The Impact of Chlamydia Pneumoniae Infection on the Immune Status of Children

Author(s):  
I. Solovyeva ◽  
L. Shalunova ◽  
A. Solovyeva ◽  
K. Zakuraeva ◽  
T. Krivozubova ◽  
...  
mBio ◽  
2018 ◽  
Vol 9 (4) ◽  
Author(s):  
Kuppan Gokulan ◽  
Matthew G. Arnold ◽  
Jake Jensen ◽  
Michelle Vanlandingham ◽  
Nathan C. Twaddle ◽  
...  

ABSTRACT Intestinal microbiota composition and gut-associated immune response can contribute to the toxicity of arsenic. We investigated the potential toxicity of short-term arsenic exposure on gut microbiome composition, intestinal immune status, microbial arsenic resistance gene, and arsenic metabolic profiles in adult and developmental stages of CD-1 mice. The potential toxicity of arsenite [As(III)] was determined for two life stages: (i) adult animals at 24 or 48 h after single gavage (0.05 mg/kg body weight [b.w.] [low dose], 0.1 mg/kg b.w. [medium dose], and 0.2 mg/kg b.w. [high dose]) and repeated exposure at 1 mg/liter for 8 days and (ii) postnatal day 10 (PND10) and PND21 after single gavage (0.05 mg/kg b.w.). Dose- and time-dependent responses in bacterial recovery/microbial composition were observed in adults after a single gavage. Repeated exposure caused a transient decrease in the recovery of intestinal bacteria, a shift in the bacterial population with abundance of arsenic resistance genes, and evidence for host metabolism of arsenite into less-reactive trivalent methylated species. Arsenic exposure in adult animals induced high levels of CC chemokines and of proinflammatory and anti-inflammatory cytokine secretion in intestine. Arsenic exposure at PND21 resulted in the development of distinct bacterial populations. Results of this study highlight significant changes in the intestinal microbiome and gut-associated immune status during a single or repeated exposure to arsenic in juvenile and adult animals. The data warrant investigation of the long-term effects of oral arsenic exposure on the microbiome and of immune system development and responses. IMPORTANCE Transformation of organic arsenic to toxic inorganic arsenic (iAs) is likely carried out by intestinal bacteria, and iAs may alter the viability of certain microbial populations. This study addressed the impact of arsenic exposure on intestinal microbiota diversity and host gut-associated immune mediators during early development or adulthood using scenarios of acute or repeated doses. During acute arsenic exposure, animals developed defense functions characterized by higher abundances of bacteria that are involved in arsenic resistance or detoxification mechanisms. Arsenite had a negative effect on the abundance of bacterial species that are involved in the conversion of protein to butyrate, which is an alternative energy source in the intestine. The intestinal mucosal immune cytokine profile reflected a mechanism of protection from arsenic toxicity.


2020 ◽  
Vol 125 (1) ◽  
pp. 62-70 ◽  
Author(s):  
Jun Chen ◽  
Jiaming Chen ◽  
Yinzhi Zhang ◽  
Yantao Lv ◽  
Hanzhen Qiao ◽  
...  

AbstractThe present study was conducted to evaluate the impact of dietary fully oxidised β-carotene (OxBC, C40H60O15) supplementation during the perinatal period on immune status and productivity in a sow model. At day 85 of pregnancy, 150 sows were allocated to one of three dietary treatments with fifty sows per treatment. The three experimental diets were supplemented with 0, 4 or 8 mg/kg OxBC in the basal diet. The feeding trial was conducted from gestation day 85 until day 21 of lactation. Dietary OxBC supplementation greatly enhanced colostrum IgM, IgA and IgG levels, and the IgM and IgG content of 14-d milk. Dietary OxBC supplementation decreased the TNF-α and IL-8 levels in colostrum, as well as the TNF-α and IL-18 levels in 14-d milk. There was also a tendency towards an increase in the soluble CD14 level in 14-d milk. Although dietary treatments did not affect average daily feed intake nor backfat thickness loss during lactation, dietary OxBC supplementation tended to enhance litter weight and individual piglet weight at weaning. There was a trend towards increased lactose concentration in 14-d milk with increasing dietary OxBC. It is concluded that dietary supplementation with OxBC during the perinatal period enhances the lactose concentration of sow milk and the immune status of sows, which is reflected by improved cytokine status and immunoglobulin concentrations in colostrum and milk, and thus tending to increase litter weight and individual piglet weight at weaning. The results also provide a scientific nutritional reference for perinatal mothers due to the biological similarity between pigs and humans.


2020 ◽  
Vol 9_2020 ◽  
pp. 129-137
Author(s):  
Dolgushina N.V. Dolgushina ◽  
Krechetova L.V. Krechetova ◽  
Ivanets T.Yu. Ivanets ◽  
Vtorushina V.V. Vtorushina ◽  
Inviyaeva E.V. Inviyaeva ◽  
...  
Keyword(s):  

2012 ◽  
Vol 30 (15_suppl) ◽  
pp. 8590-8590
Author(s):  
Sean Donovan ◽  
Amy Weaver ◽  
Clark Otley ◽  
Richard Wayne Joseph

8590 Background: Merkel Cell Carcinoma (MCC) is an aggressive cutaneous malignancy of neuroendocrine origin associated with immunosuppression presumably through infection with Merkel Cell Polyomavirus present in >80% of patients (pts). The impact of immune status on clinical outcomes in pts with MCC is unknown. The primary objective of this study was to compare clinical characteristics and outcomes of pts with MCC who are immunosuppressed (ISP) versus non-immunosuppressed (non-ISP). Methods: We performed a retrospective chart review on pts with MCC diagnosed at the Mayo Clinic between 1981 and 2009. A dermatopathologist confirmed all cases. ISP was defined as pts diagnosed with chronic lymphocytic leukemia, HIV, solid organ transplant recipients, or chronic immunosuppressive medication. The association between ISP status and overall survival was summarized using the hazard ratio (HR) and 95% confidence interval (CI) estimated from a Cox regression model. Results: Of the 268 pts identified and included in the study, 38 (14%) were ISP. We found no differences in age, tumor size, tumor location, stage of disease, or recurrence rate in ISP vs Non-ISP. Among pts who had Stage 3-4 disease, there was no difference in the size of the primary between groups. Among pts with Stage 1-2 disease, ISP status was not significantly associated with poorer survival (HR 1.5, 95% CI 0.7-3.3). However, among pts with Stage 3-4 disease, ISP pts had significantly poorer survival compared to non-ISP pts (HR 2.7, 95% CI 1.2 - 6.2). Conclusions: Baseline clinical characteristics of pts with MCC do not differ based on immunosuppression, and outcomes do not differ in pts in regards to immunosuppression in early stage MCC (Stage 1-2). However, in pts with Stage III-IV MCC, ISP pts have a worse clinical outcome suggesting that metastatic MCC either behaves more aggressively in ISP pts either through intrinsic differences in the biology of the tumor or improved immune evasion in ISP pts. These results should be cautiously interpreted given the small number (n=12) of immunosuppressed pts with advanced stage MCC. The authors will update their data with an additional 58 patients by the date of presentation.


2005 ◽  
Vol 73 (7) ◽  
pp. 4315-4322 ◽  
Author(s):  
Kambiz Yaraei ◽  
Lee Ann Campbell ◽  
Xiaodong Zhu ◽  
W. Conrad Liles ◽  
Cho-chou Kuo ◽  
...  

ABSTRACT Chlamydia pneumoniae is a common respiratory pathogen that is associated with an increased risk of cardiovascular disease. However, the mechanisms by which C. pneumoniae contributes to cardiovascular disease have not been determined yet. C. pneumoniae infection may accelerate the death of cells within atherosclerotic lesions and contribute to the formation of unstable lesions. To test this hypothesis, the impact of C. pneumoniae infection on the death of lipid-loaded mouse macrophages was investigated. It was observed that RAW 264.7 cells are highly susceptible to the toxic effects of oxidized low-density lipoprotein (LDL) and exhibit markers of cell death within 24 h of treatment with as little as 5 μg/ml oxidized LDL. Subsequent infection with either live C. pneumoniae or heat-killed or UV-inactivated C. pneumoniae at a low multiplicity of infection for 24 to 72 h stimulated both additional binding of annexin V and the uptake of propidium iodide. Thus, C. pneumoniae augments the effects of oxidized LDL on cell death independent of a sustained infection. However, unlike oxidized LDL, C. pneumoniae infection does not activate caspase 3 or induce formation of the mitochondrial transition pore or the fragmentation of DNA, all of which are classical markers of apoptosis. Furthermore, primary bone marrow macrophages isolated from mice deficient in Toll-like receptor 2 (TLR-2) but not TLR-4 are resistant to C. pneumoniae-induced death. These data suggest that C. pneumoniae kills cells by a caspase-independent pathway and that the process is potentially mediated by activation of TLR-2.


1987 ◽  
Vol 1 (2) ◽  
pp. 12-15
Author(s):  
T W Wong ◽  
YC Chan ◽  
HC Tan

In 1986, a seroepidemiological study on rubella antibody was conducted in a public housing community in Singapore using the direct latex agglutination method. The overall seropositive rate was 78.1% (95% confidence limit: 73.5% to 82.7%). There was no significant association between age and immune status for both sexes. However, the seropositive rates for females aged 15 to 19 years and 20 to 24 years were significantly higher than for females in other age groups, reflecting the impact of the rubella immunisation programme launched in 1976. There is still a considerable number of susceptible females in the reproductive age group. An extension of the present programme to cover all persons above 12 months of age is recommended, as this would reduce the overall incidence of rubella, and hence congenital rubella, by conferring immunity to young children who presently act as reservoirs of infections.


2012 ◽  
Vol 9 (75) ◽  
pp. 2603-2613 ◽  
Author(s):  
Shishi Luo ◽  
Michael Reed ◽  
Jonathan C. Mattingly ◽  
Katia Koelle

Antigenically evolving pathogens such as influenza viruses are difficult to control owing to their ability to evade host immunity by producing immune escape variants. Experimental studies have repeatedly demonstrated that viral immune escape variants emerge more often from immunized hosts than from naive hosts. This empirical relationship between host immune status and within-host immune escape is not fully understood theoretically, nor has its impact on antigenic evolution at the population level been evaluated. Here, we show that this relationship can be understood as a trade-off between the probability that a new antigenic variant is produced and the level of viraemia it reaches within a host. Scaling up this intra-host level trade-off to a simple population level model, we obtain a distribution for variant persistence times that is consistent with influenza A/H3N2 antigenic variant data. At the within-host level, our results show that target cell limitation, or a functional equivalent, provides a parsimonious explanation for how host immune status drives the generation of immune escape mutants. At the population level, our analysis also offers an alternative explanation for the observed tempo of antigenic evolution, namely that the production rate of immune escape variants is driven by the accumulation of herd immunity. Overall, our results suggest that disease control strategies should be further assessed by considering the impact that increased immunity—through vaccination—has on the production of new antigenic variants.


Author(s):  
V. O. Velichko

Analysis of literature data and the results of our own research show that even with intensive rearing of animals with the use of balanced feeding and keeping them in accordance with the technology - it is almost impossible to avoid stress. And especially, excessive man-made load on agroecosystems also has a negative impact on animal life. Factors that cause a decrease in immune status and the emergence of immune pathology in animals include: industrial technology of animal husbandry, chemicalization in crop and livestock production, man-made pressure, dietary imbalance in nutrients and biologically active substances. This increases the impact on the body of heavy metals, which displace nutrients from body tissues, in particular trace elements and replace them in metabolic processes, which is a potential prerequisite for the development of oxidative stress. The mechanism of development of stress reaction of an organism is closely connected with activity of POL (lipid peroxidation) and depression of antioxidant potential. Under these conditions, the ability of the organism to mobilize protective and adaptive capabilities in response to the action of negative factors becomes especially important. Keeping productive animals in adverse conditions, unbalanced feeding are components of immobilization stress, which reduces their productivity, affects reproductive function, metabolic and functional disorders, reducing nonspecific and specific resistance of the organism (Fedoruk & Kravtsiv, 2003; Velychko, 2008; Velychko, 2011). Under conditions of man-caused load on the environment, respectively, and animals – it is promising to develop effective methods for regulating the activity of the enzymatic system of antioxidant protection with the help of biologically active substances, in particular trace elements. The results of research confirm that this has a positive effect on the formation of productive and adaptive properties of animals. The system of antioxidant protection is a necessary part of non-specific reactions of the organism, a component of the processes of its adaptation to environmental conditions, a component of normal life, a factor in maintaining homeostasis. Widespread immunodeficiency and elucidation of the main links of their pathogenesis have exacerbated the problem of regulating disorders of the immune system. Therefore, knowledge of the patterns of formation of the immune status of animals, especially in the early postnatal period, is important in the development of methods for the correction of immunodeficiency, antioxidant protection.


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