1.
Andersson, Sören, 1957-, et al.
(författare)
CHIMERIC MOMP ANTIGEN
2015
Patent (populärvet., debatt m.m.)
2.
Gustafsson, Lars, et al.
(författare)
Infectious disease, reproductive effort and the cost of reproduction in birds
1994
Ingår i: Philosophical transactions of the Royal Society of London: Series B. ; :346, s. 1655-1658
Tidskriftsartikel (populärvet., debatt m.m.) abstract
Reproductive effort can have profound effects on subsequent performance. Field experiments on the collared flycatcher (Ficedula albicollis) have demonstrated a number of trade-offs between life-history traits at different ages. The mechanism by which reproductive effort is mediated into future reproductive performance remains obscure. Anti-parasite adaptations such as cell-mediated immunity may probably also be costly. Hence the possibility exists of a trade-off between reproductive effort and the ability to resist parasitic infection. Serological tests on unmanipulated collared flycatchers show that pre-breeding nutritional status correlates positively with reproductive success and negatively with susceptibility to parasitism (viruses, bacteria and protozoan parasites). Both immune response and several indicators of infectious disease correlate negatively with reproductive success. Similar relations are found between secondary sexual characters and infection parameters. For brood-size-manipulated birds there was a significant interaction between experimentally increased reproductive effort and parasitic infection rate with regard to both current and future fecundity. It seems possible that the interaction between parasitic infection, nutrition and reproductive effort can be an important mechanism in the ultimate shaping of life-history variation in avian populations.
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5.
Andersson, Sören, 1957-, et al.
(författare)
Chimeric MOMP antigen
2014
Patent (populärvet., debatt m.m.) abstract
The present invention regards polypeptides capable of eliciting an immunological response that is protective against Chlamydia trachomatis. The polypeptide comprises a first amino acid sequence which has at least 90% homology with the amino acid sequence according to SEQ ID NO: 1 and a second amino acid sequence which has at least 90% homology with the amino acid sequence according to SEQ ID NO: 2. Furthermore, production of these polypeptides and pharmaceutical compositions comprising them are also provided.
6.
Loodin, Henrik, et al.
(författare)
Beteendeförändring, tag plats!
2021
Ingår i: Efter antibiotika : Om smitta i en ny tid - Om smitta i en ny tid. - 9789189139954 ; , s. 62-72
Bokkapitel (populärvet., debatt m.m.)
7.
Massena, Sara, et al.
(författare)
Chemokine transport across the vessel wall and presentation to circulation leukocytes are regulated by vascular permeability, DARC and PAD released during inflammation
Annan publikation (populärvet., debatt m.m.) abstract
Increased vascular permeability and consequent leakage of plasma and macromolecules through endothelial cell junctions is a hallmark of inflammation. The physiological importance of this event for leukocyte recruitment has been controversial, but it might have a role in chemokine transport into blood vessels and consequently for the recruitment of circulating leukocytes. Elevated amounts of peptidyl arginine deiminases (PAD) and of their citrullinated products associate with autoimmune disorders, chronic inflammation and cancer. The role of citrullination in the inflamed microenvironment is debated, but it might be an innate mechanism for infiltrating leukocytes to resolve inflammation. In this study we investigated if increased vascular permeability facilitated the influx of chemokines from tissue into post-capillary venules, thereby affecting leukocyte recruitment. Vascular permeability and chemokine influx into post-capillary venules were simultaneously monitored by real-time in vivo confocal microscopy of the mouse cremaster muscle. We found that increased venular permeability induced by histamine, correlated with accelerated influx of the fluorescently labeled chemokine CXC ligand 2 (CXCL2/MIP-2) into post-capillary venules, which accumulated predominantly at endothelial cell junctions. Consequently, neutrophil adhesion was accelerated leading to increased neutrophil extravasation. In situ inhibition of caveolae-mediated transcytosis by filipin had no significant effect on chemokine influx to post-capillary venules, indicating that chemokine traffic across the venular wall is independent of caveolar transport. Nevertheless, neutrophil recruitment was prevented in filipin-treated mice as transmigrating neutrophils were trapped on endothelial cell domes and failed to finalize transmigration. Furthermore, we used this real-time in vivo model for studying the role of the atypical chemokine receptor 1 (DARC/ACKR1) in chemokine transport and availability. We show that the absence of DARC/ACKR1 (ACKR1-/- mice) does not impair chemokine transport. Instead it leads to increased seric levels of chemokine and increased intravascular chemokine sequestration. As a result, high numbers of firmly adherent neutrophils were found in post-capillary venules. Intraluminal neutrophil crawling was though abrogated and neutrophil transmigration prevented. Finally, we studied the role of chemokine citrullination by leukocyte-derived PAD in the inflamed tissue. The transport of citrullinated CXC ligand 8 (CXCL8/IL-8) across the venular wall, its immobilization on the luminal endothelium, and subsequent leukocyte recruitment, were monitored by real time imaging. Chemokine citrullination inhibited its transport from the inflamed tissue into blood vessels, impeding their immobilization on the luminal endothelium. Reduced intravascular chemokine bioavailability dampened leukocyte recruitment. Altogether these findings demonstrate that changes in vascular permeability regulate inflammation by affecting abluminal-to-luminal chemokine transport and thereby leukocyte recruitment to tissue. Furthermore, DARC/ACKR1 plays an important role in neutrophil recruitment by controlling intravascular chemokine availability and by shaping the intravascular chemokine gradient necessary for efficient neutrophil recruitment. Finally, citrullination of chemokines by PAD in the inflamed tissue inhibits chemokine transport into blood vessels and luminal presentation to circulating leukocytes, which dampens leukocyte recruitment
8.
Persson, Alexander, 1978-, et al.
(författare)
Apoptotic neutrophils activates the inflammatory response in macrophages –increased capacity to handle intracellular infection
Annan publikation (populärvet., debatt m.m.) abstract
Inflammation is essential to eradicate invading pathogens but an uncontrolled inflammation may develop into chronic inflammation and extensive tissue destruction unable of effectively controlling infections. At the site of infection, macrophages are the major regulators of the inflammatory response through balanced release of pro- or anti-inflammatory cytokines and therefore a key cell in the resolution of inflammation. Neutrophils effectively phagocytose and kill pathogens but they are short-lived and removal of these dead cells by macrophages is a key event in the resolution of inflammation and tissue repair. However, down-regulation of the immune response by apoptotic cells would in the presence of pathogens be detrimental to the host. In contrast to resolution of inflammation, we show that in the presence of microbial stimuli, apoptotic neutrophils in fact exert a potent pro-inflammatory activation of macrophages. This augmentation of the pro-inflammatory response is dependent on uptake of the apoptotic cells by the macrophage. In addition to secretion of TNF-α, presence of apoptotic neutrophils enhanced the capacity of the stimulated macrophages to kill intracellular Mycobacterium tuberculosis. This presents a novel role for apoptotic neutrophils in the modulation of the macrophage-dependent inflammatory response, and control of intracellular infections.
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