Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0043167 (pertussis)
 19,595 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Infection of target cells by HIV-1 requires initial binding interactions between the viral envelope glycoprotein gp120, the cell surface protein CD4, and one of the members of the seven-transmembrane G protein-coupled chemokine receptor family. Most primary isolates (R5 strains) use chemokine receptor CCR5, but some primary syncytium-inducing, as well as T cell line-adapted, strains (X4 strains) use the CXCR4 receptor. Signaling from both CCR5 and CXCR4 is mediated by pertussis toxin (PTX)-sensitive G(i) proteins and is not required for HIV-1 entry. Here, we show that the PTX holotoxin as well as its binding subunit, B-oligomer, which lacks G(i)-inhibitory activity, blocked entry of R5 but not X4 strains into primary T lymphocytes. Interestingly, B-oligomer inhibited virus production by peripheral blood mononuclear cell cultures infected with either R5 or X4 strains, indicating that it can affect HIV-1 replication at both entry and post-entry levels. T cells treated with B-oligomer did not initiate signal transduction in response to macrophage inflammatory protein (MIP)-1beta or RANTES (regulated upon activation, normal T cell expressed and secreted); however, cell surface expression of CCR5 and binding of MIP-1beta or HIV-1 to such cells were not impaired. The inhibitory effect of B-oligomer on signaling from CCR5 and on entry of R5 HIV-1 strains was reversed by protein kinase C (PKC) inhibitors, indicating that B-oligomer activity is mediated by signaling events that involve PKC. B-oligomer also blocked cocapping of CCR5 and CD4 induced by R5 HIV-1 in primary T cells, but did not affect cocapping of CXCR4 and CD4 after inoculation of the cultures with X4 HIV-1. These results suggest that the B-oligomer of PTX cross-deactivates CCR5 to impair its function as a coreceptor for HIV-1.
 ...
PMID:The B-oligomer of pertussis toxin deactivates CC chemokine receptor 5 and blocks entry of M-tropic HIV-1 strains. 1047 44

We prospectively followed 725 children under 2 years of age with laboratory-diagnosed Bordetella pertussis infection to investigate the hospitalization rate and complications. Diagnosis was made by culture and polymerase chain reaction (PCR) from nasopharyngeal swabs in 11,016 children who presented with > or = 7 days of cough at 63 pediatric practices in Germany. Of these children, 33 (4.5%) were hospitalized at a mean age of 4.8 months (range, 17 days to 19.5 months). Complications occurred in 16 (48%) of the 33 patients. Pneumonia developed in two (6%) children and a convulsion was observed in one (3%). Intensive care monitoring was required for 23 (70%) children. Further complications were bradycardia (21%), apnea (12%), conjunctivitis (12%), loss of weight (12%), otitis media (6%), atelectasis (3%) and dehydration (3%). Children aged 6-24 months who had not received any dose of pertussis vaccine had a ten-fold increased risk of hospitalization compared to those who had been partially or fully immunized (p < 0.05). Pertussis immunization should be given at an early point in time and completely in order to prevent severe courses of pertussis and hospitalization in young children.
Infection
PMID:Hospitalization and complications in children under 2 years of age with Bordetella pertussis infection. 1078 97

A total of 133 pertussis cases were studied during an outbreak in Basra from June to December 1996. Most were females and were immunized. Bordetella spp. was isolated in 48.1% of the cases. The isolation rate was highest among infants and decreased with increasing age, and was highest during the catarrhal stage. B. pertussis was the most common species; however, B. parapertussis infection did occur. There were some severe cases of pertussis among infants caused mainly by B. pertussis and dual Bordetella infection. Infection was transmitted by close contact with a pertussis case.
 ...
PMID:Outbreak of pertussis in Basra, Iraq. 1079 32

The human respiratory tract pathogen Bordetella pertussis is the major cause of whooping cough in infants and young children, and also causes chronic cough in adults. B. pertussis infection damages ciliated epithelium in the respiratory tract. However, the interaction of the bacterium with the respiratory mucosa is poorly understood, and previous studies have either utilized animal tissue which may not be appropriate, or isolated cell systems which lack the complexity of the respiratory mucosa. We have studied the interaction of B. pertussis strain BP536 with human nasal turbinate tissue in an air-interface organ culture over 5 days. We have also compared infection by BP536 with two other strains, Tohama I and CN2992, to determine whether the interactions observed with BP536 are consistent, and, in both nasal turbinate and adenoid organ cultures at 24 h, to determine whether there were differences between tissue from different parts of the respiratory tract. BP536 adhered to cilia, most commonly at their base, and disorganized their spatial arrangement, they also adhered to damaged tissue and mucus, but very rarely to unciliated cells. Within the first 24 h there was a five-fold increase in bacterial density on ciliated cells, and the total number of adherent bacteria increased up to 96 h. Infection caused increased mucus at 24h and an increase in damaged epithelium from 72 h which involved both ciliated and unciliated cells. The number of residual ciliated cells did not decrease after 72 h. The three different strains of B. pertussis exhibited similar interactions with the mucosa, and there was no tissue specificity for adenoid or turbinate tissue. We conclude that B. pertussis adhered to multiple sites on the mucosa and caused hypersecretion and epithelial damage which are the pathological changes described in vivo.
 ...
PMID:Interaction of Bordetella pertussis with human respiratory mucosa in vitro. 1095 56

Filamentous hemagglutinin (FHA) is a dominant cell surface-associated Bordetella pertussis adhesin. Recognition that this protein is secreted in significant amounts and that bacterial adhesins may have other activities, prompted an assessment of FHA effects on human macrophages. Incubation of human macrophage-like U937 cells with preparations of FHA resulted in dose-dependent cytotoxicity, with death of 95% of treated cells after 24 h. Based on the use of four independent methods, death of these cells could be largely attributed to apoptosis. FHA-associated apoptosis was also observed in THP-1 macrophage-like cells, fresh human peripheral blood monocyte-derived macrophages (MDM), and BEAS-2B human bronchial epithelial cells. Infection of MDM with wild-type B. pertussis resulted in apoptosis within 6 h, while infection with an FHA-deficient derivative strain was only 50% as effective. FHA-associated cytotoxicity was preceded by host cell secretion of tumor necrosis factor alpha (TNF-alpha), a potential proapoptotic factor. However, pretreatment of cells with a neutralizing anti-TNF-alpha monoclonal antibody inhibited only 16% of the FHA-associated apoptosis. On the other hand, a blocking monoclonal antibody directed against TNF-alpha receptor 1 inhibited FHA-associated apoptosis by 47.7% (P = 0.0001), suggesting that this receptor may play a role in the death pathway activated by FHA. Our in vitro data indicate that secreted and cell-associated FHA elicits proinflammatory and proapoptotic responses in human monocyte-like cells, MDM, and bronchial epithelial cells and suggest a previously unrecognized role for this prominent virulence factor in the B. pertussis-host interaction.
 ...
PMID:Proinflammatory and proapoptotic activities associated with Bordetella pertussis filamentous hemagglutinin. 1125 31

Infection with tissue-migrating helminths is frequently associated with intense granulocyte infiltrations. Several host-derived factors are known to mediate granulocyte recruitment to the tissues, but less attention has been paid to how parasite-derived products trigger this process. Parasite-derived chemotactic factors which selectively recruit granulocytes have been described, but nothing is known about which cellular receptors respond to these agents. The effect of products from the nematodes Ascaris suum, Toxocara canis, and Anisakis simplex on human neutrophils were studied. We monitored four parameters of activation: chemotaxis, cell polarization, intracellular Ca(2+) transients, and priming of superoxide anion production. Body fluids of A. suum (ABF) and T. canis (TcBF) induced strong directional migration, shape change, and intracellular Ca(2+) transients. ABF also primed neutrophils for production of superoxide anions. Calcium mobilization in response to A. suum-derived products was completely abrogated by pretreatment with pertussis toxin, implicating a classical G protein-coupled receptor mechanism in the response to ABF. Moreover, pretreatment with interleukin-8 (IL-8) completely abrogated the response to ABF, demonstrating desensitization of a common pathway. However, ABF was unable to fully desensitize the response to IL-8, and binding to CXCR1 or CXCR2 was excluded in experiments using RBL-2H3 cells transfected with the two human IL-8 receptors. Our results provide the first evidence for a direct interaction between a parasite-derived chemotactic factor and the host's chemotactic network, via a novel G protein-coupled receptor which interacts with the IL-8 receptor pathway.
 ...
PMID:Ascaris suum-derived products induce human neutrophil activation via a G protein-coupled receptor that interacts with the interleukin-8 receptor pathway. 1134 70

Infection with Bordetella pertussis, the causative agent of pertussis (whooping cough) in humans, is followed by the production of antibodies of several isotypes, including immunoglobulin A (IgA). Little is known, however, about the role of IgA in immunity against pertussis. Therefore, we studied targeting of B. pertussis to the myeloid receptor for IgA, FcalphaRI (CD89), using either IgA purified from immune sera of pertussis patients or bispecific antibodies directed against B. pertussis and FcalphaRI (CD89 BsAb). Both IgA and CD89 BsAb facilitated FcalphaRI-mediated binding, phagocytosis, and bacterial killing by human polymorphonuclear leukocytes (PMNL) and PMNL originating from human FcalphaRI-transgenic mice. Importantly, FcalphaRI targeting resulted in enhanced bacterial clearance in lungs of transgenic mice. These data support the capacity of IgA to induce anti-B. pertussis effector functions via the myeloid IgA receptor, FcalphaRI. Increasing the amount of IgA antibodies induced by pertussis vaccines may result in higher vaccine efficacy.
 ...
PMID:Immunoglobulin A-mediated protection against Bordetella pertussis infection. 1144 59

In the first half of the 20th century, improved living conditions, preventive measures, vaccines and antibiotics led to a marked reduction in morbidity and mortality from infectious diseases. It was predicted that the conquest of all infectious diseases was imminent. However, 50 years later, in 1999, they were still the major cause of disease worldwide, and caused nearly one third of all deaths (a total of 55.9 million). The eradication of smallpox in the 1970s and the approaching eradication of poliomyelitis represent major achievements. The prevalence of measles, pertussis and tetanus neonatorum is also markedly reduced, but still 1.5 million children in developing countries die each year because of lack of vaccines. Malaria and tuberculosis are re-emerging. Tuberculosis and HIV/AIDS are the diseases with known aetiology that cause most deaths, altogether 5 million each year. Respiratory and gastrointestinal infections cause 6.5 million deaths annually. Infections in the immunocompromised host have become a "trade mark" of today's advanced medicine. Almost every year, new diseases related to new micro-organisms are described; over the last 30 years, approximately 40 new diseases/micro-organisms have been diagnosed. Among the best known are HIV/AIDS, peptic ulcer caused by Helicobacter pylori, Legionnaires' disease, borreliosis (Lyme disease), hepatitis C, gastroenteritis caused by rotavirus, and Ebola haemorrhagic fever. Antimicrobial resistance development of micro-organisms has become one of the major health problems worldwide; a number of preventive measures are being introduced.
 ...
PMID:[Microorganisms strike back--infectious diseases during the last 50 years]. 1180 14

Infection by Helicobacter pylori causes an acute inflammatory response followed by a chronic infection of the human gastric mucosa. A neutrophil-activating protein (HP-NAP) has been identified in H.pylori, and its role in infection and immune response is currently under investigation. Here, we show that HP-NAP induces beta-hexosaminidase release and interleukin-6 production in peritoneal mast cells, two actions which are completely inhibited by pertussis toxin. We also show that in polarized epithelial cell monolayers HP-NAP translocates from the apical to the basolateral domain, where mast cells are located. These findings characterize HP-NAP as an inflammatory factor of H.pylori that is effective from the beginning of the inflammatory cascade.
 ...
PMID:The neutrophil-activating protein (HP-NAP) of Helicobacter pylori is a potent stimulant of mast cells. 1185 41

Host resistance to the intracellular protozoan Toxoplasma gondii is highly dependent on early IL-12 production by APC. We demonstrate here that both host resistance and T. gondii-induced IL-12 production are dramatically reduced in mice lacking the adaptor molecule MyD88, an important signaling element used by Toll-like receptor (TLR) family members. Infection of MyD88-deficient mice with T. gondii resulted in uncontrolled parasite replication and greatly reduced plasma IL-12 levels. Defective IL-12 responses to T. gondii Ags (soluble tachyzoite Ag (STAg)) were observed in MyD88(-/-) peritoneal macrophages, neutrophils, and splenic dendritic cells (DC). In contrast, DC from TLR2- or TLR4-deficient animals developed normal IL-12 responses to STAg. In vivo treatment with pertussis toxin abolished the residual IL-12 response displayed by STAg-stimulated DC from MyD88(-/-) mice. Taken together, these data suggest that the induction of IL-12 by T. gondii depends on a unique mechanism involving both MyD88 and G protein-coupled signaling pathways.
 ...
PMID:Cutting edge: MyD88 is required for resistance to Toxoplasma gondii infection and regulates parasite-induced IL-12 production by dendritic cells. 1205 6


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>