not show a clear separation of Th cells during contamination but revealed a coherence of an increase of interferon (IFN)- mRNA positive cells in ceca and protection. The present evaluate not only summarizes the research performed around the immune response of host birds in the course of histomonosis but also highlights the specific features of as a model organism to study immunological principles of an extracellular organism GFAP in birds. is an important flagellated parasite of RU 24969 poultry causing the disease histomonosis (syn. blackhead disease, histomoniasis, or infectious typhlohepatitis) (1). Historically, the disease was extensively investigated in the first half of the last century and thereby effective chemotherapeutics were identified to prevent and treat birds from contamination. This success neglects that for a long time the true etiology of the disease was questioned and under argument. Difficulties to determine the real cause of histomonosis in earlier studies are comprehensively recapitulated elsewhere (2). However, to date the disease is usually of high relevance in poultry flocks as effective prophylactic and therapeutic options are not available anymore in many countries for reasons of food security. As a consequence research was intensified in recent years and with it several reviews were published addressing different features of the parasite or the disease. This includes a general overview on the disease (3), updated findings of the recent years (4), a summary of experimental infections (5), a recapitulation on previous and current strategies for prevention and therapy (6), and assumptions how the disease might be controlled in the future (7). The purpose of this review is to emphasize on studies investigating mechanisms of the immune response of host birds against the RU 24969 disease. This includes early studies describing inflammatory reactions of birds’ up to recent investigations on specific immune cells and signaling proteins involved in host defense. Furthermore, the host reaction due to vaccination and its functional aspects are reviewed. Finally, might be a model to unravel peculiar immune mechanisms of extracellular pathogens considering that the avian immune response against these organisms is not as investigated in depth compared to viral or bacterial RU 24969 infections. Histomonosis, an important poultry disease Histomonosis was firstly described in turkeys by Cushman (8) more than a century ago. Infection with can occur directly or via embryonated eggs of the nematode which was already described by Graybill and Smith (9). Horizontal transmission was hypothesized to occur by active uptake via the cloaca (10) or orally, based on successful oral application of cultured histomonads (11).The first signs of histomonosis are reflected by clinical changes such as reduced appetite, depression, drowsiness, droopy wings, and ruffled feathers. Infected birds might suffer from yellowish diarrhea and succumb to death (4). The pathogenesis generally varies between species of gallinaceous birds: in turkeys (migrates into the mucosa and deeper layers of the cecal wall leading to inflammation and ulceration, resulting in a thickening of the cecal tissue and formation of fibrin. Occasionally, ulcers erode throughout the cecal wall leading to peritonitis. Following destruction of cecal tissue, the parasite is able to infiltrate into blood vessels and to reach the liver via the portal vein. As a consequence, areas of inflammation and necrosis can occur in the liver. Liver lesions are highly variable in appearance: they may be.
Categories:Glycogen Phosphorylase