Bacillus Calmette-Guérin (BCG) is an attenuated Mycobacterium tuberculosis vaccine. We performed a series of co-infection experiments with BCG-Plasmodium chabaudi chabaudi Landau, 1965 AS using C57BL/6 mice to analyse whether BCG can affect the development of protective immunity to infection with Plasmodium spp. and the mechanism of this protection. We divided mice into four groups: BCG-inoculation 4 weeks prior to P. c. chabaudi AS infection (B-4w-Pc); simultaneous BCG-inoculation and P. c. chabaudi AS infection (Pc+B); BCG-inoculation 3 days post P. c. chabaudi AS (Pc-3-B) infection; and mono-P. c. chabaudi AS infection as control (Pc). The parasitemia level in the B-4w-Pc group was noticeably higher than control group at 6-19 days post infection (dpi). Compared with the control group, the proportion of CD4+CD69+ T cells was significantly reduced 5, 8 and 12 dpi, but the proportion of CD4+CD25+Foxp3+ Tregs was significantly increased in the B-4w-Pc group on 5 and 8 dpi. The B-4w-Pc group also demonstrated reduced levels of IFN-γ and TNF-α on 5 and 8 dpi and significantly elevated level of IL-10 on 12 dpi. There were significantly fewer mDCs (CD11c+CD11b+) and pDCs (CD11c+B220+) in the B-4w-Pc group than the control group at all the time points post infection and the expression of MHC II was noticeably reduced on day 8 pi. Our findings confirmed that BCG inoculation prior to Plasmodium infection resulted in excessive activation and proliferation of Tregs and upregulation of anti-inflammatory mediators, which inhibited establishment of a Th1-dominant immune response during the early stages of Plasmodium infection by inhibiting dendritive cells response. BCG inoculation prior to P. c. chabaudi AS infection may contribute to overgrowth of parasites as well as mortality in mice., Dong-Hua Cao, Ji-Chun Wang, Jun Liu, Yun-Ting Du, Li-Wang Cui, Ya-Ming Cao., and Obsahuje bibliografii
This article summarises the current knowledge of the rabbit coccidia and the disease they cause. Various aspects, such as life cycles, localisation in the host, pathology and pathogenicity, immunity and control, are discussed.
F.xcept other functions, surface saccharide residues on trematode larvae are supposed either to be the targets of the intermediate (molluscan) and final host immune systems, or to represent candidates for molecular mimicry. Therefore, changes in surface saccharide patterns during the development of the avian schistosome Trichobilharzia szidati were characterized. Whole parasite larval stages and their tissue sections were examined using FITC-conjugated lectins. Marked surface differences were found among larval stages (miracidia, mother sporocysts, daughter sporocysts, cercariae, schistosomula). Staining by some lectins reflected known ultrastructural changes of the outer tegument. Reaction of lectins with cercarial embryos was almost negative. In case of other developmental stages, binding of at least one member from each carbohydrate-specificity group of lectins (Man/Glc-, GIcNAc-, Gal/GalNAc- and Fuc-specific) occurred. One exception is represented by mother and daughter sporocysts which practically failed to react with Fuc-specific lectins. Besides other lectins which recognized larval surfaces, a-L-fucose-specific lectins (LTA, UEA-I) and (GlcNAcfll —>4)„-spccific WGA bound very strong to certain stages. The comparison of mature intrasporocystic cercariae with those emerged from snails brought the indication that some snail glycosylated molecules adhere to the surface of schistosome larvae or that emerged cercariae express some new carbohydrate epitopes under changed environmental conditions. The result partially supports the theory of parasite mimicry/masking strategies and immune evasion in the host.
Anthropogenic environmental pollutants affect many physiological, biochemical, and endocrine actions as reproduction, metabolism, immunity, behavior and as such can interfere with any aspect of hormone action. Microbiota and their genes, microbiome, a large body of microorganisms, first of all bacteria and co-existing in the host´s gut, are now believed to be autonomous endocrine organ, participating at overall endocrine, neuroendocrine and immunoendocrine regulations. While an extensive literature is available on the physiological and pathological aspects of both players, information about their mutual relationships is scarce. In the review we attempted to show various examples where both, endocrine disruptors and microbiota are meeting and can act cooperatively or in opposition and to show the mechanism, if known, staying behind these actions., Richard Hampl, Luboslav Stárka., and Obsahuje bibliografii
Aged people are the most susceptible group to COVID-19 infection. Immunosenescence characterized by impairment of immune function with inflamm-aging contributes to pathophysiological alterations, among which endocrine and metabolic diseases are not exception. Diabetes, obesity along with impairment of disorders of thyroid functions are the most frequent ones, the common feature of which is failure of immune system including autoimmune processes. In the minireview we discussed how COVID-19 and aging impact innate and adaptive immunity, diabetes and selected neuroendocrine processes. Mentioned is also beneficial effect of vitamin D for attenuation of these diseases and related epigenetic issues. Particular attention is devoted to the role of ACE2 protein in the light of its intimate link with renin-angiotensin regulating system.
We have studied the influence of both levamisole (AL) and Freund's adjuvant (AF) on the immunisation of mice with the secretory antigens of adults of the liver fluke Fasciola hepatica Linnaeus, 1758. Total IgG antibodies were detected in all groups where the F. hepatica antigen was administered, been levels of IgG1 increased respect to IgG2a antibodies. During immunisation, IL-4 and IFN-γ were only detected in AL and AF groups, but after infection, IL-4 boosted in all groups. IFN-γ increased two fold in AF and AL groups compared to the saline solution (AS) group. Worm recovering was of 32-35% in groups administered without antigen whereas in AS, AL and AF groups recovering was of 25%, 12% and 8%, respectively. Macroscopical lesions in the liver were scarce in AL and AF groups. Our data suggest that immunisation of mice with antigens of F. hepatica enhances the immune response avoiding both liver damage and worm establishment after challenge infection. The murine model of fasciolosis has appeared to be useful to elucidate the mechanism by which the parasite modulates immune responses toward a Th2 type but also the development of Th1 type-inducing vaccines., María de los Ángeles Gutiérrez-Sánchez, Julieta Luna-Herrera, Lauro Trejo-Castro, Natividad Montenegro-Cristino, Alfredo Almanza-González, Alejandro Escobar-Gutiérrez, Jorge Luis de la Rosa-Arana., and Obsahuje bibliografii
The invasion success of gibel carp (Carassius gibelio) depends on demographic and competitive traits. The major biological trait responsible for the invasiveness of C. gibelio is the mode of reproduction. Apart from sexual reproduction, which is typical in fish, C. gibelio is a unique cyprinid species able to reproduce through asexual gynogenesis, which is also known as sperm-dependent parthenogenesis, observed in all-female populations. Though the sexual and asexual forms of C. gibelio co-exist widely in natural habitats, the gynogenetic form has the capacity to modulate the range of effective ecological niches, which may facilitate the process of invasion. In this paper, we reviewed current knowledge of the sexual and gynogenetic forms of gibel carp along with their physiological advantages, immunological traits, and ability to withstand different environmental conditions. As parasitic infection may directly alter the immunology of hosts, and also indirectly alter their investment in reproduction, we provide some insights into the role of parasites as one of the potential drivers facilitating the coexistence of asexual and sexual forms. We highlight evidence that gibel carp have been identified as a serious threat to native species; hence, its impact on the ecosystem is also discussed.
Lectins as carbohydrate recognition proteins other than enzymes or immunoglobulins play important roles in living systems, e.g., in celi celi recognition. They are considered to be involved in snail-trematode immune interactions, i.e., in a system where antibodies are lacking and lectins might at least partially substitute immunoglobulin functions. From the snail side, lectins can be located on haemocyte surfaces as receptors for foreignness and they can be found freely in plasma. The latter can function as agglutinins/opsonins helping in the recognition of parasites by haemocytes. They may also link immune cells and pathogens by recognition of surface carbohydrates on both. Lectins of parasite origin could also be involved in snail-trematode interactions. They might function as trematode surface receptors for snail glycoconjugates in parasite masking strategies. Functions other than the involvement in the snail's immune response or the parasite’s evasion strategies might be fulfilled by lectins as well. Among these may be host-finding, penetration, orientation in the host, nutrition. It cannot be omitted that lectin-saccharide reactions represent only a part of the snail-trematode interactions and thus, results obtained from lectin experiments are a rough simplification of the actual, very complicated situation. An array of immune and other reactions comprised of yet unknown bioactive molecules certainly exists in snails and, on the other hand, trematode mechanisms to escape or otherwise interact with these, might be involved at the same time. But we can certainly conclude that a more complete view of the complex snail-trematode interactions also necessitates a more profound knowledge of the identity and functioning of lectins and their ligands, in host and parasite.
Multiple sclerosis (MS) is an autoimmune neurological disease characterized by chronic inflammation of the central nervous system (CNS), leading to demyelination and axonal damage and resulting in a range of physical, mental or even psychiatric symptoms. Key role of oxidative stress (OS) in the pathogenesis of MS has been suggested, as indicated by the biochemical analysis of cerebrospinal fluid and blood samples, tissue homogenates, and animal models of multiple sclerosis. OS causes demyelination and neurodegeneration directly, by oxidation of lipids, proteins and DNA but also indirectly, by inducing a dysregulation of the immunity and favoring the state of proinflammatory response. In this review, we discuss the interrelated mechanisms of the impaired redox signaling, of which the most important are inflammation-induced production of free radicals by activated immune cells and growth factors, release of iron from myelin sheath during demyelination and mitochondrial dysfunction and consequent energy failure and impaired oxidative phosphorylation. Review also provides an overview of the interplay between inflammation, immunity and OS in MS. Finally, this review also points out new potential targets in MS regarding attenuation of OS and inflammatory response in MS.