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1

Lack of relationship between serum content of MBL, sCD14, anti-PPD and anti-Hsp65 IgG, and ingestion of Mycobacterium bovis BCG bacilli by phagocytes

100%
Paziak-Domanska B., Bonar A., Kowalewicz-Kulbat M., Klink M., Kowalski M., Karhukorpi J., Karttunen R., Jurkiewicz M., Rozalska B., Rudnicka W.
Archivum Immunologiae et Therapiae Experimentalis
|
2002
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vol. 50
|
issue 5
337-344
EN
Prophylactic vaccination against tuberculosis (TB) with a live attenuated strain of Mycobacterium bovis Bacille Calmett?e-Gerin (BCG) has been used worldwide. However, TB remains one of the most significant diseases of humans and animals. Better understanding of the mechanisms of human immunity to mycobacteria is essential for development of new vaccines and estimation of their efficacy. In this study we determined the levels of known humoral mediators of mycobacterial phagocytosis - mannose binding lectin (MBL), soluble CD14 (sCD14), antibodies of IgG class against mycobacterial purified protein derivative (PPD) and mycobacterial Hsp65 antigen, in the sera from healthy young volunteers vaccinated with BCG and presenting positive and negative Mantoux responses to PPD. Than we asked a question as to whether macrophages and polymorphonuclear leukocytes (PMNs) from the individuals with positive (TT(+)) and negative (TT(-)) tuberculin tests differ by the ability to ingest mycobacteria. Also we were looking for a relation between the intensity of mycobacterial ingestion by phagocytes in the medium with autologous sera containing different concentration of MBL, sCD14 andf anti-mycobacterial IgG. We found no significant differences between the investigated parameters for TT(+) and TT(-) volunteers. Our result suggest that ability of macrophages and PMNs to ingest mycobacteria depends on an individual intrinsic capacity of phagocytes.
2

Role of antigen-presenting cells in innate immune system

100%
Ohteki T., Koyasu S.
Archivum Immunologiae et Therapiae Experimentalis
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2001
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vol. 49
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issue 1 suppl.
47-52
EN
Activation of antigen-presenting cells (APC) and natural killer (NK) cells initiates the production of various proinflammatory cytokines, including interleukin 12 (IL-12), interferon gamma (IFN-) and nitric oxide (NO), which are important in the innate immune response for controlling infection by intracellular pathogens. In this review, we focus on these cytokines produced by APC and summarize the current understanding of how APC functions are regulated by cytokines in innate immunity.
3

Macrophages and HIV-1-associated dementia

100%
Bovem L. A.
Archivum Immunologiae et Therapiae Experimentalis
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2000
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vol. 48
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issue 4
273-279
EN
One of the strongest predictors for HIV-1-associated dementia is the presence of monocytic infiltration in perivascular areas of the brain. Therefore, macrophages have been suggested to play a major role in the development of this disease. This review focuses on possible mechanisms through which the macrophage may enhance disease progression by mediating neuronal damage.
4

Immunomodulation of macrophages by pathogenic Yersinia species

100%
Ruckdeschel K.
Archivum Immunologiae et Therapiae Experimentalis
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2002
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vol. 50
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issue 2
131-138
EN
The interaction between macrophages and bacterial pathogens plays a crucial role in the pathogenesis of infectious diseases. Pathogenic species of the gram-negative bacterium Yersinia deploy complex strategies to disarm macrophages and to disrupt their response to infection. For this purpose, Yersinia spp. engage a type III protein secretion system that mediates polarized translocation of Yersinia virulence factors, the so-called Yops, into the host cell cytoplasm. There, the Yops act on different cellular levels to neutralize a sequence of programmed phagocyte effector functions. Yersiniae initially impair the phagocytic machinery and block the generation of the bactericidal oxidative burst. Furthermore, yersiniae uncouple an array of fine-tuned signals of innate immunity, which leads to suppression of the macrophage TNF- production and to macrophage apoptosis. The impairment of cellular functions results in a scenario, by which Yersinia efficiently resist the attack of the macrophage and finally kills the macrophage by activating its intrinsic cell suicide mechanism. This review highlights the aspects of Yersinia-macrophage interaction that determine the fate of the infected cell.
5

CSF-1 as a regulator of macrophage activation and immune responses

100%
Sweet M. J., Hume D. A.
Archivum Immunologiae et Therapiae Experimentalis
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2003
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vol. 51
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issue 3
169-177
EN
Macrophage activation is a key determinant of susceptibility and pathology in a variety of inflammatory diseases. The extent of macrophage activation is tightly regulated by a number of pro-inflammatory cytokines (e.g. IFN-gamma, IL-2, GM-CSF, IL-3) and anti-inflammatory cytokines (e.g. IL-4, IL-10, TGF-beta). Macrophage colony stimulating factor (CSF-1/M-CSF) is a key differentiation, growth and survival factor for monocytes/macrophages and osteoclasts. The role of this factor in regulating macrophage activation is often overlooked. This review will summarise our current understanding of the effects of CSF-1 on the activation state of mature macrophages and its role in regulating immune responses.
6

PPAR ? an important regulator of monocyte/macrophage function

100%
von K. A., Brune B.
Archivum Immunologiae et Therapiae Experimentalis
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2003
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vol. 51
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issue 4
219-226
EN
Regulation of monocyte/macrophage function is important to coordinate immune responses. Their contact with invading pathogens activates signaling pathways that provoke pro-inflammatory gene expression and thus causing a locally restricted inflammation. Recently, the peroxisome proliferator activated receptor (PPAR) has been identified to antagonize pro-inflammatory responses in monocytes/macrophages causing an anti-inflammatory and/or desensitized phenotype to predominate. For PPAR general mechanisms in facilitating the transition from a pro- to an anti-inflammatory phenotype have been elucidated. PPAR is a member of the nuclear receptor superfamily and activated upon endogenous as well as exogenous agonist binding. Here we focus on its role in monocyte/macrophage biology in affecting inflammation. Summarizing current information, a model is proposed, giving rise to potential new therapeutic possibilities for the treatment of diseases presumably involving PPAR-dependent regulatory circuits.
7

HIV-macrophage interactions at the cellular and molecular level

100%
Khat M., James W., Gordon S.
Archivum Immunologiae et Therapiae Experimentalis
|
2001
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vol. 49
|
issue 5
367-378
EN
Macrophages, centrally involved in both the innate and adaptive arms of the immune system, are not only the chief target of the human immunodeficiency virus (HIV), but also its main reservoir and vehicle of transmission. Macrophage-tropic viruses are responsible for the initial infection, predominate in the asymptomatic phase, and persist throughout infection, even after the emergence of preferential T cell- and/or dual-tropic HIV-1 variants. Functional impairment of HIV-infected macrophages plays a role in the immune dysregulation characteristic of AIDS (acquired immunodeficiency syndrome). Efforts directed ant understanding the cellular and molecular mechanisms underlying HIV-macrophage interactions remain the basis for devising novel and efficacious therapeutic strategies against HIV and the AIDS epidemic
8
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Exuberant cellular reaction of the optic nerves in experimental Creutzfeldt-Jakob disease

100%
Liberski P. P., Sikorska B., Bratosiewicz-Wasik J., Walis A., Brown P., Brown D.
Acta Neurobiologiae Experimentalis
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2003
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vol. 63
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issue 4
309-318
EN
We report here on the exuberant glial reaction in the optic nerves affected by prion diseases. Optic nerves from CJD- and GSS-, and scrapie-infected mice and hamsters showed severe pathology. These lesions were qualitatively indistinguishable from each other but were more intense in the Fujisaki model than in the hamsters inoculated with Echigo-1. Exuberant cellular reaction comprised of macrophages containing numerous mitochondria, abundant rough endoplasmic reticulum, and secondary lysosomes filled with digested myelin debris, electron-dense material and occasionally, entire myelin-bound vacuoles were readily observed in both models. Macrophages actively digesting myelin fragments and containing lyre-like bodies and paracrystalline inclusions were frequently noted. Some macrophages extended long filopodia to form labyrinth-like structures, and within a few macrophages, concentric arrays of cisterns and channels sequestrated part of the cytoplasm. An analogous network of narrow cisterns was seen to surround whole segments of the myelinated fibers.
9

Monocyte-related immunopathologies in trauma patients

88%
Laudanski K., Wyczechowska D.
Archivum Immunologiae et Therapiae Experimentalis
|
2005
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vol. 53
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issue 4
321-328
EN
Mechanical trauma is one of the most important causes of morbidity in the developed world. The response of the immune system to mechanical insult is of paramount importance for the patient's recovery. Shortly after trauma, the indiscriminate saystemic inflammatory response syndrome (SIRS) is mediated by circulating monocytes (Ms) and other innate immunity components. Then acquired immunity, limited to the offending pathogen and the site of injury, gradually preponderates. SIRS is followed by the compensatory anti-inflammatory response syndrome (CARS), where the initial inflammatory response is quenched by anti-inflammatory mediators. This precisely regulated process of immune system activation in response to trauma can be easily deviated, resulting in multi-organ failure (MOF) and increased mortality. Excessive activation of inflammatory Ms in the SIRS phase, premature or exorbitant CARS, a predominance of macrophages (Macs) in the blood stream and peripheral tissues, as well as a depletion of dendritic cells are often seen in trauma patients and contribute to the development of MOF. Here we explore several mechanisms of pathological M? activation in patients with severe mechanical traumatic injury without accompanying sepsis.
10
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Interleukin-1beta affects the macrophage recruitment and proliferation in the injured brain of 6-day-old rat

88%
Pawlinski R., Setkowicz Z., Mlodzinska K., Janeczko K.
Acta Neurobiologiae Experimentalis
|
1999
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vol. 59
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issue 4
271-278
EN
Six-day-old male rats received a mechanical lesion in the left cerebral hemisphere. Thereafter, a single dose of either 5, 50 or 500 units (U) of recombinant rat interleukin-1beta (IL-1beta) was injected into the lesion cavity. One or 2 days after the injury, the rats were injected with ^3H-thymidine. Brain sections were subjected to BSI-B4 lectin histochemistry and autoradiography to visualise proliferating and non-proliferating macrophages located within the region of injury. A mitogenic effect of IL-1beta on macrophages was observed on day 2 in brains injected with the lowest 5 U dose of cytokine. Following administration of higher 50 U and 500 U doses, infiltration of the injured tissue by macrophages was significantly intensified on day 1. However, on day 2, dose-dependent reductions of the total number of macrophages as well as their proliferative activity were recorded. The findings suggest that the higher the initial quantity of macrophages, the sooner they disappeared from the injury site. It may therefore be hypothesised that IL-1beta-induced increase in macrophage recruitment at the beginning of the inflammatory response speeded the removal of tissue debris and, therefore, accelerated healing of the injured nervous tissue.
11

A two step procedure to fractionate mouse testicular macrophages with a different cytokine profile

88%
Bryniarski K., Szewczyk K., Ptak M., Bobek M., Ptak W.
Archivum Immunologiae et Therapiae Experimentalis
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2002
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vol. 50
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issue 3
225-231
EN
Cells isolated enzymatically from interstitial tissue of mouse male gonads are composed of macrophages, Leydig cells, and myofibroblasts. They can be separated on density gradients either by sedimentation (Ficoll) or flotation (Percoll) into several fractions according to different buoyant density containing mixtures of different cells. Macrophages (FcR+, esterase+) present in cell mixtures can by highly enriched in a single step to 95% purity by rosetting with opsonized erythrocytes followed by sedimentation on Lymphoprep. Separate fractions of highly purified (over 95%) macrophages obtained by successive use of density gradients and rosetting differ significantly in the production of cytokines, such as cells from fractions at lower density produce little IL-6, cells from fractions at higher density are poor producers of TNF-alpha whereas TMf in intermediate fractions produce significant amounts of both cytokines. These differences may suggest that particular subpopulations of testicular macrophages play different biological roles in the testis.
12

Mechanisms of cellular cytotoxicity. I. The stages of

88%
Janiak M., Budzynski W.
Postępy Higieny i Medycyny Doświadczalnej
|
1993
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vol. 47
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issue 3
169-182
EN
This review describes the stages of mediated by , cytotoxic , natural killer cells and .
13

Neuropeptides as modulators of macrophage functions. Regulation of cytokine production and antigen presentation by VIP and PACA

88%
Ganea D., Delgado M.
Archivum Immunologiae et Therapiae Experimentalis
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2001
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vol. 49
|
issue 2
101-110
EN
VIP, and the structurally related neuropeptide PACAP, present in the microenvironment of lymphoid organs, modulate the function of inflammatory cells through specific receptors. VIP and PACAP inhibit the production of the pro-inflammatory agents and stimulate the production of anti-inflammatory cytokines in activated macrophages. The effect is mediated through specific receptors, and involves shedding of the CD14 LPS receptor and the transcriptional regulation of cytokine genes through effects on de novo expression or nuclear translocation of NFkB, CREB, c-Jun, and IRF-1. The in vivo administration of VIP/PACAP results in a similar pattern of cytokine modulation, which presumably mediates the protective effect of VIP/PACAP in a high-endotoxic murine model for septic shock. VIP/PACAP reduce the expression of the costimulatory B7.1/B7.2 molecules, and the subsequent stimulatory activity for T helper cells in stimulated macrophages. In contrast, in unstimulated macrophages, VIP/PACAP induce specific B7.2 expression and promote Th2 cell differentiation. We propose that VIP/PACAP act as endogenous factors that regulate immune homeostasis, and that the physiological consequences of the VIP/PACAP presence in the immune microenvironment depends on the timing of the neuropeptide release and the activation stage of the neighboring immune cells.
14

Cellular responses to attaching and effacing bacteria: activation and implication of the innate immune system

88%
Gobert A. P., Wilson K. T., Martin C.
Archivum Immunologiae et Therapiae Experimentalis
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2005
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vol. 53
|
issue 3
234-244
EN
During the last decade, research on attaching-effacing (A/E) bacteria/host cell interactions has revealed much of the molecular basis of colonization and lesion formation. The colonic mucosa represents the first line of defense against these pathogens, and its integrity is required to avoid translocation of bacteria or bacterial soluble factors into the infected host. Therefore, the cellular immune response to A/E pathogens plays an important role in bacterial pathogenesis since it can clear the bacteria or modulate the inflammatory processes. Data obtained from infected patients demonstrate a correlation between the production of pro-inflammatory cytokines and the severity of the disease. In vitro studies of infected epithelial cells have clearly elucidated A/E bacteria-induced host signal transduction events. However, the identification of the bacterial factors responsible for cellular activation remains a subject of controversy. Experimental studies with knock-out mice infected with Citrobacter rodentium, a rodent A/E pathogen, indicate that innate immunity is an essential component of pathogenesis. This review summarizes in vivo and in vitro evidence for the induction and potential role of the innate immune system during infection with A/E bacteria.
15

Cartilage formed by syngeneic rat chondrocytes in joint surface defects is rejected in animals sensitized with allogeneic chondrocytes: involvement of the synovial lining

88%
Moskalewski S., Osiecka-Iwan A., Hyc A., Niderla J.
Archivum Immunologiae et Therapiae Experimentalis
|
2005
|
vol. 53
|
issue 2
159-168
EN
The aim of the study was to discover the mechanism of rejection of chondrocyte transplants introduced into articular cartilage defects. Chondrocytes from 3?5-day-old Lewis or WAG rats were liberated by enzymatic digesand tion from articular-epiphyseal cartilage complexes and implanted into defects made in the subpatellar region of the femur condyle of naive Lewis rats. Syngeneic transplants were also done after sensitization of the recipients with allogeneic chondrocytes injected intramuscularly. The transplants and synovial membrane were studied in periodate-lysineparaformaldehyde- fixed material with antibodies against B lymphocytes, CD4+ and CD8+ cells, NK cells, and macrophages. For detection of humoral response, chondrocyte lysates were subjected to protein electrophoresis and Western blotting with sera from the transplant recipients. Cartilage produced in intracartilaginous transplants of syngeneic chondrocytes did not show any signs of rejection. CD8+ lymphocytes and macrophages accumulated in the vicinity of cartilage produced by similar transplants in animals sensitized with intramuscular transplants of allogeneic WAG chondrocytes or bearing transplants of allogeneic WAG chondrocytes. CD8+ cells penetrated into the peripheral part of the cartilage, while macrophages advanced much more deeply. No specific anti-chondrocyte antibody was detected. The synovium from rats bearing intracartilaginous transplants of allogeneic chondrocytes or syngeneic chondrocytes after sensitization contained macrophages and CD8+ cells. The rejection of cartilage formed by syngeneic chondrocyte transplants in sensitized animals argues in favor of a chondrocyte-specific antigen expression. The involvement of the synovial membrane during transplant rejection suggests that it should be included in observations of the behavior of chondrocyte transplants introduced into articular cartilage.
16

The role of oxidatively modified low density lipoprotein in the pathogenesis of atherosclerosis

88%
Siennicka A., Zapolska-Downar D.
Postępy Higieny i Medycyny Doświadczalnej
|
2003
|
vol. 57
|
issue 2
219-237
EN
The precise mechanisms of LDL oxidation in vivo are not well-known but the presence of several enzymes and agents capable of modifying LDL particles was noted in arterial wall. These reactive agents modify lipid, protein as well as antioxidant component of the LDL particles. Postsecretory modification in LDL structure trigger its atherogenic potential. LDL particles retained in the artery wall interact with the various forms of proteoglycans in the extracellular matrix, that increases the resident time of LDL in endothelial space and allows extensive modification. The modified forms of LDL are able to activate intimal cells and to trigger various inflammatory signals. In turn, activated intimal cells can secrete enzymes and agents capable of modifying LDL. These processes can initiate and maintain a vicious circle in the intima and lead to lesion progression.
17

1-Methylnicotinamide and nicotinamide: two related anti-inflammatory agents that differentially affect the functions of activated macrophages

88%
Biedron R., Ciszek M., Tokarczyk M., Bobek M., Kurnyta M., Slominska E. M., Smolenski R. T., Marcinkiewicz J.
Archivum Immunologiae et Therapiae Experimentalis
|
2008
|
vol. 56
|
issue 2
127-134
EN
1-Methylnicotinamide (MNA), a major metabolite of nicotinamide (NA), is known to exert anti-inflammatory effects in vivo. Treatment of inflammatory skin diseases by topical application of MNA provides certain advantages over the use of NA. However, in contrast to NA, the molecular mechanisms of the anti-inflammatory properties of MNA are not well known. In this study the influence of exogenous MNA and NA in vitro on the generation of inflammatory mediators by macrophages (Mo) was investigated. Materials and Methods: Peritoneal Mo of CBA/J mice were activated in vitro with lipopolysaccharide and incubated with MNA or NA. The effect of these compounds on biological functions of Mo was measured by evaluation of the production of reactive oxygen species (ROS) by luminol-dependent chemiluminescence, cytokines and prostaglandin E2 (PGE2) by ELISA, and nitric oxide (NO) by the Griess method. Moreover, the expressions of inducible NO synthase and cyclooxygenase-2 were measured by Western blotting. Results: It was shown that at non-cytotoxic concentrations, NA inhibits the production of a variety of pro-inflammatory agents, such as tumor necrosis factor alpha interleukin 6, NO, PGE2, and the generation of ROS. In contrast to NA, exogenous MNA inhibited only the generation of ROS, while its effect on the synthesis of other mediators was negligible. Conclusions: These results indicate that the anti-inflammatory properties of MNA demonstrated previously in vivo do not depend on its capacity to suppress the functions of immune cells, but more likely may be related to its action on vascular endothelium. The authors suggest that the limited permeability for exogenous MNA, in contrast to that for NA, may be responsible for its lack of suppressor activity against Mo.
18

Modulation of pulmonary innate immunity during bacterial infection: animal studies

88%
Schultz M. J., van_ d. P. T.
Archivum Immunologiae et Therapiae Experimentalis
|
2002
|
vol. 50
|
issue 3
159-168
EN
Both the increasing number of immunocompromised patients susceptible to pneumonia, and the development of bacterial resistance are significant problems related to the treatment of pneumonia. The primary outcome of treatment for pneumonia is to tip the balance to a successful host response. An ideal approach would be the combination of immunomodulation and conventional antimicrobial therapy for the treatment of pneumonia. It is of increasing importance to understand the components of innate immunity, before immunomodulatory therapy can be applied to patients. Much of our knowledge of the role of alveolar macrophages, cytokines and chemokines in the pathogenesis of pneumonia is derived from animal studies on experimental pneumonia. This article summarizes current information on the role of an alveolar macrophage (AM) and AM-derived mediators in host defense against pneumonia.
19

Biological activities of lipopolysaccharide

88%
Lukasiewicz J., Lugowski C.
Postępy Higieny i Medycyny Doświadczalnej
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2003
|
vol. 57
|
issue 1
33-53
EN
Lipopolysaccharides (LPS, endotoxin) are known to be responsible for the initiation of endotoxic shock, therefore they can be targets for new preventive and therapeutic strategies. This review describes the biological and physicochemical properties of endotoxin ? major component of the outer membrane of Gram-negative bacteria. The paper focuses on response of the host to endotoxin, recent knowledge about the target cells and receptors for LPS, mechanisms of innate immune response and cell signal transduction due to the LPS recognition. It also summaries results of studies on LPS structure influence on its biological activity.
20

Eicosanoid regulation of pulmonary innate immunity post-hematopoietic stem cell transplantation

75%
Ballinger M. N., McMillan T. R., Moore B. B.
Archivum Immunologiae et Therapiae Experimentalis
|
2007
|
vol. 55
|
issue 1
1-12
EN
Hematopoietic stem cell transplantation (HSCT) is a therapeutic option for a number of malignant and inherited disorders. However, the efficacy of this therapy is limited by a number of serious infectious and noninfectious complications. Pulmonary infections represent a significant cause of morbidity and mortality post-HSCT and can occur both pre- and post-hematopoietic reconstitution. Susceptibility to Gram-negative bacterial infections despite full hematopoietic engraftment suggests that innate immunity remains impaired months to years post-HSCT. This review will describe the process and complications of HSCT and will summarize what is known about innate immune reconstitution post-HSCT. Data from the literature as well as our own laboratory will be presented to suggest that an eicosanoid imbalance characterized by over-production of prostaglandins and under-production of leukotrienes leads to impaired lung phagocyte function post-HSCT. Of therapeutic interest, strategies which limit production of prostaglandins can improve pulmonary host defense in animal HSCT models, which suggests that this may also be beneficial for human HSCT recipients.
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