Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0036690 (sepsis)
 59,461 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The tonsils are portal of entry and a site of multiplication and persistence for a variety of pathogens, including Streptococcus suis (S. suis), which is a common cause of meningitis, septicemia and arthritis in pigs. Understanding the early changes that occur in the first barrier of the tonsil, i.e. the crypt epithelium, in response to S. suis infection is critical in clarifying the pathogenesis of this disease and for the future development of efficient methods of mucosal vaccination. In this study, we investigated the early changes, from 18 to 72 h, that occur in leucocyte subpopulations of the crypt epithelium of the palatine tonsils of 3-week-old pigs in response to S. suis type 2 infection. Monoclonal antibodies against leucocyte markers CD3, CD4, CD8, gammadelta T cell receptor, lambda-immunoglobulin light-chain, myeloid cells, and major histocompatibility complex class II molecule (MHC-II) were used in an avidin-biotin immunoperoxidase technique. An increase in the number of lambda-immunoglobulin light-chain positive cells (B cell subset) was noticed in crypts of S. suis-infected animals from 18 h after infection onwards. This increase was significant at 18 and 48 h after infection. The number of CD4 and CD8 cells was greater from 18 h onwards, with a significant increase at 24 and 72 h post-infection. No significant difference in numbers of CD3, gammadelta T cell receptor and MHC-II positive cells was detected in the crypts of infected animals compared to controls. Macrophages, neutrophils and crypt epithelial cells stained positively with the myeloid marker, and the area of crypt epithelium positive for this marker was increased in the crypts of infected animals, with a significant difference detected at 24 and 72 h after infection. These results suggest that there is participation of the innate immunity in the early phase of S. suis infection, represented by neutrophils, macrophages and likely epithelial cells, and that there is a potential for the initiation of both humoral and cellular responses against S. suis within the crypt epithelium of the palatine tonsil.
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PMID:Changes in the leucocyte subpopulations of the palatine tonsillar crypt epithelium of pigs in response to Streptococcus suis type 2 infection. 1205 42

In a 1 year study, 342 patients admitted to the Burns Unit at Queen Elizabeth Central Hospital (QECH), Blantyre, Malawi underwent a voluntary HIV test. Forty (11.7%) tested HIV positive: of those aged above 15 years, 31% (34 out of 112) were HIV positive, whilst 3% (6 of 231) aged under 15 were HIV positive of whom the majority were in those aged under 5 years (5 of 125, 4%). Patients who were HIV positive had an increased risk of death (P=0.04) which was mainly due to sepsis, but those HIV patients, who did not develop infection or recovered from an episode of sepsis, had similar hospital stay, need for skin grafting and graft take as nonHIV patients. There was no difference in pathogens cultured from wound swabs taken from HIV positive and negative patients. HIV positive patients had significantly lower CD4 counts as compared to HIV negative patients (mean 383mm3 (S.D. 320) and 937mm3 (S.D. 497), respectively). However, low CD4 counts were also found in the HIV negative patients (mean 901, range 131-1964) and 24% had CD4 <500/mm3. Both HIV status and the total body surface area (TBSA) burned were independent predictors of CD4 count. TBSA was an independent risk factor for death (odds ratio 1.3; 95% CI 1.1, 1.4). In patients with TBSA burns of over 30%, mortality approached 100% irrespective of HIV status, but in patients with burns of 11-20% TBSA and who were HIV positive have a mortality of 25% compared to 12% in HIV negative patients; for 21-30% TBSA burns mortality was 100% compared to 50% for HIV positive and HIV negative patients, respectively.
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PMID:The prevalence of HIV infection among burn patients in a burns unit in Malawi and its influence on outcome. 1254 46

Abscess formation associated with intra-abdominal sepsis causes severe morbidity and can be fatal. Previous studies have implicated T cells in the pathogenesis of abscess formation, and we have recently shown that CD4(+) T cells activated in vitro by zwitterionic capsular polysaccharides from abscess-inducing bacteria such as Staphylococcus aureus and Bacteroides fragilis initiate this host response when transferred to naive rats. In this study, we show that mice deficient in alphabetaTCR-bearing T cells or CD4(+) T cells fail to develop abscesses following challenge with B. fragilis or abscess-inducing zwitterionic polysaccharides, compared with CD8(-/-) or wild-type animals. Transfer of CD4(+) T cells from wild-type mice to alphabetaTCR(-/-) animals reconstituted this ability. The induction of abscesses required T cell costimulation via the CD28-B7 pathway, and T cell transfer experiments with STAT4(-/-) and STAT6(-/-) mice demonstrated that this host response is dependent on STAT4 signaling. Significantly higher levels of IL-17, a proinflammatory cytokine produced almost exclusively by activated CD4(+) T cells, were associated with abscess formation in Th2-impaired (STAT6(-/-)) mice, while STAT4(-/-) mice had significantly lower levels of this cytokine than control animals. The formation of abscesses was preceded by an increase in the number of activated CD4(+) T cells in the peritoneal cavity 24 h following bacterial challenge. Confocal laser-scanning microscopy analysis revealed that CD4(+) T cells comprise the abscess wall in these animals and produce IL-17 at this site. Administration of a neutralizing Ab specific for IL-17 prevented abscess formation following bacterial challenge in mice. These data delineate the specific T cell response necessary for the development of intra-abdominal abscesses and underscore the role of IL-17 in this disease process.
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PMID:CD4+ T cells mediate abscess formation in intra-abdominal sepsis by an IL-17-dependent mechanism. 1257 64

The authors report a retrospective study about 92 cases of HIV-1 infections among adult tunisian women hospitalised or consulting in the department of infectious diseases at Rabta hospital over a period of 15 years and 6 months. The middle age is 33.2 years. 64.1% of patients are married, and the conjoint is HIV-1 positive in 84.1% of cases. The route of transmission is sexual in 75%, parenteral in 22.8% and unknown in 2.2%. According to CD4 level and clinical symptoms, patients are at AIDS stage in 75.5%. The main clinical symptoms are: oral candidiasis in 92.4%, diarrhea in 54.3%, pneumocystis carinii pneumoniae in 11.9%, cerebral toxoplasmosis in 10.9%, septicemia caused particularly by salmonella in 9.7%, tuberculosis in 6.7%, cryptococcal meningitis in 4.3% an Kaposi's sarcoma in 3.2%. Mother to child HIV transmission is found in 33.3%, and the mortality is noted in 43.5% of cases.
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PMID:[AIDS in Tunisian women. Study of 92 cases]. 1261 50

Sepsis causes lymphopenia which is inversely correlated with patient survival. The role of apoptosis-specific immune-activation and activation-induced cell-death in sepsis is incompletely understood. Fifteen septic patients and 20 healthy controls were included. T-cell proliferation was measured by [3H]thymidine uptake. Apoptosis and cell phenotype were determined by FACS. sTNFR1, sCD95, interleukin-1beta converting enzyme (sICE), and interleukin (IL)-10 were measured by ELISA. PHA and CD3-driven T-cell proliferation were significantly decreased in septic patients. The percentages of CD3(+) and CD4(+) T cells and CD19(+) B cells were significantly reduced. Percent memory T-cells (CD45RO(+)) and cells undergoing apoptosis (CD95(+)/annexin-V(+)) were significantly increased in sepsis. Moreover, sCD95, sTNFRI, and ICE were significantly increased. Anti-CD3 antibody triggering induced a 56% increase of CD4 T-cell death in septic patients vs. 7.5% in controls relative to IgG. Serum level of IL-10, a Th2 cytokine, was enhanced. These findings strongly suggest that in septic patients Th1 T-cells are selectively susceptible to undergo apoptosis. This observation provides an additional pathophysiological concept in the genesis of Th2 dominance.
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PMID:Susceptibility to programmed cell death in T-lymphocytes from septic patients: a mechanism for lymphopenia and Th2 predominance. 1292 95

This retrospective study evaluated complications associated with caesarean section in HIV-infected women. For each HIV-positive patient ( n=45) a control group of ten seronegative women ( n=450) was matched for age, number of foetuses, gestational age, indication for caesarean section, status of the membranes and kind of anaesthesia. All women delivered in the same hospital using a uniform protocol. We evaluated the duration of stay in hospital after operation, the need for antibiotics after caesarean section, the incidence of minor postoperative complications (mild anaemia, mild temperature or fever 24 h after surgery, wound haematoma or infection, urinary tract infection, endometritis) and major postoperative complications (severe anaemia, pneumonia, pleural effusion, peritonitis, sepsis, disseminated intravascular coagulation, thromboembolism). Most HIV-positive women (64.5%) had a complicated recovery after surgery. A higher incidence of major and minor postoperative complications were observed in the HIV-positive group than in the control group. There was a statistically significant greater incidence of mild anaemia, mild temperature or fever, urinary tract infection and pneumonia in the HIV-positive group. HIV-positive women with less than 500x10(6) CD4(+) lymphocytest/l had higher post-caesarean section morbidity than HIV-positive women with more than 500x10(6) CD4(+) lymphocytest/l. The median duration of hospital stay was significantly higher in the HIV-positive group (median 7 days) than in the HIV-negative group (median 4 days). The rate of HIV vertical transmission was 8.8%. Higher post-caesarean section morbidity was found in HIV-positive women than in controls. Unfortunately, the HIV-positive women (with low CD4 lymphocytes counts), whose infants theoretically will benefit most from caesarean delivery, are also the women who are most likely to experience post-operative complications.
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PMID:Post-operative complications after caesarean section in HIV-infected women. 1450 67

We have previously demonstrated that the detergent Tyloxapol is effective in preventing reactions to endotoxin. We studied the effects of Tyloxapol on the morbidity and mortality from endotoxemia in rabbits and on the mortality in rats with sepsis. The effects of Tyloxapol on endotoxin binding and macrophage activation were studied in the macrophage cell line RAW264.7 and CHO cells expressing CD14. Isolated human leukocytes were used to study the effects of Tyloxapol on immune reactions, leukocyte motility, and phagocytosis. Intravenous Tyloxapol (200 mg/kg), given prior to or at the time of endotoxin infusion protected rabbits from developing shock. In rats with peritoneal sepsis, a lipid-rich diet and Tyloxapol given at the time of induction of peritonitis protected them from septic death. In vitro, Tyloxapol blocked the binding of endotoxin to murine macrophages and CHO cells expressing CD14, activation of macrophages, and also some antigen-antibody immune reactions (mediated by CD2, CD4, CD22, HLA-DR). Tyloxapol may prevent the reaction to endotoxin by desensitizing endotoxin-recognizing receptors.
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PMID:Tyloxapol attenuates the pathologic effects of endotoxin in rabbits and mortality following cecal ligation and puncture in rats by blockade of endotoxin receptor-ligand interactions. 1452 71

Citrobacter rodentium uses virulence factors similar to the enteropathogenic Escherichia coli to produce attaching and effacing lesions in the distal colon of mice. We used this infection model to determine components of adaptive immunity needed to survive infection. During acute infection, wild-type mice develop breaks across infected epithelial surfaces but resolve infection. Surprisingly, mice markedly deficient in mucosal lymphocyte populations from beta(7) integrin deficiency resolve infection, as do CD8alpha-/- or TCR-delta-/- mice. In contrast, CD4-/- or TCR-beta-/- mice develop polymicrobial sepsis and end-organ damage, and succumb during acute infection, despite epithelial damage similar to wild-type mice. B cell-deficient (MuMT-/-) or B and T cell-deficient (recombinase-activating gene 2-/-) mice develop severe pathology in colon and internal organs, and deteriorate rapidly during acute infection. Surviving mice develop robust Citrobacter-specific serum IgM responses during acute infection, whereas mice that succumb do not. However, CD4-/- mice receiving serum Igs from infected wild-type mice survive and clear the infection. Our data show that survival of apparently self-limited and luminal mucosal infections requires a systemic T cell-dependent Ab response against bacteria that enter through damaged mucosa. These findings have implications for understanding host defense against mucosal infections, including the pathogenesis of these diseases in immunocompromised populations.
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PMID:Critical role of T cell-dependent serum antibody, but not the gut-associated lymphoid tissue, for surviving acute mucosal infection with Citrobacter rodentium, an attaching and effacing pathogen. 1468 52

We have generated transgenic mice expressing the leech anticoagulant hirudin and human tissue factor pathway inhibitor tethered to the cell surface by fusion with fragments of human CD4 and P-selectin. Expression of the transgenes is under the control of the CD31 (platelet endothelial cell adhesion molecule [PECAM]) promoter, limiting expression to endothelial cells, monocytes, and platelets. In addition, the P-selectin sequence directs expression to secretory granules. Functional cell surface expression only occurs when the cells are activated. In a mouse model of systemic lipopolysaccharide (LPS)-induced endotoxemia, we show that expression of either anticoagulant on activated endothelium inhibits the widespread intravascular thrombosis, thrombocytopenia, and consumptive coagulopathy associated with endotoxemia. Importantly, non- LPS-treated transgenic mice had normal baseline bleeding times. We speculate that targeted delivery of anticoagulants to the endothelium may be a strategy worth pursuing in clinical sepsis to improve efficacy of systemic anticoagulation while minimizing potential hemorrhagic side effects.
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PMID:Inhibition of intravascular thrombosis in murine endotoxemia by targeted expression of hirudin and tissue factor pathway inhibitor analogs to activated endothelium. 1512 22

The physiological alterations induced by acute inflammation present significant management challenges for anaesthesiologists. Major surgery, trauma, burns and sepsis all have large inflammatory components. Acute inflammation is characterized by vasodilatation, fluid exudation and neutrophil infiltration. These processes are activated and amplified by a series of intracellular and extracellular factors that tightly co-ordinate the inflammatory process. The innate immune system responds rapidly to infection or injury. Macrophages, natural killer cells, CD8 + T-lymphocytes and neutrophils provide an early response to injurious factors in an effort to contain and eliminate harmful stimuli. The adaptive immune response requires prior exposure to microbial antigens, is mediated primarily by CD4 + T-lymphocytes and serves to further amplify acute inflammation. Although acute inflammation is fundamentally beneficial, severe inflammation can precipitate the systemic inflammatory response syndrome. This syndrome is characterized by hyperinflammation and can cause organ injury, shock and death in its most severe forms. Overall, our understanding of inflammation has increased tremendously during the past 20 years. However, these basic science advances have not yet translated into widespread benefit for patients suffering from trauma, sepsis and systemic inflammation.
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PMID:Mechanisms of the inflammatory response. 1521 35


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